Cattle Flashcards

0
Q

What are the benefits of a compact calving pattern?

A

Even batches of calves to rear > easy management of calves, efficient feeding of calves
Cows at same stage of pregnancy and lactation - efficient feeding of cows and efficient supervision at calving > easy calvings, fewer deaths, fertile cows for rebreeding. Good milk supply, calves of optimum birthweight, fewer difficult calvings, healthy calves with a high potential for growth, cows in correct body condition, fertile cows for re breeding.

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1
Q

What is the aim of an efficient beef suckler herd?

A

To calve the herd over a short season 9-12 weeks at the same tim each year and wean one calf per cow.

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2
Q

How can you achieve a compact calving period?

A

Have fertile cows, cycling at the start of breeding period, have fertile bulls run with cows for a restricted breeding period (9-10 weeks), have a good replacement heifer breeding policy, avoid introducing infectious infertility diseases.

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3
Q

How can cow fertility be maximised?

A

Key to beef cow fertility is in nutritional management. when calculating winter rations for beef cows one must make allowance for maintenance, pregnancy and lactation requirements. cows in good body condition can be allowed to mobilise body fat to contribute to daily ME requirement and save on feed costs. Body condition score BCS at calving directly related to post calving anoestrus period/fertility. Cows BCS 2 or less at calving les likely to conceive during a restricted mating period as may be anoestrus during much of breeding period. aim for target condition scores at key times of the year. Seperate off thin cows and feed extra or wean early, ensure adequate trace element vitamin mineral supplementation. copper and selenium may often require supplemenation. avoid sudden changes in level of feeding untill 6 weeks post mating period. minimise periparturient problems eg dystocia. have control measures to avoid introduction of infectious diseases that may affect fertility e.g venereal campylobacter, leptospirosis, BVD, IBR. Pd cows 6-8 weeks after end of breeding period and plan culling poly.

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4
Q

How should bulls be selected?

A

Ideal bull produces calves that are born easily, grow rapidly and produce carcases of good conformation. estimated breeding values available for common breeds to aid bull selected as they assess the genetic potential of an animal. BLUP (best linear unbiased prediction) system utilises data from performance records of the animal itself, its relatives and progeny and removes environmental effects where possible. Newly purchased young bulls should be screened for BVD status and if >2 yo for johnes and or where possible sourced from disease free herd. other disease screening eg, IBR, lepto depends on herd status and may simply choose to vaccinate. Hire bulls and non virgin mature bulls are a major disease risk especially campylobacter fetus venerealis.

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5
Q

Describe a breeding soundness evaluation for bulls

A

Ideally all bulls should have annual breeding soundness assessment to help avoid economic losses due to use of infertile bulls.
1 - physical examination, general health, musculoskeletal system.
2 - reproductive system examination - visual appraisal of scrotum shape. measure scrotal circumference (in general over 15 months >31cm, over 2yo > 34 cm, separate breed standards available), Palpate testicles and epididymides carefully (orchitis, epididymitis, edegeneration), palpate accessory sex glands (vesiculitis), palpate sheath and inspect tip of penis (haematoma, trauma, phymosis, persistent frenulum, fibropapilloma).
3. Semen evaluation - collect semen by electro ejaculation, artificial vagina or rectal massage and assess volume/density, motility, gross and progressive, minimum 60% progressive motiity) and % normal sperm morphology (minimum 70% normal), handling of semen sample is critical (temperature.
4. Serving capacity assessment - need to observe bull mating females to ensure good libido and normal intromission.
A full breeding soundness evaluation should include all 4 components but even doing parts 1 and 2 will help to ensure unsound bulls are not used.

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6
Q

What bull to cow ratio should be used?

A

young bull - 20/30 cows max

Mature bull - 40/50 cows max

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7
Q

What general management should be used for bulls?

A

Nutrition - young bulls <2 1/2 years old require fed for maintenance and growht. bulls should be fit not fat.
Housing - when not working keep in well fenced, outdoor paddock or bull pen with exercise area. foot care - regular foot trimming essential. lameness is most common problem of bulls. don forget to include bulls in herd vaccination and worming programmes.

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8
Q

Describe replacement heifer breeding management

A

Best source of replacements is to buy yearling bulling heifers from known source. aim is to have heifers calving down at 2-21/2 year old to easy calving bull in good body condition, 2-3 weeks ahead of main herd calving period. isolate from main herd for 2-3 weeks and screen purchased replacements for BVD status, vaccinate for leptospirosis, BVD, IBR depending on herd health status, check for freemartins/non breders and misalliance pregnancies. Ensure adequate nutrition prior to and during mating period. feed for maintenance and growth. aim for critical minimum mating weight at first service of around 65% of mature cow weight. ensure no trace element deficiencies or parasite problems prior to mating. mate with easy calving bull for 6-7 weeks only. PD and remove non pregnant heifers for sale. Feed during pregnancy for CS3 at calving, too fat - dystocia, too thin - extended post partum anoestrus. if possible run first calvers as a separate group untill pregnant again.

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9
Q

What are the advantages and disadvantages of AI?

A

Advantages - allows use of best bulls with known EBVs for various traits. reduces costs of keeping stock bulls, removes risk of venereally transmitted diseases. may tighten calving period as all cows receive first service on day 1 of breeding period. Disadvantages - heat detection may be a problem if not using fixed time AI, handling for AI, cost.

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10
Q

Describe the double prostaglandin injection for oestrus synchronisation?

A

Double prostaglandin injection - cows/heifers injected twice with PG, 11 days apart and fixed time AI 72 and 96 hours following second iinjection. best restricted to maiden heifers as results may be poor in cows due to anoestrus at the time of synchrony.

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11
Q

Describe progesterone releasing intravaginal devices for oestrus synchronisation?

A

Device inserted for 8-10 days with prostaglandin luteolytic injection given 1-2 days before device removed. AI at 48 and 72 hours after device removed or once at 56 hours. Progesterone based synchrony is superior in beef cows as it will induce oestrus and ovulation in cows that may be anoestrus. the degree of synchrony is superior to double PG programmes especially if GnRH injection is given at the time of CIR insertion to cause emergence of a new follicular wave.

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12
Q

How do you maximise pregnancy rate with fixed time AI?

A

Ensure cows/heifers on a good steady plane of nutrition and cyclical before synchrony and for six weeks following AI. ensure no trace element deficiencies parasite problems and that infectious diseases controlled, have good handling system for AI etc, minimise stress, will get higher pregnancy rates if use double AI. realistic pregnancy rates achieved to synchronised AI, cows 55-65% and heifers 65-75%.

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13
Q

What are the key targets indicating high fertility performance in a beef herd?

A

Barren cow rate 65%, calf crop > 94%.

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14
Q

What is the average milk price in the EU?

A

31ppl

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15
Q

What are the aims and objectives of preventative medicine?

A

Optimising health status, by prevention of disease and losses due to subclinical disease. Increased efficiency and productivity, increased longevity by reducing forced culling death rates, ensuring good animal welfare and husbandry, production of good quality produce and ensuring food safety, maximising profitability.

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16
Q

Describe the objectives set in health plans?

A
Must be SMART
Specific
Measurable
Achievable
Relevant
Time  based - met within a reasonable period if not the reasons for failure should be examined. Targets can be set using data from standard texts. They must be up to date and specific for each individual farm. The costs for some of the most important disease conditions have been worked out and thus the value of these targets can be demonstrated to the farmer.
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17
Q

Describe the overview components of a preventative medicine programme

A

Objectives - defining objectives is a basic component of any preventative medicine programme and the key point is that these vary from farm to farm. Each farm must be treated as an individual. The targets must be agreed between the farmer and the vet. Implementation of a programme - data evaluation - method of recording farm health data to assess current performance. Clinical examination of the animals. Farm inspection - will concentrate on management of the farm and includes ration evaluation, feeding and pasture management, milking routine. Decision making - based on monitoring, evaluation and interpretation of all the factors discussed in implementation of your advice. Follow up.

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18
Q

What are the different sections of a preventative medicine or health plan?

A
  1. DEtails of farm. 2 current production data. 3. production targets - monitoring and recording of past and current performance. Setting of targets in context of farm and husbandry erformance. 4. reproductive performance. 5. nutritional management. although detailed nutritional management and ration formulation is usually left to Nutritional advisers. Health plans should incorporate regular body scoring, use of metabolic profiles, advice on changes in ration etc. 6. replacement policy -will vary depending on whether or not the farm is closed or not. 7. Disease contorl. 8. Control of infectious disease. 9.Parasite control - may be necessary for endo parasites such as gastrointestinal, lungworm, fasciolosis, ectoparasites such as lice, sheep scab, mange mites, blowfly and tick borne diseases. 10. neonatal care. 11. Biosecurity. 12. Medicines usage. 13. Stockmanship and management. 14. Calendar of health plan.
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19
Q

Describe the Biosecurity measures which help in the control and even eradication of diseases resulting in reduced drug usage and increased profitability?

A

Maintain a closed herd/flock. Most common source of new diseases. Operate an isolation policy for purchased stock - ideally animals should be bought from a herd/flock of known health status that matches that of the receipient herd. Purchased stock should be isolated away from all other stock for a minimum period of 4 weeks and regularly inspected for signs of disease. 3. Provide clean feed and water -food and water eg streams, rivers and flooded pastures may all represent a risk and the introduction of disease e.g salmonella, liver fluke. 4. Control visitors and vehicles - high risk visitors including lambing help, contractors, veterinary surgeons, feed companies, knacker services. 5. control rodents and birds, 6. Define and monitor health status in addition to the prevention of new infections the herd/flock needs to be monitored regularly to assess the health status. Operate a disease control programme which involves vaccination, strategic medication, culling, husbandry and nutritional advice.

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20
Q

What is the average lifespan of a dairy cow?

A

Only 3.04 lactations. The overall culling rate remains constant at about 20-24%.

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21
Q

What are the main reasons for culling?

A

Forced or involuntary culls - These are animals that must be culled due to death disease or poor reproductive performance and represent over half of all cows culled. the three most common reasons are infertility, mastitis and lameness. Selected or voluntary culls - these are animals that the farmer chooses to cull for reasons such as poor milk yield, old age, poor conformation, temperament etc. the ideal situation is for the dairy farmer to minimise culling through forced reasons and thus have control over which cows are culled. Infetility 4.9%, mastitis 3.5%, lameness 2.2%, age 3.6%, yield 0.9% other including death 6.3%.

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22
Q

What are the major disease problems in UK dairy herdS?

A

Infertility, mastitis and lameness. for every 100 cows per year -
Fertility 26.1, mastitis 37.5, lameness 22.3. They are all associated with peri parturient cow and in particular the metabolic sterss of early lactation. They all have a multifactorial aetiology. they may not be seen as spectacular individual cases but the farmer may be unaware of the extent of the problem. Observed clinical cases are usually only the tip of the iceberg with far greater number of subclinical cases that will be inhibiting milk production. they are inter related and can increase susceptibility to each other e.g a cow with milk fever will be more susceptible to mastitis. They all cost money. Other production diseases include assisted calving, digestive disease including LDAs, hypomagnesaemia, hypocalcaemia, ketosis, lameness, injury.

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23
Q

Describe the two main types of costs associated with disease:

A

Direct costs - treatment cost, veterinary costs, labour costs (herdsmans time), discarded milk (antibiotic withdrawal), reduction in milk yield, mortality.

Indirect costs - increased culling rate, possible risk of fatality, susceptibility to other disease, extended calving interval, extra services per conception.

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24
Q

What is the cost of culling a dairy cow?

A

a farmer will receive approx £600 from the sale of a cull cow. However the cost of replacement heifer is £2000 on average in the UK. other costs that must be taken into account include the lower milk yield from a heifer (14000 litres for the subsequent lactation equating to £322) and the smaller calf from a heifer (£8). Figure in 2012 for the cost of a cull cow range from £1328 for a live cull at the end of lactation to £3307 for a fatality in early lactation. The cost of a fatality is even greater as farmer will not receive any income from dead cow and will pay to get her removed.

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25
Q

What is the cost of infertility to the farmer?

A

Failure to get the cow back in calf when the farmer wants. a 365 day calving interval is still accepted as being the target for the average dairy herd in the UK. The cost of an extra day on the calving interval is often quoted to be £3 per day. This is made up of reduced milk per cow per year as well as reduced calf sales and extra AI costs.

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26
Q

What is the cost of mastitis to the farmer?

A

Although mastitis rates have fallen in the last 40 years, rates have steadied at around 40 cases/100 cows/ year. the major costs are due to treatment costs - relatively minor by herdsman. cost of discarded milk, lower milk yields - reduces lactation by approximately 5% - 15% in severe cases. higher culling rate. 90% of mastitis will be mild, and 0.2% fatal, average cost of mastitis is £201. can be up to £1709 for a fatal case.

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27
Q

What are the costs of lameness to a UK dairy farmer?

A

Main economic losses due to poorer fertility - delayed return to oestrus and poor demonstration of oestrus signs, reduced intakes of food, prolonged NEB in early lactation - increased calving interval, increased number of services per conception. Higher culling rate, lower milk yields 21/2-5%, severe up to 15%. Predisposition to other diseases. An average case of lameness based on 41% digital lameness, 38 interdigital and 21% solar ulcers will cost 178£ ranging from 81- £324 for a solar ulcer.

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28
Q

What is the average cost of a case of milk fever?

A

Costs involved in the majority of cases that respond to farmers treatment alone are relatively low (£40) but can escalate markedly if the case becomes complicated. An average case has been calculated to cost £209.62.

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29
Q

What is the aim of an efficient beef suckler herd?

A

To calve the herd over a short season (9-12 weeks) at the same time each year and wean one calf/cow. The benefits of a compact calving period include - even batches of calves to rear so easy management of calves and efficient feeding of calves. Cows at same stage of pregnancy and lactation so efficient supervision at calving, efficient feeding of cows.

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30
Q

How can a compact calving period be achieved?

A

Have fertile cows, cycling at the start of the breeding period. Have fertile bulls run with cows for a restricted breeding period (9-10 weeks). Have good replacement heifer breeding policy. Avoid introducing infectious infertility diseases.

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31
Q

How can cow fertility be maximised?

A

Key to beef cow fertility is in nutritional management. When calculating winter rations for beef cows one must make allowance for maintenance, pregnancy and lactation requirements. Cows in good body condition can be allowed to mobilise body fat to contribute to daily ME requirement and save on feed costs. One Kg of LWL provides approx 35 MJ/ME to the cow. Body condition score BCS at calving is directly related to post calving Anoestrus period/fertility. Cows BCS 2 or less at calving are less likely to conceive during a restricted mating period as may be anoestrus during much of breeding period. Aim for target condition scores at key times of year. separate off thin cows and feed extra or wean early. Ensure adequate trace element/vitamin/mineral supplementation. copper and selenium may often require supplementation. Avoid sudden changes in level of feeding until 6 weeks post mating period. Minimise peri parturient problems eg dystocia. Have control measures to avoid introduction of infectious diseases that may affect fertility e.g venereal campylobacter, leptospirosis, BVD, IBR. PD cows 6-8 weeks after end of b reeding period and plan culling policy.

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32
Q

How should bulls be selected for optimum fertility?

A

Ideal bull produces calves that are born easilsy, grow rapidly and produce carcases of good conformation. Estimated breeding values available for common breeds to aid in bull selection as they assess the genetic potential of an animal. BLUP system utilises data from performance records of the animal itself, its relatives and progeny and removes environmental effects where possible. Newly purchased young bulls should always be screened for BVD status and if > 2 yo for johnes where possible sourced from disease free herd. Other disease screening e.g IBR, lepto, depends on herd status and may simply choose to vaccinate. Hire bulls and non virgin mature bulls are a major disease risk especially campylobacter fetus venerealis.

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33
Q

Describe a bull breeding soundness evaluation?

A

Should consist of 1. physical examination - general health, musculoskeletal system. 2 Reproductive system examination - visual appraisal of scrotum shape, measure scrotal circumference ( in general over 15 months > 31cm, over 2yo > 34 cm, separate breed standards available.) palpate testicles and epididymides carefully (orchitis, epididymitis, degeneration), palpate accessory sex glands (vesiculitis), palpate sheath and inspect tip of penis (haematoma, trauma, paraphymosis, persistent frenulum, fibropapilloma). 3. semen evaluation - collect semen by electro ejaculation, artificial vagina or rectal massage, and assess volume/density, motility and % sperm morphology. 4. Serving capacity assessment - need to observe bull mating females to ensure good libido and normal intromission. A full breeding soundness evaluation should include all 4 components but even doing parts 1 and 2 will help to ensure unsound bulls are not used.

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34
Q

What should minimum sperm motility and morphology be?

A

60% progressive motility minimum and 70% normal sperm morphology.

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35
Q

What is the appropriate bull to cow ratio?

A

Young bull - 20-30 cows maximum. Mature bull - 40/50 cows maximum.

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36
Q

Describe general management of bulls

A

Nutrition - remember young bulls t forget to include bulls in herd vaccination and worming programmes.

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37
Q

Describe replacement heifer breeding management?

A

Best source of replacements is to buy yearling/bulling heifers from known source. Aim is to have heifers calving down at 2-21/2 years old to easy calving bull in good condition (CS2-3 weeks) ahead of main herd calving period. Isolate from main herd for 3-4 weeks and screen purchased replacements for BVD status, vaccinate for leptospirosis, BVD and IBR, depending on herd health status. Check for freemartins/non breeders and misalliance pregnancies. Ensure adequate nutrition prior to and during mating period. Feed for maintenance and growth (0.7kg/day). Aim for critical minimum mating weight at first service o around 65% of mature cow weight. Ensure no trace element deficiencies or parasite problems prior to mating. Mate with easy calving bull for 6-7 weeks only. PD and remove non pregnant heifers for sale. Feed during pregnancy for CS3 at calving, too fat - dystocia too thin - extended post partum anoestrus. If possible run first calvers as a separate group until pregnant again.

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38
Q

What are the advantages and disadvantages of aI in beef herds?

A

Advantages of AI - allows use of best bulls with known EBVs for various traits. Reduces costs of keeping stock bulls. Removes risk of venereally transmitted diseases. May tighten calving period as all cows receive first service on day 1 of breeding period. disadvantages - heat detection may be a problem if not using fixed time AI, handling for AI etc, cost.

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39
Q

What are the two different oestrus synchronization methods available for fixed time AI?

A

Double prostaglandin injection - cows/heifers injected twice with PG, 11 ays apart and fixed time AI 72 and 96 hours following second injection. Best restricted to maiden heifers as results may be poor in cows due to anoestrus at the time of synchrony.
Progesterone releasing intravaginal devices - Device inserted for 8-10 days with prostaglandin (luteolytic) injection given 1-2 days before device removed. AI at 48 hours and 72 hours after device removed or once at 56 hours. Progesterone based synchrony is superior in beef cows as it will induce oestrus and ovulation in cows that may be anoestrus. The degree of synchrony is superior to double PG programmes especially if GnRH injection is given at the time of CIDR insertion to cause emergence of a new follicular wave.

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40
Q

How can you maximise pregnancy rate with fixed time AI?

A

Ensure cows/heifers on a good steady plane of nutrition and cyclical before synchrony and for six weeks following AI. Ensure no trace element deficiencies/parasite problems and that infectious diseases are controlled. Have good handling system for AI etc, minimise stress. will get higher pregnancy rates if using double AI. Realistic pregnancy rates achieved to synchronise AI - cos 55-65% and heifers 65-75%.

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41
Q

Describe a typical synchronisation programme for fixed time AI in beef cows

A
Day 0 - insert CIDR
Day 7 - Inject PG
day 9 - Remove CIDR
Day 11 - 1st AI
Day 12 - 2nd AI
Day 13 - introduce sweeper bulls
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42
Q

What are the key targets indicating high fertility performance in a beef herd?

A

Barren cow rate - 65%

Calf crop >94%

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43
Q

Describe the cascade for food producing species

A

In all species - if there is a product that is licensed for the particular condition being treated and the particular species then this product should be used. If no such product exists then a product licensed for use in that species for a different condition may b e used OR a product licensed for that condition in another food producing species may be used. If no such product exists in 1 then a product available in another member state (EU) may be imported but only provided that the product is licensed for use in a food producing species in that state. In addition the prescribing veterinary surgeon must ensure that the treatment is only used for animals on a single holding. Ensure that the drug is listed in the EU table of permitted substances. The vet must also specify a withdrawal period - if the medicine prescribed does not state a withdrawal period for that species then the VS must stipulate a withdrawal period which should not be less than 7 days for milk and eggs and 28 days for meat and 500 degree days for meat from fish. Keep appropriate records for a period of 5 years which include name and address of owner, identification of animals treated, date, diagnosis, details of drug and dose used including batch numbers, duration of treatment, withdrawal period applied.

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44
Q

What are MRLs and ADIs?

A

ADI - when an individual eats meat, milk eggs honey etc there is an assurance that levels of drugs in these products are within safe limits. Maximum residue limits MRLs are set for certain drugs based on the calculated ADI (acceptable daily intake) for that particular drug. Withdrawal periods are then established which take into account the MRL for the drug and its pharmacokinetics in the animal; allowing a determination of the amount of time it takes for levels of the drug to fall below the MRL and hence identifying a suitable withdrawal period for that product.

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45
Q

How are withdrawal periods set?

A

Withdrawal periods are then established which take into account the MRL for the drug and its pharmacokinetics in the animal allowing a determination of the amount of time it takes for levels of the drug to fall below the MRL and hence identifying a suitable withdrawal period for that product.

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46
Q

What are the ADIs for milk, meat eggs and honey?

A

The calculation of the ADI includes an extremely large safety factor. The MRL calculation assumes an average daily intake per person of 500g of meat, 1.5 litres of milk, 2 eggs and 20g of honey.

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47
Q

What records should be kept for food producing animals receiving drugs?

A

At the time of purchase - proof of purchase, name and address of supplier, name and batch number of drug, date of purchase, quantity, withdrawal period. At the time of administration - name of product, amount of product, date of administration, withdrawal period, identification of animals treated. if product administered by the veterinary surgeon then the vet can enter the information directly into your records or give you the information which should also include the name and address of the administering veterinary surgeon. At the time of disposal - name of product, amount disposed of, how disposed of. All records must be kept for five years.

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48
Q

What records should the veterinary surgeon keep when prescribing to food producing animals?

A

Date and nature of transaction, identification of the product, quantity, name and address of either the supplier or the recipient, a copy of any prescriptions and the name and address of the person who wrote the prescription, batch number and date once product is in use. Remember the legal categories of veterinary medicines. Think of the list and see which ones are relevant to drugs used in farm

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49
Q

What records should be kept for drugs prescribed under the cascade:

A

Date of examination of animal, name and address of owner, identification of animals treated, diagnosis, trade name of the product if there is one, batch number, name and quantity of active ingredient, dose administered duration of treatment, withdrawal period.

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50
Q

Describe in feed medication

A

Medicines that are incorporated into feed are now either classified as POM -v or POM VPS under the new legislation. Since they are POM drugs then a prescription is required. in the case of written prescriptions these require a specific MFSp medicated feed stuff prescription which will contain additional details to a standard prescription.

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51
Q

What information must be present on a MFSp?

A

The name and address of the person prescribing product, qualifications of person, name and address of owner, species of animal, identification and number of animals, premises at which the animals are kept if this is different, date of prescription, signature or other authentication of the person prescribing the product, name and amount of product prescribed, dosage and administration instructions, necessary warnings, withdrawal period if relevant, manufacturer or distributor of feed stuffs, inclusion rate of veterinary product and inclusion rate of active substance, any special instructions, percentage of the prescribed feedingstuffs to be added to the daily ration.

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52
Q

Describe how the absorption of drugs is different in ruminants?

A

The ruminal microflora is capable of catalysing hydrolytic and reductive reactions and so may readily inactivate orally administered drugs before they ever reach the systemic circulation. Orally administered drugs may adversely affect gastrointestinal microflora and interfere with normal digestive processes. This may occur particularly with orally administered drugs but may also be associated with systemic administration. Oral modified drug release delivery systems (boluses) take advantage of the unique anatomy. Bolus retained in the rumen which allows time for the sustained or pulsatile release of drugs to occur.

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53
Q

Describe how the metabolism of drugs differs in ruminant species?

A

In ruminant species highly significant changes are observed in metabolic capability in preruminant versus the ruminant. This is associated with changes in the diet resulting in a change in the nature and complexity of nutrients to which the liver is exposed. Differences in hepatic metabolism of certain anthelmintic drugs such as benzimidazoles, clorsulon, probably explains the higher dose requirement seen in cattle and goats verrsus sheep for these anthelmintics. For drugs that undergo hepatic metabolism, half lives seem to be shorter in cattle and horses compared to dogs and cats. Exceptions include theophylline in the horse and phenylbutazone in cattle.

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54
Q

Describe the differences in excretion of drugs in ruminant animals?

A

Urinary pH - the urinary pH in herbivorous animals such as sheep cattle and horses is generally alkaline ph 7-9. in contrast to carnivorous animals where urinary ph is acidic 5–5.7. This may affect elimination of certain drugs through the urinary tract. in general acidic drugs will be predominantly ionised in an alkaline pH and elimination should be enhanced since the drug will remain in the urine. by contrast alkaline drugs will be primarily unionised and therefore are more readily reabsorbed from the urine reducing the rate of their elimination. note that milk fed animals generally excrete an acidic urine.

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55
Q

How do the pharmacodynamics differ in ruminant animals?

A

Differences may occur at the receptor level. eg for example a2 adrenoceptor agonist xylazine. the dose required on a mg/kg basis in cattle is very significantly less than in some other species - thought to be an increaed sensitivity of the receptor site in this species.

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56
Q

Describe the practical aspects of farm and production therapeutics in terms of bulk administration, rumen boluses, long acting injections etc.

A

Bulk administration in feed or water - dose needs to be based on the expected feed or water consumption and obviously there will be an individual animal variation. Rumen boluses primarily employed for the delivery of anthelmintics to cattle. the use of multi dose injectors are used to deliver IM or SC injections.. It is very important to change the needle at regular intervals. pour ons primarily used for certain anthelmintics. Long acting injections especially relevant in relation to antimicrobials. certain drugs by nature of the drug itself or the formulation have long half lives reducing the need for repeated treatments.

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57
Q

what can be done to prevent injection site lesiosn occuring? What are the consequences?

A

Lesions caused in young calves often will not resolve and may often enlarge as the animal matures. in an ideal world injections should be given s/c but need too have a carcass friendly injection site and still adhere to the label requirements for the drug. Ideally i/m injections should be given in the neck away from the more expensive cuts of meat. Maximum volume for injection should be 10mls. Needle selection can be important. 16 or guage needle depending on size of the animal. 5/8 or 1/2 inch ideal for s/c an 1 or 1 1/2 inch ideal for IM. keep injection sites 4 inches apart if possible.

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58
Q

What are the targets for heifer rearing?

A

calve at 22-26 months old, conception at 15 months, 85% adult body weight at calving, 60% adult body weight by service. For a calf born at 40Kg growing to be 700kg adult weight this means an average daily weight gain of 0.9Kg.

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59
Q

Describe the best start for calves in terms of husbandry

A

Manage dry cow nutrition and consider whether pre calving vaccination is necessary. Provide clean dry well lit calving pens. ensure navels are dipped as soon as possible after birth e.g iodine. Ensure adequate colostrum intake. 10% body weight by 6 hours old and a further 2.5% by 12 hours old. Ensure adequate colostrum quality (encourage monitoring by farmer or you). Use colostrometer or specific gravity refractometer. Monitor levels of passive transfer - serum total protein >5.2g/L is the target, <4.8g/dL is inadequate. 5.5g/dL has been correlated with low levels of disease. Zinc sulphate turbidity test or gamma globulins.

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60
Q

Describe the onward management for optimum growth of calves

A

It is not recommended to feed calves waste milk (significant contamination with bacteria and possible antibiotic residue). Calves should be offered milk at least twice a day from clean buckets or bottles. Some producers use large drums with teat feeders or robotic milk feeders which allow more frequent feeding. Important that milk replacer is made up correctly. Calves should be offered creep concentrate feed from two weeks of age and should have access to good quality forage. Calves should have access to fresh clean water from birth onwards. Calves require four to six litres of water for every 1Kg of concentrate consumed. encourage measurement and recording of calf weights (calf weigh bridge or measurement of heart girth using a weigh tape.) this measurement should continue once youngstock are no longer in small groups (measure height to withers if heart girth not possible) weigh opportunistically when heifers being handled for other reasons.

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61
Q

What procedures should be taken by the vet/farmer when things go wrong with calves?

A

Encourage farmers to keep records of mortality and causes when possible. Mortality should be >3% but may be 10%. Encourage farmers to record treatments. Calves must be checked twice daily. Consider calf scoring to help record ill health and guide farmer decision making. Encourage the farmer to call the vet early for advice. Congenital problems are not uncommon. Carefully auscultate the heart when opportunities arise. Calves suffer from digestive problems sometimes (failure of oesophageal groove closure, failure of milk clot formation, liquid milk overflow to duodenum, Abomasal bloat, rumenal impaction). These problems are often associated with poor husbandry around feeding. Calves can get post weaning scour. Calves can also suffer from trace element deficiencies (hypomagnesaemia, vitamin E, selenium). Naval ill and its consequences can be prevented but will need prompt treatment with broad spectrum antibiotics to prevent sequelae such as joint ill, septicaemia, meningitis.

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62
Q

What do the welfare of farmed animals regulations state for calves?

A

Must have bovine colostrum within 6 hours of birth, sufficient iron to maintain good health and a mean haemoglobin conc of 4.5mmol/l. when they reach >2 weeks old, 100g/d fibrous food must be fed increasing to 250g/day at 20 weeks old. Must be fed at least twice a day. Must be fed a sufficient quantity of fresh drinking water per day. If hot weather or calf is ill, must be fed fresh drinking water at all times. Sick or injured calves must be isolated as necessary with dry bedding, no individual stalls after 8 weeks unless veterinary instruction, access to dry bedded lying area. Inspection - housed calves 2 x day, outside calves 1 x day. No transport until navel healed. No markets until 7 days old, no more than 1 market in 28 days.

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63
Q

What happens with male calves?

A

To reduce the number of unwated male dairy calves some farms use sexed semen. Male and excess female dairy breed calves may not have the conformation required for the traditional beef market however if carefully reared and butchered it can enter the bull beef market. Rearing of dairy calves for veal is controversial. 100% milk diets have been banned there has been a growing interest in rose veal (6-12 month old dairy produced calves). Dairy farmers may choose to breed some of their cows or heifers to a beef breed bull to produce calves that have better confirmation for the beef trade. These are reared as for the dairy heifers and sometimes will be sold on to calf rearing, store or finishing units. the lifetime feed costs of such animals are likely to be higher than for more traditional beef breeds, not least because they are usually reared on artificial milk replacer for at least the first few weeks and are weaned much earlier than beef calves.

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64
Q

Describe the stack effect

A

On still days in a livestock building the heat produced by the stock as a by product of their metabolism of energy, is available to warm the air. this warm air rises and leavs via the ridge. if it is wide enough to allow this. This stale air is replaced by colder fresher air entering at eaves level. If this moist air is not allowed out at the ridge, it condenses on the underside of the cold roof and falls as condensation droplets.

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65
Q

What are the factors involved in generating a stack effect?

A

The factors involved are the height difference between the inlet and outlet, the temperature difference, inside temperature and out, the inlet area, the outlet area and the velocity of arflow to the outside gnerated by the housed livestock. The difference in density of warm air and cold air generates a hydrostatic pressure head, which causes airflow in at lower level and out at a higher level. Steeper pitched roofs vent better than shallow roofs because of a greater height difference between inlet and outlet. Flat roofs are to be avoided for livestock housing because of the problems in creating natural airflow. The most influential factor in creating good stack efect is a decent opening at the ridge.

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66
Q

What is the minimum sq m outlet area per calf?

A

0.04sq m outlet area per calf (4sq m outlet per 100 calves) to balance this outlet the inlet area should be four times the outlet area. for large dairy cows, allow about 0.1sq m outlet per cow (10 sq m per 100 cows), again with about four times the minimum inlet area.

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67
Q

Describe a healthy environment for calves?

A

Ensure good siting of the bilding on an open sunny location away from other stock. do not have too many calves in a single airspace, split the facilities so reducing the risk of airborne infection. provide adequate ventilation, preferably natural but with fans if necessary. ensure protection from draughts. keep dust and pathogen levels low. Never restrict ventilation in an attempt to raise air temperature. provide good natural light levels. keep out birds and vermin.

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68
Q

What is a stress free environment for calves?

A

Newly arrived calves must be allowed time to rest and acclimatise. newly arrived calves should be kept apart from other calves for long enough to avoid cross infection. Allow good visual contact between individually penned calves with perforated walls which allow the calves to have visual and tactile contact. all calves above 8 weeks old must be group penned. keep groups small and well matched for size without overcrowding. provide spacious follow on penning in airy buildings as calves grow and progress through the sysetm, keeping groups intact to avoid stress. Be organised, keep calm and quiet avoiding unnecessary noise.

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69
Q

How can you provide a dry lying area for calves?

A

Provide a generous amont of good dry bedding, maintain a dry bed, design pens to drain directly to an external channel never through adjacent pens which can encourage the spread of disease, prevent water spillage or leaks into pens, especially within lying areas, avoid condensation drips caused by poor ventilation, prevent roof leakage due to poor maintenance..

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70
Q

How much space is adequate for calves?

A

Each calf must be able to adopt a comfortable lying poositioon whatever teh housing system but especially when individually penned. individual pens should be at least 1m wide and preferably 1.8m long. calves in groups should be able to choose locations within the pen for lying down to avoid draughts and away from feeding and drinking points. Provide good pen space to encourage healthy exercise.

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71
Q

What problems can be seen with too much moisture in a livestock building?

A

supports microbial activity, promotes bacterial growth, absorbs energy, acts as a transport medium, increases slippery floors - stress. Seen as dirty water lying, dirty cattle, damp floors in areas that could be dry, water ingress, leaking drinkers, condensation, staining of underside of roof

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72
Q

What problems can be seen with too little fresh air in a livestock building?

A

Lack of fresh air increases survival time of airborne pathogens, lack of fresh air increases concentration of gaseous emissions, lack of fresh air can reduce oxygen concentrations. Smells of ammonia/dampness, elevated air temperatures, no ventilation in corners

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73
Q

What can be the problems associated with too much or too little air speed in a livestock building?

A

Too much - associated with excessive energy losses - animals avoiding certain areas, huddling, hairy coat, high intake/low production rates.
too little - associated with lack of fresh air, animals avoiding certain areas, smell.

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74
Q

What are potential solutions to too much moisture in a building?

A

Drainage 1 in 60 or 1 in 20 below straw. Drainage within pen between bens within building and outside. manure management and straw management, air inlets and outlets, decent gutters and downpipes, consider concrete

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75
Q

What solutions are there to problems with too much air speed?

A

Air inlets and outlets - protection from wind to above animal height, greater use of perforated wall caldding, elimination of draughts at animal height.

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76
Q

How do you assess the air inlets and outlets of a building?

A

Assess roof - No outlets - guarunteed contribution to problems. Area of opening in roof - depends primarily on slope of roof and energy density within building. Flat roof bad > 17 degree slope good. Area of opening in roof 2- only two ball park figures - 0.04m2 per calf, 200mm wide open ridge for adult and growing cattle. Area of inlet at least twice the area of outlet. Always look to eliminate draughts at animal height. Large openings do not control air speed they increase them. Large openings that may create stress should have galebreaker type, space boarding, or yorkshire boarding. inlet and outlet areas are best as a series of diffuse openings along the ridge and walls. Less risk of stagnant areas within the building.

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77
Q

Describe the aetiology of rotavirus infection in calves

A

Most common cause of diarrhoea in neonatal calves. Rotavirus can be isolate from up to 40 percent of normal calves. Infection results from the ingestion of faecal contaminated material. The virus attacks epithelial cells of the upper mid then lower small intestine causing desquamation. Loss of these cells results in reduction of absorptive capacity and secretory defence mechanisms. Loss of mature differentiated cells with absorptive capacity at the tips of the illi and survival of cells in the crypts secreting fluidds, exacerbates the problem. Loss of cells secreting disaccharidases so sugars are fermented in large colon producing organic acids with the hydrogen ions contributing to the metabolic acidosis. Diarrhoea results in loss of water, sodium, chloride and bicarbonate ions. Loss of intracellular potassium ions occurs because hydrogen ion replacement occurs (buffering in an attempt to reduce metabolic acidosis).

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78
Q

What are the clinical signs of rotavirus?

A

Range from no observed abnormality through to severe diarrhoea and dehydration with high mortality. the incubation period is 1-3 ays depending upon the level of viral challenge. Calves most commonly affected at 8-14 days old. Acute onset of diarrhoea with passage of watery yellow/green faeces. Typical early signs include a reluctance to stand and suck, mild depression and salivation. Without fluid therapy the calf rapidly becomes dehydrated hypothermic and recumbent. The abomasum and intestines are often distended with fluid and gas and sloth when balloted. The eyes are sunken and the ski becomes tight and inelastic. Calves treated with oral rehydration have normal hydration status but have become severely acidotic causing depression/stupor, weakness and recumbency.

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79
Q

How is diagnosis of rotavirus made?

A

In a typical beef herd outbreak, the high morbidity of scour affecting calves age 8-14 days with losses occurring despite oral fluid therapy should suggest rotavirus as the primary causal agent. Same day confirmation by PAGE test on fresh faeces can be obtained from a veterinary laboratories. Four or more calves should be sampled (30g faeces not swabs) to allow a meaningful interpretation of the herd problem. Rotavirus frequently isolated from normal calves without diarrhoea.

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80
Q

What is the treatment of rotavirus?

A

The calf should be isolated in a warm dry and well bedded pen. Intravenous fluids are essential because severely affected calves are acidotic with variable degrees of dehydration. A 16 Gauge catheter should be stitched in a jugular vein as this makes fluid administration much easier because the calf can be left unattended. A typical treatment regime would be: 1 litre of isotonic saline plus 50 percent of estimated bicarbonate deficit during first 20 min then 3 more litres of isotonic saline plus remainder of estimated bicarbonate deficit over next 2-4 hours. 1 litre of oral electrolyte 4 to 8 times daily. Oral antibiotics coontraindicated. Parenteral antibiotics should be used to control concurrent focal infections eg navel ill. milk should not be diluted with electrolyte solution. alternate milk and electrolyte solution every two hours. offer fluid by teat not oesophageal feeder.

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81
Q

What factors are likely to increase the level of rotavirus challenge in a dairy herd?

A

The persistence of infection in dirty calving boxes/yards
the failure to feed sufficient good quality colostrum at the correct time. not feeding calves stored colostrum during the first two weeks of calfs life.

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82
Q

What factors are likely to increase the level of virus challenge in beef herds?

A
  1. A protracted calving period in the same field or building especially if the cows calve in that field every year.
  2. Failure to remove newly calved cows and calves from the group still to calve.
  3. The purchase of calves from markets to set on to cows which have lost a calf is an excellent source of enteropathogens.
  4. concurrent cryptosporidial infections . these are most severe when the same field is used for lambing in the spring and for calving cows in the autumn.
  5. Factors which lead to the lack of production or ingestion of suitable quantities of good quality colostrum.
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83
Q

Should cows be vaccinated for rotavirus?

A

Once a herd has experienced losses due to rotavirus infection, annual/alternate years vaccination is ssneitla. in the face of an outbreak it takes 14 days for adequate antibody to accumulate in the colostrum. In subsequent years cows must be vaccinated 1-3 months before the calving date. vaccination against rotavirus infection every second year appears to be an effective programme on many farms. Vaccination reduces the mortality to almost zero if used in conjunction with sound husbandry practices but bouts of diarrhoea can still occur when the calf is 10-14 days old. these outbreaks are usually mild and controlled using oral electrolytes as supportive therapy.

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84
Q

Describe a typical outbreak of coronavirus infection in calfs

A

Coronavirus diarrhoea are similar to or more severe than those observed for rotavirus infection. coronavirus infection is much less common than rotavirus. Typical clinical signs include depression, reluctance to suck and passage of faeces containing mucus and milk curds. The disease can progress rapidly to weakness, recumbency, severe dehydration and death. Coronavirus infections cause diarrhoea in calves up to 20 days old.

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85
Q

Describe the aetiology of coronavirus

A

Coronavirus infections differ from rotavirus infections in that the coronavirus replicates in the epithelial cells causing severe damage in the small intestine and progresses caudally into the colon. Infection of epithelial cells with virus results in the loss of cell function causing abnormal absorption and secretion before desquamation occurs 48-96 hours later. The loss of epithelial cells results in shortened villi and occasionally adjacent villi fuse. Cuboidal epithelium replaces the previous columnar cells. The regenerating epithelium consists of functionally immature cells which like in rotavirus cases are unable to carry out normal absorptive and secretory functions.

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86
Q

What is the treatment and control for Coronavirus?

A

Treatment for coronavirus infection is as for rotavirus. Annual/alternate year vaccination with a combined rotavirus, coronavirus and K99 combined vaccine is an invaluable insurance policy in all beef herds but is perceived as costly by farmers.

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87
Q

What is Enterotoxigenic E. coli? How does it cause disease?

A

Refers to strains of E. coli possessing the K99 antigen. Recent surveys have shown the incidence of K99 E. coli is low but when it does occur in a herd losses can be high. The ability to adhere to the gut mucosa and the production of a heat stable toxin results in the hypersecretion of fluids into the gut with rapid dehydration collapse and death. ETEC are non invasive and the villi remain intact. K99 E. coli rarely produces systemic colibacillosis.

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88
Q

What are the clinical signs of Enterotoxigenic E. coli?

A

The disease characteristically affects calves aged 1-3 days old. There is sudden onset of profuse yellow white diarrhoea without mucus or blood. There is rapid and severe dehydration. The calf quickly becomes recumbent. Sequestration of fluid in the abomasum and intestines give the abdomen a bloated appearance which sloshes on succussion. The rectal temperature may be elevated in the early stages but rapidly falls to subnormal. Affected calves are rarely acidotic. Diagnosis based on severe diarrhoea with high mortality affecting calves 1-3 days old. Confirmation following isolation of K99 + E. coli from 30gfaecal samples.

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89
Q

What is the DDx for Enterotoxigenic E. coli?

A

Recumbency in 1-3 day old calves could include congenital heart defects, Neosporosis and atresia coli/ani, events at parturition such as femoral nerve paralysis and neonatal infections - septicaemia/bacterial meningoencephalitis.

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90
Q

What is the treatment of Enterotoxigenic E. coli?

A

fluid therapy (these calves are rarely acidotic) antibiotic resistance is not a problem with most K99+ isolates. Always check for the presence of navel ill/septicaemia as such cases require parenteral antibiotics. Control by the movement of all pregnant cows to clean pastures and isolation of newly calved cows should markedly reduce the incidence of ETEC disease.

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91
Q

How does specific K99 antibody work?

A

It acts locally in the small intestine by interfering with the attachment of ETEC to the intestinal mucosa. Locatim (vetoquinol) is a concentrated bovine lacto serum containing specific immunoglobulins G against E. coli F5. Vaccinate all pregnant animals immediately with Rotavec corona K99 but it will take 10-14 days for sufficient protective antibody to accumulate in the colostrum. Oral antibiotics may be administered at birth as temporary prophylactic measure. Ensure all calves receive equivalent to 10% body weight of colostrum within the first six hours of life.

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92
Q

What is septicaemic colibacillosis?

A

It occurs in calves less than 2 weeks old on farms with poor husbandry standards. Scour is only seen in the agonal stages. Two factors are critical in the development of septicaemic colibacillosis; 1 inadequate passive immunity from colostral immunoglobulins.
2) exposure and invasion via the nasal, oropharyngeal and mucous membranes, tonsil, upper resp, or intestine of E. coli serotype able to produce an overwhelming bacteraemia , endo toxaemia and death. the umbilicus is not a major portal of entry for bacteria. Calves with sufficient circulating immunoglobulins are resistant to septicaemic colibacillosis. it has been suggested that nil to minimal immunoglobulin concentrations allow a septicaemia whereas more marginal concentrations allow a bacteraemia with bacteria localising in joints, endocardium or meninges.

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93
Q

What are the clinical signs of septicaemic colibacillosis?

A

Calves less than 2 weeks old. Incubation period of 24 hours between challenge and clinical signs with a course as short as 6-8 hours in septicaemic cases Diarrhoea is a terminal clinical sign. Septicaemia - lethargy, depression, failure to suck, recumbency. Bacteraemia - localisation in the eye, joints, endocardium etc. Episcleral injection. Salivation and yellow mucoid diarrhoea occur terminally, seizure activity, periods of opisthotonus, nystagmus and death.

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94
Q

What is the treatment for septicaemic colibacilosis?

A

Septicaemic case - florfenicol as most commonly caused by E. coli. Hopeless prognosis if calf showing seizure activity. Meningitis - florfenicol. supportive therapy including NSAIDS. High dose of soluble corticosteroid to reduce cerebral oedema remains controversial in the treatment of bacterial meningoencephalitis. poor prognosis unless treated very early. Polyarthritis - parenteral antibiotics and more importantly thorough joint lavage with lactated ringers solution. Do not flush joints with diluted antiseptic solutions. poor prognosis if carpal/hock joints involved. Prevention - with colostrum and hygienic calving accomodation.

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95
Q

Describe when cryptosporidiosis infection is most likely to occur?

A

C parvum is not a host specific and severe outbreaks occur when there is a build up of infection towards the end of calving period especially if the same fields or buildings are used for autumn/winter calving then spring lambing as the protozoan parasite can remain dormant on pasture for months. Cryptosporidiosis is more frequently recorded in beef calves than dairy calves. Cryptosporidiosis is a zoonotic disease and has been frequently reported in school children visiting open farms.

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96
Q

What are the clinical signs of Cryptosporidiosis?

A

Diarrhoea is caused by the physical loss of villous absorptive area and exacerbates viral infections. In some instances no clinical disease results from cryptosporidium spp infection. Beef calves aged 10-21 days old are most commonly affected. There is profuse yellow green diarrhoea with much mucus present. There is only mild dehydration but the calf rapidly looses condition over 2-5 days and has a dull tucked up apperaance. there is a reluctance to suck and examination of the dam often reveals a full udder. Whilst morbidity is high the mortality rate in uncomplicated cases is usually low.

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97
Q

Describe cryptosporidiosis in lambs

A

Most cases occur during the second half of the lambing period in housed flocks. lambs aged 3-7 days are most commonly affected. There is profuse yellow green diarrhoea with only some mucus. Affected lambs quickly become dull, tucked up and reluctant to move often standing hunched behind shelters. There is rapid dehydration in severe cases with recumbency and eventual death. Unlike calves a severe challenge of C parvum can cause lamb losses during adverse weather conditions if supportive therapy is not administered. Convalescence of surviving lambs is protracted.

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98
Q

How is diagnosis of cryptosporidiosis made?

A

Calves - change the calving accomodation and move cows and their newborn calves as soon as they are born from the remainder of the herd. in lambs - diagnosis is difficult because the clinical signs and epidemiological findings also fit E. coli infections in lambs aged 3-5 days. Demonstration of cryptosporidia spp oocysts on faecal smear after giemsa stain. Other enteropathogens may also be involved. Identification of organisms on stained gut sections of post mortem material is the preffered laboratory method.

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99
Q

What is the treatment of cryptosporidiosis?

A

In uncomplicated cases ensure that the calf is properly hydrated and use oral electrolyte solutions as necessary. Halofuginone lactate is licensed for the prevention and treatment of diarrhoea caused by C parvum. For prevention of diarrhoea, calves should be dosed for seven consecutive days starting within one to two days of birth. For treatment, calves should be dosed for seven consecutive days starting within one day of the onset of diarrhoea. Halofuginone lactate has a low toxicity index and the data sheet instructions must be carefully followed. Lambs - oral flui therapy is essential and 150-200 mls of oral rehydration solution 4-6 times daily is recommended.

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100
Q

How can cryptosporidiosis be controlled?

A

Do not use same fields for calving/lambing. Change field every year or when clinical cases occur int hat season. Move newborn animals immediately onto clean pasture.

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101
Q

What is coccidiosis?

A

A problem of housed, intensively reared lambs. Disease can occur in calves during dry summer months associated with contaminated water courses and feed areas (E alabamensis). There is speculation that periweaning scour syndrome of dairy calves is caused by coccidiosis.

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102
Q

What is the aetiology of coccidiosis?

A

Caused by infection by the protozoan eimeria spp which parasitizes the epithelium lining the alimentary tract E zuernii, E bovis and E alabamensis.

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103
Q

What are the clinical signs of coccidiosis?

A

It was a problem in weaned dairy calves confined outdoors during the summer months in small dirty paddocks where faecal contamination of grazing and feed troughs rapidly builds up. Now coccidiosis is more common in spring born beef calves at pasture during summer months with infection acquired from contaminated surface water. In severe clinical coccidiosis there is a sudden onset of profuse foetid diarrhoea containing mucus and flecks of fresh blood. There is considerable staining of the perineum and tail. Straining with partial eversion of the rectum which may result in prolapse. Clinical signs are more usually less marked with chronic wasting and poor appetite the presenting signs. Small clots of fresh blood and mucus are passed but the diarrhoea is not so marked. Anaemia is uncommon. Rectal temp often normal. Morbidity is high but mortality even in severe cases is low.

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104
Q

What is the DDx for crypto?

A

Calves - parasitic gastroenteritis, salmonellosis, lead poisoning. If only one calf - intussusception, BVD, necrotic enteritis, ragwort. Lambs outdoors - PGE especially nematodiriasis.
Indoors - Poor nutrition of both lamb and dam, strongyloids westeri infestation, liver abscessation/pyaemia, chronic pneumonia.

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105
Q

What is the treatment for crypto?

A

Move from infected pastures. sulphamezathine given orally for 3 days was the standard treatment. Fluid therapy may be indicated in certain cases. Decoquinate and diclazuril can be used for the treatent and prophylaxis of coccidiosis in lambs. toltrazuril and diclazuril can be used for both treatment and prophylaxis in calves. decoquinate can be used in feed for prevention of coccidiosis in dairy calves.

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106
Q

What are wheezes?

A

Continuous single pitch sound which usually occurs during inspiration and occasionally during both inspiration and expiration. result from vibration of airway walls caused by air turbulence in narrowed airways.

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107
Q

What are crackles?

A

Sudden sound towards the end of inspiration or less frequently during both inspiration and expiration. Caused by sudden opening of small airways plugged by mucus, pus and other debris.

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108
Q

What is pasteurellosis? (transit fever)

A

An acute infection resulting in broncho pneumonia affecting cattle aged between 3 months and 2 years old.

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109
Q

Describe the aetiology of pasteurellosis? (transit fever)

A

Genetic selection has resulted in domesticated cattle with small lungs relative to metabolic demands and such reduced respiratory capacity can contribute to decreased resistance to Aerogenous exposure to infectious agents particularly during periods of exertion. Reductions in body weight which occur over transportation of long distances, poor appetite after arrival and changes in ration may compromise immune system function and predispose calves to respiratory disease. The importance of the respiratory tract innate defences - intact epithelium including ciliated cells, mucus, interferon, and phagocytes.
PAsteurellae are part of the normal flora of the nasopharynx. A number of factors including Pi3, BRSV or IBR infection, stress, overcrowding poorly ventilated buildings, transportation, starvation, allow increases in numbers or virulence of pasteurellae in the nasopharynx. Mannheimia haemolytica is believed to be responsible for up to 90% of cases. others attributed to P multocida.

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110
Q

What are the clinical signs of pasteurellosis?

A

The farmer notices that the animal does not come forward for concentrate feeding. The affected animal is often dull and may stand by itself in a corner of the pen. the rectal temperature is elevated but the animal does not appear ill, there is a mild serous ocular and nasal discharge. there is an increased respiratory rate and effort. the animal may appear gaunt if it has been inappetent for more than one day. Coughing is not a feature of pneumonic pasteurellosis. there are few abnormal sounds to be heard on auscultation of the chest.

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111
Q

How is diagnosis of pasteurellosis made and what are the DDx?

A

IBR - check other cattle in the group for clinical signs of IBR. nasal swabs are of little use to diagnose pasteurellosis as these bacteria are commensals of the upper respiratory tract. DDX - IBR hepatocaval thrombosis in individual animal.

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112
Q

What is the treatment of pasteurellosis?

A

Up to 50% of affected animals may recover in 3-7 days without antibiotic treatment. 75-80% of lung isolates of pasteurellae are sensitive to oxytetracycline but this drug is now rarely used by vets. recommended dose 10mg kg/iv. Continue treatment with single long acting injection or for 3-5 consecutive days. Rectal temperature should fall to near normal by the third day of treatment. tilmicosin has advantage of a single long acting injection. Has been ovetaken by tulathromycin (draxxin), gamithromycin (zactran) and tildipirosin. Florfenicol can be administered on day 1 and day 3 or as a single long acting injection. Enrofloxacin and other fluoroquinolones are highly effective against pasteurellae spp should be held in reserve. Marbofloxacin would be choice.

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113
Q

How can response to antibiotic treatment be monitored?

A

Antibiotic re treatments should be based upon recurrence of significant pyrexia during the monitoring of recovering cattle which takes place at regular two to four days intervals after completion of the initial treatment course. Field studies have demonstrated a marked reduction in calf rectal temperature 24 hours after the start of antibiotic treatments indicating efficacy of that antibiotic in the treatment of bacterial respiratory disease.

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114
Q

When should antibiotic re treatment be undertaken?

A

Antibiotic re treatment becomes necessary when bacterial infection recurs during the period of viral induced compromise of host defence mechanisms in the upper respiratory tract. Recurrence of pyrexia 5-14 days after first antibiotic treatment can occur in 20% -50% of treated calves. Use the same antibiotic because re infection of compromised lung has occurred. Antibiotic re treatment rates are considerably higher in calves 2-5 months old than weaned cattle.

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115
Q

When is the antibiotic treatment defined as a failure?

A

When there has been a failure of the rectal temperature to fall after 48 hours or recurrence of pyrexia 2-4 days after first antibiotic treatment. With the exception of peracute BRSV cases where the animal is severely dyspnoeic, corticosteroids should be avoided untill the rectal temperature begins to fall.

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116
Q

How is pasteurellosis controlled?

A

No obvious measures for pasteurellosis have been shown to work consistently well. improved ventilation of buildings and delaying stressful procedures may help to reduce the disease prevalence. Pasteurella vaccines not found to be very successful in the UK. Metaphylactic antibiotic injection- No evidence to support - expensive and not consistent with good practice especially if using a fluoroquinolone. There are obvious animal welfare benefits from the early detection and effective treatment of respiratory disease by the vet.

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117
Q

What is haemophilus somni? What is the treatment?

A

Aetiology and clinical signs similar to those described for pasteurellosis and specific diagnosis can only reliably be made at necropsy findings with marked fibrinous pleuritis and pleuopneumonia. Florfenicol and fluoroquinolone drugs effective. Occasionally thromboembolic meningo encephalitis reported in cattle following episodes of H soni respiratory disease. syndrome presently very uncommon in the UK. Animals become obtunded, ataxic and sternally recumbent.

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118
Q

What is chronic suppurative pulmonary disease?

A

Bacterial in origin developing as a result of unsuccessful treatment or incomplete recovery from earlier pneumonia episodes. Recrudescence of infection is often associated with a stressor such as transport, sale or calving. CSPD often associated with persistent BVD in growing cattle. affected growing cattle are dull, in poor condition, pot bellied, with a dry rough and starig coat, and are intermittently febrile. Affected animals cough frequently and have an occasional muco purulent nasal discharge. the respiratory rate is increased with an obvious abdominall component to respiration. the appetite is poor. Obvious crackles are heard. Clinical signs in adult cattle are poorly defined and often present with a normal rectal temperatuer, poor milk yield, reduce appetite and weight loss.

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119
Q

What is the treatment of Chronic suppurative pulmonary disease?

A

Growing cattle are unlikely to grow well and should be culled. treatment with procaine penicillin for secondary infection of lung pathology with T pyogenes injected daily for 6 weeks. success rate much higher for recently calved heifers and adult cattle.

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120
Q

What is infectious bovine rhinotracheitis?

A

IBR is a highly contagious infectious disease affecting cattle of all ages. the disease is characterised by sever inflammation of the upper respiratory tract. Bovine herpes virus 1, also causes infectious pustular vulvo vaginitis in the female and infectious balanoposthitis in the male.

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121
Q

What are the clinical signs of Infectious bovine rhinotracheitis?

A

Clinical signs generally first appear either 2-3 weeks following housing or other stressful events such as calving. The morbidity rate may be 100% but the mortality rate is less than 2%. Sudden onset illness, febrile 41-42, purulent ocular and nasal discharges, affected animals are inappetant, very depressed, slow to rise and stand with the head held lowered. Conjunctivae are oedematous and there is partial prolapse of the third eyelid. Tear staining of the face is pronounced. there is halitosis due to pus in larynx and trachea and varying degrees of dyspnoea. Affected animals cough frequently and palpation of the larynx is resented. Milder clinical signs with occasional coughing and poor production can occur. IBR virus has been found to enhance the pathogenicity of moraxella bovis. This is important in herds with endemic IBR infection where severe IKC lesions can develop in calves.

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122
Q

How is diagnosis of IBR made?

A

Careful inspection of all animals in the group. fluorescent antibody test FAT requires cells so rub corneal sac vigorously. If veterinary laboratory not local, make smears on glass slides and dry in air before posting. Never believe a negative FAT test.

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123
Q

What is the treatment and control options for IBR?

A

Vaccinate all animals in the group immediately if IBR is suspected on clinical findings. Marker gE vacines are available for more sophisticated control programmes. sick animals should be treated daily for three to seven days with a parenteral procaine penicillin. Never use corticosteroids. IBR vaccination is relatively inexpensive at £3 per dose either by single intranasal or intramuscular injection and should be boosted annually.

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124
Q

What is bovine respiratory syncytial virus?

A

BRSV is considered to be the most important respiratory virus predisposing to pneumonia in young cattle and in severe infections can precipitate disease and sudden death without bacterial infection.

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125
Q

What are the clinical signs of bovine respiratory syncytial virus?

A

In some outbreaks one or two animals may be found in severe respiratory distress with mouth breathing, rapid abdominal movements and death within 12 hours. In other studies involving housed calves seroconversion to BRSV has occurred without any clinical signs of respiratory disease. In most respiratory disease outbreaks involving BRSV there is an increased respiratory rate and frequent coughing. A serous nasal discharge is usually observed. There is no occular involvement. Secondary bacterial invasion frequently occurs which makes the prognosis even more guarded. the rectal temperature ranges from 39.5 to 42.

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126
Q

How is a diagnosis of BRSV made?

A

Lavage to obtain virus identified by FAT is the most useful test in acute respiratory disease. FAT on frozen lung sections requires a dead anima in the acute phase of the disease process. paired serology from 4-6 calves, 2-3 weeks apart, is costly and of little use in tackling the problem at the start of an outbreak. A four fold increase in titre 25% of sample population is considered indicative of BRSV involvement.

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127
Q

What is the treatment of BRSV?

A

In severly dyspnoeic calves a single injection of corticosteroids such as dexmathasone may be life saving. the rationale for such treatment is that inhalation of virus into the caudo dorsal lung field sets up an allergic reaction with the development of extensive emphysema, NSAIDs are not nearly so effective. Bronchial smooth muscle relaxants are of little benefit in the acute phase of the disease. Recurrence of fever and respiratory disease signs are common 5-14 days after the first episode. the same antibiotic should be used to treat these reinfections as that used successfully in the first outbreak.

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128
Q

How is control of BRSV implemented?

A

Vaccination is widely used to control BRSV induced respiratory disease. Rispoval 4 is a live attenuated bovine respiratory syncytial virus, Containing IBR, Pi3, BDV antigens which is administered intramuscularly on two occasions, four weeks apart, two weeks prior to the anticipated challenge eg housing. Single intranasal vaccination with rispoval RS (also contains Pi3 antigen) is as effective as two intramuscular injections and is claimed to be effective in the face of a BRSV induced respiratory disease outbreak. Reducing stocking density and improving ventilation/reducing humidity wherever possible would improve the disease situation on most units.

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129
Q

Describe Pi3 infection

A

the clinical signs attributable to Pi3 infection as defined by seroconversion during the respiratory disease outbreak, are generally mild. most outbreaks occur during october/november and are common following housing. it is not uncommon for Pi3 and BRSV infections to occur simultaneously.

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130
Q

What is mycoplasma (enzootic or cuffing pneumonia)

A

Poorly defined clinical disease where mycoplasma dispar may act in conjunction with Pi3 infection. Insidious onset disease more commonly encountered in young weaned dairy replacement heifers where young susceptible calves are mixed with or placed in pens adjacent to older cattle. there may be a considerable range in calves rectal temperatures 39.2-40.5. Appear dull, unthrifty, with a dry staring coat. there are usually no ocular or nasal discharges. frequent bouts of coughing are noticeable when the animals are handled.

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131
Q

What is the treatment of M bovis?

A

Few reports of outbreaks i the uK. may also cause severe intractable mastitis and polyarthritis. treatment is with florfenicol or fluoroquinolone but not tilmicosin or tulathromycin.

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132
Q

What is pulmonary thromboembolism from the caudal vena cava (hepatocaval thrombosis)

A

An uncommon condition which develops following the haematogneous spread of a large number of septic emboli from a thrombus in the caudal vena cava. Pulmonary arterial thrombo embolism occurs with eventual fatal rupture of pulmonary arterial aneurysms. Animal may be found dead having bled to death through respiratory tract. in the majority of cases there is a history of respiratory disease. clinical signs develop rapidly initially resembling pasteurellosis. Febrile 41 degrees C, apparent response to antibiotic therapy although short term as signs re appear 3-10 days later. Respiratory rate is increased with shallow painful respirations, coughing. at this stage frank blood at nostrils or coughed up - death follows in 1-14 days from massive intrabronchial haemorrhage with the animal found in a pool of bloos.

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133
Q

Describe chronic suppurative pulmonary disease?

A

Bacterial in origin developing as a result of unsuccessful treatment or incomplete recovery from earlier pneumonia episodes. it is a flare up of infection from a chronic septic focus which is responsible for the occasional adult animal presenting with signs of an apparently sudden onset disease. Recrudescence of infection is often associated with a stressor such as transport or calving.

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134
Q

What are the clinical signs of chronic suppurative pulmonary disease?

A

Typical cases are dull with chronic weight loss, intermittently febrile 39-39.5, production rate is reduced to 50-75% of predicted milk yield. there is increased respiratory rate around 40 breaths per minute with an abdominal respiratory component and a moist productive cough. there may be evidence of a purulent nasal discharge most obvious when the animal lowers its head to eat. there may be evidence of thoracic pain, crackles may occasionally be heard in the antero ventral chest but such sounds may not be obvious.

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135
Q

Describe diagnosis in adult cattle of chronic suppurative pulmonary disese?

A

Difficult in adult cattle as clinical signs are vague. serum protein profile indicating chronic bacterial infection is helpful but not specific to lung disease. fibrinogen assay does not warrant extra cost. ultrasonographic examination of both lungs/pleurae is quick. can use linear 5Mhz scanner. DDx - endocarditis, liver abscesses, Tuberculosis

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136
Q

What is the treatment of chronic suppurative pulmonary disease?

A

Main bacterial isolate is A pyogenes. attempt treatment of adult cattle with procaine penicillin injected daily for 6 weeks. Cost is 40-50 for treatment course. Success rate is approximately 50%. poorer prognosis when sonographic changes extend 5-10cm dorsally above the point of the cows elbow. Check BVDv status even in calved heifers. Correct treatment of respiratory disease as calves.

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137
Q

What is fog fever?

A

An atypical interstitial pneumonia of cattle/acute bovine pulmonary emphysema. Fog fever has a sudden onset causing severe respiratory distress in adult beef suckler cows 1-2 weeks after moving on to a lush silage hay aftermath in july august. Circumstential evidence links the disease with the ingestion of large amounts of the amino acid L tryptophan and its conversion in the rumen to 3-methyl indole and indole acetic acid.

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138
Q

What are the clinical signs of fog fever?

A

There is a sudden onset of severe respiratory disease. an expiratory grunt can often be heard from 30 yards away. the animal stands with its neck extended, head lowered, and moves very reluctantly. the nostrils are flared and the animal mouth braethes. the mucous membranes are cyanotic. there is frothy saliva around the protruding tongue. the rectal temperature is normal. rapid pulse 80-120 beats per minute. mortality rate in severely affected cases is 95%. Less severely affected cattle improve over a 10-14 day period. subcutaneous emphysema often develops over the thorax and along the back. Auscultation reveals widespread harsh crackles. usually no more than 2-5 percent of cattle at risk are Severely affected. mild fog fever - sleepy looking, tachypnoeic, and hyperneoic.

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139
Q

What is farmers lung?

A

An extrinsic allergic bronchiolo-alveolitis which develops in housed adult cattle following repeated exposure to mouldy hay containing spores derived from micropolyspora faeni and thermoactinomyces vulgaris. farmers lung is now rare due to improvements in beef cow nutrition and housng. individual animals show a sudden onset of severe dyspnoea, occasionally with mouth braething. there is frequent coughing with the production of thick mucus. the animal is alert, the reduced milk yield and anorexia which may be present are secondary to the respiratory diistress. mild to moderate attacks may go unnoticed, or dyspnoea may appear after exercise. The respiratory rate is increased with loud crackles audible antero ventrally due to the presence of tenacious mucus in the airways. Treatment - corticoseroids not in the last 5 months of pregnancy. Control - avoid mouldy hay. feed silage/barley straw.

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140
Q

What is vegetative endocarditis?

A

the provisional diagnosis of vegetative endocarditis is based upon clinical findings of chronic weight loss, pyrexia and often multiple joint effusions. typically encountered two to four months after parturition where the uterus is a potential source of infection, other septic foci act as the source of the bacteraemia in younger animals. Animals typically present with poor milk yied of several days to weeks and weight loss manifest as poorer body condition compared to other animals in the group. rectal temp marginally elevated. typically obvious effusion of hock carpal and fetlock joints. stifle and elbow less commonly. Heartrate may be elevated but may be no murmur. Lesions involving the tricuspid valve may result in ascites and peripheral oedema.

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141
Q

What is the DDx for vegetative endocarditis? How is it treated?

A

Bacterial polyarthritis - uncommon in adult sheep. Pleurisy and traumatic reticulitis (pain). Treatment with procaine penicillin for 10 days or more - usually unsucessful. Prevention based on timely and effective treatment of focal bacterial infections eg metritis, mastitis foot abscess.

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142
Q

What is dilated cariomyopathy?

A

Occasionally reported in 2-3 year old hostein cattle - genetic component. Bright and alert with normal appetite until agonal stages. clinical signs include marked peripheral oedema, jugular distension, ascites and pleural effusion which develop over several mnths. The heart rate is increased but sounds often muffled due to pleural effusions. DDx - right sided heart failure due to lung pathology or mediastinal mass. No treatment for DCM and affected cattle should be eutanased. necropsy reveals enlargement of the heart with a rounded globose shape.

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143
Q

Which congenital abnormalities may occur in the bovine gastro intestinal tract?

A

Cleft palate/harelip, pro/brachygnathia, atresia ilei (gut distension so may cause dystocia), coli: not uncommon, progressive abdominal distension by 2-3 days of age( surgical repair rarely possible. Ani: die within 1 week if untreated - surgical repair possible in some cases.

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144
Q

What is stomatitis/pharyngitis? What is the cause?

A

Inflammation of the mouth/pharynx. Physical injury - dosing guns, stomach tubes scrapie i/d boluses, foreign bodies, tooth maloclusion. Clinical signs: salivation, halitosis, quidding, submandibular and pharyngeal swelling. treatment: symptomatic relief with anti inflammatories/antibiotics. poor prognosis with iatrogenic pharyngeal rupture.

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145
Q

What is bovine papular stomatitis?

A

Parapoxvirus same as pseudocowpox virus. Zoonosis. Clinical signs: calves 1-12 months commonly affected. Expanding papular rings on muzzle. Nostrils and buccal mucosa. May be transient anorexia, salivation, mild pyrexia. spread by contact. Treatment: none required, recovery in 4-7 days though lesions slower to heal improve.

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146
Q

What is the presentation of actinobacillosis infection?

A

Can present in various forms:
wooden tongue - most common
Intestinal form - rare, lesions in oesophagus, oesophageal groove, cardia, rumen reticulum.
Cutaneous form - rare. caused by actinobacillus lignieresii a commensal gram -ve bacteria.

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147
Q

What are the clinical signs of actinobacillosis?

A

wooden tongue - salivation, dysphagia/anorexia, tongue protruding, enlarged submandibular Lns, selling under jaw. oral examination reveals painful swollen tongue, yellow lesions visible below mucosa.
Intestinal - insidious onset, chronic progression. Ruminal bloat most marked following eating. Non painful. Afebrile. rumination abnormal - prolonged gurgling pus retching. wt loss with normal appetite.
Cutaneous - often several animals, large granulomas and ulcers mouth head and chest.

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148
Q

What is the treatment of wooden tongue?

A

5 day course of streptomycin (penstrep combo) or potentiated sulphonamides. Or devomycin.
Iodides (not in pregnant animals. (older treatment, can break down granulomatous lesions).

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149
Q

What is seen in infection with actinomycoses? (lumpy jaw)

A

Actinomyces bovis gram + bacteria causing pyogranulomatous ostitis/osteomyelitis in bones of the head especially mandible. rarely soft tissue - alimentary tract. Clinical signs are firm bony swelling on jaw usually at level of central cheek teeth. surrounding painful soft tissue swelling usually present. dysphagia with gradual emaciation. animal bright. discharging sinuses internal or external. possible tooth displacement and pathological fractures. Treatment as for wooden tongue but prognosis very poor. can try high dose penicillin/streptomycin for 14 days in early caises. aim for remission then slaughter.

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150
Q

Describe infection with oral and laryngeal necrobacillosis? (calf diptheria)

A

Fusobacterium necrophorum bacteria plus trauma. concurrent disease or nutritional deficiency may predispose. Clinical signs - usually affects calves 1-3 months of age but laryngeal form may affect older calves. oral form - swelling of cheeks, necrotic halitosis, anorexia, salivation & pyrexia. Examination of oral cavity reveals lesions on cheeks, tongue etc. Occasionally overwhelming spread of infection. Laryngeal form - anorexia, pyrexia, cough, inspiratory stridor and dyspnoea, salivation, halitosis. swollen and painful laryngeal region.

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151
Q

What is the treatment of oral and laryngeal necrobacillosis?

A

Systemic antibiotics (potentiated sulphonamides, oxytetracycline, penicillin). Laryngeal: long term high dose antibiotics (lincomycin injection reported to be successful but not licensed in cattle). corticosteroids in acute stages to reduce laryngeal oedema. Tracheostomy if necessary. Poor prognosis in advanced cases due to suppurative chondritis.

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152
Q

What is choke?

A

Obstruction at the larynx, thoracic inlet, or thoracic oesophagus. Potatoes fed whole and not chewed. chopped swede or turnip unchewed. Salivation and repeated attempts to swallow. Progressive bloat according to nature of obstruction. Diagnosis: history of feeding, visual and palpatioon. Treatment - assess severity of rumenal tympany. emergency trocharize if necessary. Relax oesophagus eg buscopan injection. Allow 5 minute, gag then attempt to massage obstruction up to pharynx. If thoracic obstruction - use orogastric tube or probang to gently push in on the rumen. Last resort - create temporary rumenostomy and allow obstruction to degenerate over 3-4days, risk of oesophageal necrosis/rupture. Always give antibiosis and anti inflammatory treatment.

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153
Q

What is upper alimentary squamous neoplasia?

A

Bracken toxin inducing bovine papilloma virus. Signs - oropharyngeal - wasting, coughing, salivation. 2 - oesophageal - wasting, signs of choke, bloat. 3. rumenal tumours in association with 1 or 2. exacerbate wasting with diarrhoea. No treatment.

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154
Q

What is megaoesophagus?

A

Rare. Can be congenital. or acquired due to neurological damge. Signs are recurrent bloat, regurgitation and discomfort on eating. Diagnosis with contrast radiography. Treatment - supportive (+ temporary rumenotomy) treat any infection

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155
Q

Describe simple indigestion

A

Sudden diet change - upset in rumen microflora. Moderate CHO excess, excess oral antibiotic, sour/fermenting food etc. Signs are rumenal atony, inappetance, milk drop, dullness + colic. Reduced faecal quantity becoming diarrhoeic. Non pyrexic. Diagnosis - signs, history, full clinical examination - rule out other causes of rumen stasis. Treatment - rumen stimulants and palatable forage. Rumen inoculum; probioitcs, multi B vitamin injections. Calcium borogluconate in early lactation cows. Control - good nutritional management.

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156
Q

Why does carbohydrate overload cause disease? (Ruminal lactic acidosis, barley poisoning)

A

Imbalanced concentrate to roughage ratio. CHO engorgement following access to feed store usually, feed change or using finely ground cereal. As easily fermentable CHO is digested VFA production increases & rumen pH falls water absorbed from systemic circulation causing dehydration. Low rumen pH reduces motility - stasis and mild bloat. G-ve bacteria killed > release of endotoxin. Chemical damage to rumen wall > rumenitis.

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157
Q

What are the clinical signs of carbohydrate overload (barley poisoning)

A

Mild - discomfort, anorexia, reduced ruminal activity, ruminal distension, diarrhoea. Severe - anorexia, depression, dehydration, tachycardia, rumen stasis, abdominal pain, laminitis. Toxaemia > pyrexia then hypothermia, hyperaemic of mm’s, scleral congestion etc. acidosis > tachypnoea, weakness, ataxia, reduced vision, recumbency, opisthotonus, coma, death. Sequelae - progressive systemic acidosis, circulatory shock and death in severe cases. Recovered cases may get fungal rumenitis and chronic bloat. secondary liver abscessation. F necrophorum and actinomyces pyogenes, laminitis, cerebro cortical necrosis all possible

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158
Q

What is the treatment of carbohydrate overload?

A

if pulse >100bpm and rumen ph 10% roughage in any diet. prevent escapes and have locked food bins. crack or roll grains - do not grind.

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159
Q

What is rumen parakeratosis?

A

seen in animals fed 100% concentrate diet, or secondary to CHO overload. There is rumenitis > escape of rumen flora, liver abscesses, laminitis. Signs: vague illness, pain, indigestion. treatment - balanced diet, antibiosis. .

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160
Q

What is juvenile ruminal tympany?

A

Juvenile - failure in oesophageal closure so milk enters rumen, subsequent fermentation acidosis and rumenal atony. rapid onset L flank distension following milk feed, discomfoort and chronic pasty scour. treatment - decompression - stomach tube/needle/trochar, oral antibiosis, feeding management.

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161
Q

Describe frothy bloat in adult cattle?

A

Usually high protein levels in lush leguminous pasture - clover rich swards. V common on N zealand. bloat causing legumes are susceptible to rapid digestion by rumen microflora. occasionally seen in feedlot cattle fed finely ground grain. Rumen fluid viscosity raised therefore small bubbles form from rumen fermentation products. froth forms which cannot be eructated normally. Signs: acute rumen tympany, distress, recumbency, death in extreme cases. Diagnosis - usually a group problem, with a history of lush grazing, failure to relieve bloat with stomach tube, froth blocks tube. Treatment- move affected animals off pasture. drench/stomach tube with anti foaming agent eg vegetable oil or silicone drench. trocarisation of rumen can be done to relieve tympany. gradual introduction to risk pasture will prevent it. daily drenching with anti foaming agent. monensin in supplementary feed or bolus.

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162
Q

What causes free gas bloat?

A

Any condition causing oesophageal obstuction or interference with normal eructation may cause free gas bloat eg lesions of oesophageal groove, actinobacillosis or papillomatosis, physical obstruction/choke, physical pressure on oesphagus/vagal nerve by enlarged mediastinal bronchial LNs, common in 3-6 month old stirks following chronic pneumonia. thoracic mass eg thymic lymphosarcoma, neurogenic causes, tetanus, vagal indigestion, lateral recumbency, milk fever.

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163
Q

What are the signs of free gas bloat? how is it treated?

A

Distended left sublumbar fossa, progressive distress, usually a single animal, passage of stomach tube confirms free gas. Treeatment: pass tube to relieve bloat, insert trocar/canula or create surgical fistula if recurrent problem. Establihs primary cause if possible and treat accordingly eg antibiotics for actino.

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164
Q

What is vagal indigestion?

A

A fairly rare sporadic disease of adult cattle. damage/irritation to vagal nerve which may occur at different sites? most commonly associated with anterior peritonitis (traumatic reticulitis), liver abscess, mediastinal abscess and lymphosarcoma. Mechanical impairment of reticular motility leads to failure of normal ingesta passage through reticulo-omasal orifice and pylorus. this outflow abnormality of the reticulo rumen and abomasum leads to the signs seen - enlargeed impacted rumen with initial hypermotility, chronic enlargement of dorsal and ventral rumen sacs leads to Ll shaped distension of abdomen, progressive inanition/weight loss/dehydration, scant faeces, occasional bradycardia.

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165
Q

What causes traumatic reticulitis?

A

Occurs sporadically in adult airy cattle following ingestion of sharp metal objects and their localisation in the reticular wall. Outbreaks of disease have been reported caused by disintegration of tyres used on silage clamps and their incorporation into the mixed wagon, and following farm building work, bonfires etc.

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166
Q

What are the clinical signs of traumatic reticulitis?

A

Classical clinical signs are only observed when the foreign body is in contact with the peritoneal lining of the abdominal cavity and may last only 2-3 days then adhesions restrict movement. the rectal temperature is within the range 39-39.5. Sudden on set anorexia, dramatic fall in milk production e.g 30 litres/day to 2-3 litres/day. animal stands with an arched back and moves reluctantly last to enter the milking parlour. described by the farmer as stiff. complete ruminal atony, initial abdominal distension then becomes tucked up and gaunt resulting from poor appetite and shrunken rumen. Animal shows evidence of anteior abdominal pain, taut abdomen, refusal to turn sharp corners, ears back, fixed glazed stare. animal is constipated. defecation and urination frequently accompanied by grunt. pain response elicited, grunt or kick when back dipped behind withers or pressure applied slowly behind the xiphisternum with a pole then suddenly released (hyperalgesia). In cases where the foreign body has penetrated the reticular wall and is in contact with the diaphragm or omasum the clinical signs are less well defined and no grunt can be elicited.

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167
Q

How is diagnosis of traumatic reticulitis made?

A

Made on clinical findings and confirmed during surgery. ultrasonography will identify excess peritoneal fluid/exudate/fibrinous reaction surrounding the penetrating foreign body. reticular abscesses are identified after about 10 days by which time this reaction will seriously affect the outcome. linear array 5Mhz canners, used for bovine fertility work will provide diagnostic quality images. Metal detectors are a waste of time due to other metallic material collecting in the reticulum. routine haemoatology is non specific. peritoneal sampling - high protein and cell count comprised of mainly neutrophils and presence of bacteria, indicates septic peritonitis.

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168
Q

Describe surgery for Treatment of traumatic reticulitis

A

High left flank laparotomy under distal paravertebral analgesia. two 5mm nylon tape loops placed 15cm apart in muscular layer of rumen wall following its exteriorisation. incise into rumen between tape loops using scissors. place rumen on to right arm while an assistant holds tape loops. pass arm through 20cm raft of dry fibrous rumen content before entering fluid. angle hand toward xiphisternum taking rumen back in through wound if necessary providing that the rumen incision is small enough to fit tightly around your arm and there has been no leakage of rumen contents. the wall between the rumen and reticulum is 15cm high off the abdominal floor. pass hand along rumen floor then upward and forward into the reticulum. Carefully search the honeycomb lining for the wire. Check for adhesions. Remove foreign body. Rumen closed with an inversion suture of 3 metris chronic catgut. abdominal wound closed routinely. recovery even after successful removal of a foreign body is slow and it may take the cow four weeks to regain previous milk yield due to localised peritonitis interfering with reticular contractility and propulsion of digesta.

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169
Q

What is an LDA? When does it occur?

A

Left sided abomasal displacement. Occurs during the winter housing period in dairy cows most commonly but not exclusively in the month following calving. some association with hypocalcaemia, twinning, endometritis and high concentrate, low fibre rations. increasingly, LDA is seen in recently calved heifers and during the summer months. never seen in suckler cows or intensively fattened cattle.

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170
Q

What are the clinical signs of an LDA?

A

Variable, may be complicated by presence of other disease conditions namely metritis and secondary acetonaemia. Most severe when LDA occurs in conjunction with acute metritis in the 5-7 days after calving. the cow is often febrile, depressed, toxaemic, anorexic with a reduced milk yield. There is profuse often foetid diarrhoea, the animal is drawn up and flanks sunken, there may be moderate dehydration. The distended abomasum occupies the craniodorsal area of the left side of the abdominal cavity and auscultation and succussion reveals high pitched tinkling sounds. Rumen movements can be heard caudally in the sublumbar fossa. Rectal examination fails to reveal any abnormality. in cases occuring more than 10 days after calving there are typically clinical signs of chronic endometritis and secondary ketosis. a typical case is presented 15-30 days post calving ,history of poor milk yield, reduced appetite with chronic weight loss up to 50kg since calving, one unit of condition score, the cow is slow to move and dull. the coat is dry and staring. rectal temperature is often normal.

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171
Q

How is diagnosis of an LDA madE?

A

Diagnosis is based on thorough clinical examination remembering that more than one condition may exist at the same time i.e metritis and LDA, and secondary ketosis and LDA. diagnosis is confirmed on surgery. Parecentesis of the displaced abomasum contents (aided by ultrasonography) would reveal the presence of fluid containing no protozoa and a pH of 2 but such testing is rarely undertaken/necessary.

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172
Q

is roling the cow the correct treatment for an LDA?

A

Treatment - rolling the cow takes time, requires three people and may only be 40% effective at best. there is the risk of inhalation of rumen contents when the cow is in dorsal recumbency especially if she has been heavily sedated. surgical correction of LDA is the preferred option. There are many surgical techniques but right flank omentopexy is the preferred method. In some practices, toggling is performed because of perceived cost saviour to the farmer but this method is not without its problems (85% sucess rate).

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173
Q

Describe the right flank approach to LDA surgery.

A

Intravenous NSAID such as ketoprofen or flunixin administered preoperatively to effect analgesia. Surgery is performed in the standing cow under distal paravertebral analgesia. The abomasum is football sized and lies high up on the left side under the costal arch boyed by its gas content. A right laparotomy incision is made and the abomasum deflated using a 14 guage needle connected to a flutter valve or suction pump. upon release of the gas the abomasum sinks towards the midline pulled down by its liquid contents. The greater omentum is grasped with your left hand as near to the ventral midline as possible and gently pulled up to the ventral margin of the incision. the sows ear and pylorus can readily be identified and an omentopexy or pylorpexy performed whereby a continuous suture taking 4cm bites of omentum or pylorus is made and this suture continued to close the peritoneum and internal oblique muscle layer. the laparotomy wound is then closed routinely. Oral fluids 50-60 litres to distend shrunken rumen.

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174
Q

What supportive therapy should be given for LDA surgery?

A

for acute endometritis with LDA: treat for 3 consecutive days with oxytetracycline, administered intravenously on day 1. NSAID such as ketoprofen or flunixin to treat toxaemia - preoperatively to effect analgesia. 3 litres of 7.2% hypertonic saline intravenously on day 1 to treat endotoxaemia. Secondary acetonaemia: corticosteroid such as dexamethasone and 400mls 50% dextrose i/v, propylene glycol orally b.i.d.

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175
Q

How can LDA be controlled?

A

As the aetiology is incompletely understood control measures are vague btu the following are suggested: prompt treatment of retained placenta and early cases of metritis, provision of long fibre i.e h ay in early post partum period. avoid high concentrate levels immediately following calving. control measures for hypocalcaemia including use of acidifying diets during the dry period. Prevent over fatness of dry cows/heifers.

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176
Q

Toggling of the aboasum through the ventral abdominal wall overlying the tympanitic abomasum has been described as a more cost effective procedure. Describe how this procedure is done?

A

The cow is cast i nto orsal recumbency and the abomasum located in the midline by percussion. two toggles with nylon sutures are introduced into the abomasum through wide bore trochars approximately 5-10 cms apart, the trochars are removed and the nylon sutures tied together. Failure to accurately locate the abomasum may result in toggling other viscera although this method is reported to be about 85% effective.

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177
Q

Describe dilation and right sided displacement of the abomasum?

A

This occurs occasionally in dairy cows 3-6 weeks following calving. Less common than LDA. Probable cause is primary distension of the abomasum due to atony caused by high concentrate intake and secondary fermentation. Accumulation of fluid and gas leads to distension and dorsal displacement on the right hand side of the abdomen. Clinical signs include history of poor milk yield, inappetance and weight loss. auscultation reveals high pitched tympanic sounds just cranial to the right sublumbar fossa. torsion of the abomasum may occasionally result. Treatment - reported treatments for abomasal dilation include 400mls 40% calcium borogluconate i/v and substitute concentrates with hay for 2-5 days, plus oral and iv fluids as necessary. Hyoscine has been reported to be useful but there is little supporting evidence. Right omentopexy may relieve the problem but why such surgery should be successful is uncertain.

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178
Q

What is an abomasal volvulus?

A

Following dilatation a 180-270 torsion may occur resulting in an abdominal catastrophe. once torsion occurs the cows condition deteriorates rapidly within 12 hours. The cow may be recumbent and there is obvious right sided abdominal swelling. rapid dehydration, toxic injected mucus membranes. rapid heart rate >100/minute. cold sweat with subnormal rectal temperature. Obvious tympanic viscus occupying most of the right side abdomen extending as far forward as the seventh intercostal space. the liver becomes displaced from the abdominal wall - no longer identifiable during ultrasound examination.

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179
Q

What is the treatment for abomasal volvulus?

A

Surgical correction of the torsion is difficult but can be attempted in the standing patient using a right flank approach. improve cardiovascular function prior to surgery by administering hypertonic saline followed by rapid intravenous infusion of large volumes of isotonic saline. Prognosis is poor in cows with heart rate >100/minute and serum chloride <80mmolL due to sequestration of chloride ions in abomasum.

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180
Q

Describe abomasal ulcers in calves

A

In young calves (2-3 week old) this condition is likely to be complicated by secondary fungal infection of the ulcer as such cases have often received prolonged oral antibiotic treatment by the farmer. Oral electrolytes made up to 2 litres given 4 times daily will maintain the calf but the prognosis is poor for those cases which will not suck or eat within 3-4 days.

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181
Q

Describe abomasal ulcers in adult dairy cows?

A

Clinical signs include poor milk production in the early post partum period, weight loss and melena. Few cows bleed to death despite very low PCV values as low as 10%. In severely affected cows, emergency slaughter may be the best option. In less Severely affected cases supportive therapy including i/v fluids, kaolin and pectin, magnesium oxide have all been recommended but are ineffective. most cows recover over a period of several weeks.

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182
Q

What is abomasal impaction?

A

It is sometimes recognised during the winter months in beef cattle fed poor quality diets of wheat straw and liquid urea supplements only. pregnant suckler cows may suffer from this condition when on similar diets but the development of starvation ketosis and other metabolic disturbances assume greater importance. The animal is often in poor condition, slow, dull with a long dry winter coat and abdomen is often pear shaped. very scant hard balls of faeces with copious mucus in rectum. Very sluggish rumen. The rumen can easily be pitted. Ddx - inadequate diet/starvation, vagus indigestion, peritonitis. Treat with 250g sodium chloride in 25-50 L water by stomach tube. Multivitamins given IV. !6-24 L saline iv. Repeat treatment day 2 if necessary. 5-10 litres mineral oil or liqud paraffin.

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183
Q

Describe when hair balls occur in cattle?

A

May occur in association with heavy louse infestation. hair balls are a common coincidental finding at post mortem of young calves. Where blockage of the pylorus occurs there is an acute onset of abdominal pian, kicking at its belly, frequently getting up and down. auscultation reveals a fluid and gas filled viscus under considerable pressure in the lower right hand side of the abdomen. The role of hair balls in cases of ill thrift is uncertain - they may simply be result rather than a cause.

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184
Q

Describe caecal dilation and torsion?

A

Occurs in dairy cows fed restricted roughage and high levels of concentrates. also may occur following change of pasture. Incompletely fermented carbohydrate reaching the caecum is fermented and the resultant volatile fatty acids produced cause caecal atony. Decreased motility leads to dilation impaction and possible torsion. there is a drop in milk yield over several days and poor appetite. the animal shows tenesmus but there are scant faeces in the rectum. rumen activity is normal but the cow is drawn in. On rectal examination a 15-25 cm diameter cylindrical blind ended viscus is easily palpable extending into the pelvis. The caecum may kink on itself (retroflex) and therefore not be palpable on rectal exam.

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185
Q

What is the treatment of caecal torsion and dilation?

A

Rectal palpation of the blind end of the caecum extending into the pelvis is pathognomonic. Remission of the caecal dilation has been recorded following transportation to surgery facility. Access is achieved through a right flank laparotomy under distal paravertebral anaesthesia. exteriorisation and drainage through an incision made in the blind end of the caecum is a simple procedure. recovery of previous milk yield may take several weeks.

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186
Q

Describe umbilical hernias in cattle. When might they need treated?

A

Umbilical hernias less than 5cm diameter are of no consequences. Larger hernias frequently contain omentum and small intestine and are most commonly presented for cosmetic reasons in breeding heifers, strangulation of hernia sac contents is very uncommon in cattle. hernia rings greater than 10cms may require a mesh during closure. umbilical hernias can be readily distinguished from umbilical abscesses during clinical examination but occasionally both conditions can occur together when the extent of the infection can be determined ultrasonographically.

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187
Q

What is a patent urachus?

A

A tubular connection between the bladder and umbilicus which persists after birth with small quantitis of urine dribbled from the umbilicus. can be difficult to detect when there is concurrent omphalophlebitis/umbilical abscess and purulent discharge. clinical signs usually not detected until the urachus/bladder becomes infected or a urachal abscess and adhesions develop. More common in male calves. The condition may be overlooked and resolve with time.

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188
Q

Describe a calf with an infected patent urachus

A

Affected calves are poorly grown, intermittently febrile and may show pain on urination, they often have cystitis. urinalysis is helpful in the diagnosis - ascending infections of the urinary tract via the urethra are very uncommon in young ruminants. a corded structure up to 2cm in diameter may be felt on deep palpation extending from the umbilicus to the apex of the bladder but this is not always easy especially if there is considerable painful umbilical reaction. ultrasonographic findings may prove difficult to interpret. Do not mistake digesta in small intestine for infected urachus.

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189
Q

Which bacteria are most commonly isolated from urachal abscesses?

A

Trueperella pyogenes, streptococci, and staphylococci most commonly isolated therefore treatment with penicillin - excreted in urine for up to 4-6 weeks is indicated but the prognosis is poor. surgical resection is difficult because of adhesions to small intestine and possibly the bladder. Such surgery is often further complicated by umbilical infection. wound breakdown of resected umbilical lesions is not uncommon.

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190
Q

Describe the legislation in place for castration?

A

Calves, lambs and goat kids can be castrated by rubber ring 2 months of age by any method requires local anaesthetic and in lambs > 3 months of age requires anaesthetic. Pigs castrated > 7 days of age require an anaesthetic.

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191
Q

How can calves be castrated?

A

Calves can be castrated by rubber ring if applied <7 days of age. this is an efficient and safe technique if carried out at the correct age and requires no local anaestheetic. complications are limited to failure to apply ring properly leaving a rig calf. Illegal application of rings to older calves can lead to gangrenous ischaemia of scrotum and possibly tetanus.

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192
Q

Describe the open surgical castration of calves.

A

This is an act of veterinary surgery in calves > 2 months of age and requires an anaesthetic. Ideally carried out at 1-3 months of age but farmers often present beef calves for castration at 6+ months. Local anaesthesia is carried out by injection 3-5ml of procaine under the scrotal skin into the testicle. Lignocaine no longer licensed for food animal use. GA only considered for mature bulls or complicated cases. Combination of xylazine and ketamine suitable for field anaesthesia or deep sedation. Make large J shaped incision on lateral wall of scrotum over tensed testicle extending through vaginal tunic. Ensure incision extends into base of scrotum to llow adequate post op drainage. grasp testicle and separate vascular part of spermatic cord from non vascular epididymal ligament complex. Make several rotational turns of testicle to twist proximal cord and then wrap around forefinger before applying steady traction to cord to rupture vessels within abdomen. The ruptured vessels will recoil within the abdomen and cause haemostasis. If remnant of ductus deferens is hanging from base of scrotum it should be pulled distally and trimmed. spray scrotal wound with topical oxytetracycline. Some give post op penicillin. Unlike horses, tetanus anti toxin not routinely given.

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193
Q

What are the potential complications with open surgical castration?

A

Haemorrhage may be seen where the vascular portion of the cord is snapped off close to the testes. Avoid this by ensuring the cord is grasped as high up as possible before applying traction. The vascular cord can be grasped with a pair of clean artery forceps and pulled out of the scrotal neck before applying traction. In most cases a clot will form and the haemorrhage will be controlled. if b lood continues to run out in a steady stream then packing of the scrotum can be attempted. often develop a large scrotal haematoma/abscess which needs drained. gut tie is a rare complication of surgical castration of older calves - the remnant of the spermatic cord recoils into the abdomen and can become adherent to the abdominal wall or viscera causing slow onset mechanical obstruction of the bowel.

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194
Q

What are rig calves/ incomplete testicular descent?

A

Cryptorchid calves are occasionally presented for castration. If only one testicle is descended the calf should not be unilaterally castrated as the remaining testicle may descend at a later date and the bull calf become fertile leading to unexpected misalliance pregnancies. Cryptorchid calves should be left entire and reared as bulls. in some cases a partially descended testicle will be palpable in the inguinal area and can be removed with care. sedation/anaesthesia may be required to facilitate this surgery.

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195
Q

Describe bloodless castration with burdizzo.

A

Burdizzo castration is often carried out by stockmen and should be carried out before 2 months of age otherwise local anaesthetic is required. The technique involves pulling down on the testicles to get access to the neck of the scrotum. The burdizzo clamp is applied twice across each side of the spermatic cord taking care to stagger the position of crushing. the clamps cause crushing of the spermatic vessels which leads to ischemic necrosis of the testicles over the following weeks. Calves should be checked after 1-2 months to ensure the technique has been effective. Poor technique or using burdizzos that are not matched to size of calf can lead to partial castration leaving calves that may be sterile due to blockage of epididymis but continue to develop as bulls due to testosterone production from viable testicle. Subsequent surgical castration of these calves is difficult due to adhesions within the vaginal tunic and cord.

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196
Q

How should lambs and goat kits be castrated?

A

They should be castrated by rubber ring <7 days of age. Otherwise, the simplest method is to grasp the base of the scrotum with forceps and remove with a single cut. the testicle can then be grasped within their tunics and are removed with simple traction. in older lambs or adult sheep local or preferably GA (xylazine and ketamine) is required. closed or open castration with emasculation of the cord is preferred to reduce risk of haemorrhage. Ligatures can be applied before emasculation of the cord however this requires good surgical cleanliness. protection against tetanus s required and most sheep/goats are vaccinated with multivalent clostridial vaccines. post operative antibiotic and analgesia should be given following surgical castration of older lambs/goats. Drugs such as flunixin, ketoprofen and meloxicam are licensed for cattle and can be used under the cascade legislation for sheep/goats.

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197
Q

What is vasectomy? how is the surgery done?

A

Vasectomy is used as a technique to produce teaser rams and occasionally bulls and boars. The ram is positioned on its hind quarters or in dorsal recumbency following sedation (xylazine) and local anaesthesia or epidural. Local must be carefully injected subcutaneously in the site of incision over the spermatic cord without puncturing the cord as this will cause peri operative swelling/haematoma. General anaesthesia with pentobarbitone or xylazine/ketamine is preferred by some practitioners. An incision is made in the skin over the spermatic cord at the level of the Accessory teats. The spermatic cord is exteriorised following blunt dissection and the vas deferens localised medially within the spermatic cord between the thumb and index finger. the tunic is nicked with the scalpel blade and vas deferens freed from connective tissue, it is then ligated twice and the section between sutures is removed. The ligated ends of the vas deferens are incorporated into different fascial planes during closure to reduce possibility of re canalisation. The skin incision is closed with interrupted mattress suture. Sperm granulomas may develop but do not affect behaviour.

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198
Q

Describe the legislation in place for dehorning/disbuding?

A

Chemical cautery eg hornex paste can be applied <7days of age without need for anaesthetic however all methods of disbudding and dehorning in cattle of any age require an anaesthetic. disbudding/dehorning calves is not an act of veterinary surgery and can be carried out by trained stockpersons.

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199
Q

How can cattle be disbudded/dehorned?

A

ideally at 2-6 weeks when easily handled and horn bud still small. following a cornual nerve block using 2-4 ml procaine per side the bud is removed by red hot gas/electric disbuding iron. the bud should be totally removed by burning the surrounding tissue right down to the surface of the skull. the skull of the calf is thick in this area. topical antibiotic spray should be applied to the wound but is noot essential. haemorrhage is normally completely controlled by the cauterising effect of the disbudding iron though occasionally calves will rub the skull wounds. calves 1-3 months will develop horn buds that may be too large for removal with hot iron and these will require cutting with hoof shears or dehorning scoops prior to thermal cautery. At around 6 months dehorning shears or embryotomy wire will be required for horn removal. With both these techniques the horn must be cut level with the base of the skull, normally exposing the frontal sinus and ring of horn vessels. The cut ends of the cornual artery should be identified, clamped and pulled with artery forceps to assist haemostasis. When dehorning large beef calves add 3-4ml of 2% xylazine injection to a bottle of 100ml local anaesthetic. Giving this gives local analgesia plus mild sedation.

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200
Q

What complications may follow dehorning?

A

Haemorrhage from the nose is often seen immediately after dehorning older cattle and is simply due to blood running through the sinuses and draining into the nasal cavity. it is not a cause for concern. Rarely, fatal haemorrhage from cornual artery bleeding can occur following dehorning of large calves so calves should always be checked for spurters after dehorning and haemostasis. sinusitis is occasionally seen in older cattle after dehorning. cattle may appear dull and reluctant to feed at barriers and may have obvious purulent discharge from dehorning wound. treatment by reuglar flushing with dilute povidone iodine along with systemic antibiotics is normally effective and sinus trephination rarely needed.

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201
Q

Describe the disbudding of goat kids

A

Goat kids have a much larger area of horn bud relative to calves and the horn grows rapidly necessitating early disbudding <7 days old. ideally a short acting general is give (eg saffan or propofol) which can be supplemented by local anaesthetic. local anaesthesia of the horn bud requires blocking of the cornual branches of the lacrimal and infratrochlear nerves using a maximum of 1ml 2% lignocaine per kid to prevent toxicity. A red hot iron is applied briefly to the skull ensuring a large enough area of skin surrounding the bud is destroyed before gently scooping off the bud. NB the skull is much thinner than calves and overheating can cause brain damage so the iron must only be applied with gentle pressure for short periods only.

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202
Q

Describe umbilical hernias in calves

A

Umbilical hernia is a relatively common hereditary defect in holstein dairy calves. uncomplicated cases present as variable sized, soft, reducible swellings at the umbilicus. Most hernial rings are <5cm will normally cause no clinical problems and become insignificant as calves grow. Larger hernias may lea to problems as abomasum enters the hernial sac and forms local adhesions leading to motility problems. surgery indicated in larger hernias and when clinical problems develop. Surgery is carried out with the calf in dorsa recumbency following xylazine sedation and local. The sac is dissected free and returned into the abdominal cavity. Large umbilical hernias may require closure with polypropylene mesh implants though this may nto be economically viable in most cases.

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203
Q

Describe what can happen with complicated umbilical hernias in calves?

A

Umbilical hernias may be complicated by the presence of subcutaneous abscessation or infection of the umbilical vessel/urachal remnants. this will lead to painful, inflamed umbilical swelling that may be hard to reduce. there is often an intermittent purulent discharge from the umbilicus at the most ventral point of the hernia. ultrasound is useful for investigating the extent and type of infection present. simple subcutaneous abscesses will require lancing and drainage. Infection of the umbilical vein or urachus may require radical surgical excision via laparotomy before any hernial defect is repaired. Conservative treatment of calves with chronic purulent omphalophlebitis/urachitis with or without associated hernia, using systemic antibiotics is rarely successful and these calves often fail to thrive.

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204
Q

How should bull nose ringing be done?

A

All mature stock bulls should have nose rings inserted to aid handling and restraint. to insert a copper nose ring the bull must be restrained in a crush and a halter applied. light sedation with xylazine may be required in fractious bulls. local anaesthetic is injected with a fine needle into the nasal septum. the septum is punctured just cranial to the cartilaginous septum using a leather lunch or trocar before pushing the sharp end of the open ring through the defect. the ring is closed and the retaining screw is carefully tightened and snapped off flush. Rings smaller than 3 inches are rarely inserted as young bulls will quickly outgrow smaller rings.

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205
Q

How does infection with leptospira hardjo occur?

A

Infection follows bacterial penetration of mucous membranes/skin. In non immune lactating or pregnant animal rapid multiplication in uterus or udder followed by bacteraemia. BActeraemia persists for 6-9 days until humoral antibodies appear. leptospira can persist after initial bacteraemia in CNS, repro tract and kidneys. following acute infection renal shedding of leptospires in urine occurs after about 114 days and may persist for months or intermittent shedding may occurs for years. Pasteurisation will destroy any lepto excreted in milk. Following infection antibody titre may disappear but carrier state still exists.

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206
Q

What are the different routes of transmission of leptospira hardjo?

A

Infection arises frmo contact with infected urine or from water/pasture contaminated with urine. products of abortion also source of infection. most spread probably occurs in spring/summer at pasture. venereal transmission possible from bulls carrying lepto in accessory sex glands. Leptospira hardjo not carried by vermin/wildlife. sheep can carry and excrete leptospira hardjo. LEptospires do not tolerate drying, exposure to sunlight, ph <5.8 or extremes of temperature. pasture unlikely to remain infected for more than two months after animals are taken off it. Risk factors for lepto infection: open herd, shared bulls, mixed grazing with sheep, shared grazing/water courses.

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207
Q

What are the clinical syndromes of infection with leptospira hardjo?

A
  1. Milk drop - occurs 2-7 days after initial infection of non immune cow. sudden reduction or cessation of yield. may get thick colostrum like blood tinged milk in all quarters. udder goes soft and flabby. may be slightly lethargic/stiffness and anorexia with pyrexia.
  2. Abortion - abortion may occur 3-12 weeks following infection, most abortions occur in last trimester. may also get weak/premature calves born.
  3. Inferility - May cause embryonic death. venereal transmission possible. May not effect pregnancy as lepto killed by uterine defenses around oestrus. semen from AI stud bulls has streptomycin added. split herd vaccination trials show some evidence of overall improved fertility parameters.
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208
Q

How is diagnosis of leptospira hardjo made?

A

Microscopic agglutination test (MAT) used to detect antibodies to lepto hardjo in serum and more recently this is being replaced by an ELISA. problems in interpretation of serology with lepto infection in cattle. Carrier animals may have negative MAT test. False positives also occur. In acute infection paired serum samples taken 3-4 weeks apart will Normally demonstrate seroconversion. Maternal serology may be of limited use as serotitre may be high low or negative by time abortion occurs. in abortion outbreak, some aborted cows have MAT titres of > 1/400 then this is likely to be significant. ELISA titre likely to remain positive for much longer following infection. Antibodies in foetal fluids - may indicate exposure to lepto in utero after period of immunocompetence >4 months. foetus may die before mounting an immune response. fluorescent antibody test to detect lepto antigen in foetal tissues eg kidney, liver. Best test to confirm diagnosis of lept abortion but in practice labs seldom get positive results as delay in submitting samples.

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209
Q

What is the treatment of leptospira hardjo?

A

Streptomycin/dihydrotreptomycin single i/m dose of 25mg/kg will probably eliminate infection in most cases. This dose is higher than data sheet recommendations. oxytetracycline or amoxycillin also likely to be effective. antibiotic treatment may still leave carrier state in some cattle. Antibiotic treatment of clinical milk drop case indicated to reduce excretion and zoonotic risk.

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210
Q

Describe the control/preevention of lepto hardjo?

A

Combination of management decisions to reuce risk of infection, antibiotic treatment and vaccination. two killed, adjuvanted vaccines available in the UK. primary course of immunisation consists of two injections 4 weeks apart followed by annual boosting. vaccinal MAT titres may fall to low levels within 3-4 months but are not correlated to protective immunity. ELISA test detects vaccinal antibodies for up to a year or more. vaccination should prevent urine shedding following exposure and will protect against milk drop and abortion. In some herds which have been fully vaccinated for several years there may still be renal carriers of infection so cessation of vaccination may lead to reappearance of clinical disease.

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211
Q

Describe different control strategies for control of leptospira Hardjo.

A
  1. Closed herd - no evidence of previous infection - avoid mixed grazing with sheep and fields with shared water courses. any additions to breeding herd including bulls should be isolated for 3 weeks and treated with streptomycin 25/mg/kg twice 10-14 days apart. 2. herd experiencing acute infection for first time - milk drop, abortions etc - consider whole herd antibiotic treatment to reduce risk of spread of infection and zoonotic risk. start vaccination programme for whole herd. bought in replacements should be vaccinated before entry. 3. Herd with evidence of endemic infection from herd screening or abortion serology etc - decision must be made on economic/ COSHH grounds whether vaccination worthwhile. if herd vaccination started should continue annual booster for whole herd. heifers should complete vaccination course before first mating.
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212
Q

Describe the key points regarding leptospira hardjo blood tests, source of infection and vaccinations.

A

Blood tests cannot be used to classify individuals as infected or non infected. seronegative animals may be infected and seropositive animals may have overcome their infection. Serology if of value in assessing the status of a herd or in the diagnosis of acute infection. The commonest source of infection is the purcahse or hire of an infected animal or contact with infected animals on common grazing. Vermin or other wildlife species play no part in spreading L hardjo infection. Clinical disease may only be apparent when infected first enters a herd. herds may be chronically infected without apparent diseaese. Vaccination can prevent clinical disease (abortions and milk drop) but may not eradicate infection. The COSHH regulations cover exposure to infected urine or uterine discharges. the regulations require a herd owner to ensure that his employees are informed of the potential risks from L hardjo and offer protection from infection risk. for this reason many dairy herds are vaccinated.

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213
Q

Describe the epidemiology of Malignant catarrhal fever?

A

A herpeves virus (ovine herpes virus 2) which has not been fully characterised but is sheep associated. Sheep appear to be most likely reservoir of infection. MCF is a relatively sporadic disease affecting cattle and deer. it is unusual to see more than one case on a single farm over a long time period. Contact with sheep or goats around lambing seems to be necessary for transmission to cattle. method of transmission unknown. May occur months after contact with sheep suggesting prolonged incubation or latent infection. virus is very fragile and will not survive more than a day outside the carrier host. Cattle are dead end hosts and don’t transmit MCF.

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214
Q

What are the clinical signs of MCF?

A

Acute onset illness with depression, anorexia and pyrexia. other characteristic signs include intense scleral congestion, erosive stomatitis of the buccal mucosa and muzzle, profuse muco purulent occulo nasal discharge, leads to stertor, generalised superficial lymph node enlargement, muscle tremors, hyperaesthesia, incoordination, head pressing, generalised exudative dermatitis, diarrhoea.

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215
Q

How is diagnosis of MCF made?

A

History of sheep contact and characteristic clinical signs (CNS signs rare with any other mucosal disease). Widespread vasculitis on PM. Diff diagnosis are IBR, BVD, BTS, VSV, FMD. Serological test available for MCF antibodies but this test may not be positive at the time of initial clinical signs. demonstration of viral genome in blood.

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216
Q

What is the treatment of MCF?

A

No treatment indicated in MCF as mortality is close to 100%. high doses of corticosteroids given systemically may give temporary improvement of clinical signs. death normally occurs 5-10 days after onset of clinical signs. Euthanasia on humane grounds should be recommended. occasionally an MCF case survives the acute disease to either recover or become chronic. Chronic MCF cases may show apparent temporary recovery but often relapse and rarely survive. control relies on avoiding contact with sheep.

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217
Q

Describe the aetiology of sporadic bovine leukosis (lymphosarcoma)

A

The cause of sporadic lymphosarcoma is unknown and affected cattle are seronegative for EBLvirus (enzootic bovine leukosis) caused by a retrovirus is a notifiable disease and currently not present in the UK. The disease is rare and sporadic in cattle and appearsin 3 main forms - juvenile, thymic and skin forms although a more generalised multicentric form can be seen.

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218
Q

Describe the juvenile form of sporadic bovine leukosis

A

occurs in calves aged 2weeks to 6 months. this form is characterised by generalised enlargement of all lymph nodes. superficial LNs are visible from a distance in some cases. gradual weight loss, depression and other signs related to tumour masses in thorax and abdomen. death inevitable after a variable length of illness.

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219
Q

Describe the thymic form of sporadic bovine leukosis

A

Occurs in older cattle typically 1-2 years of age. characterised by massive enlargement of thymus and local LNs. Thymic mass causes jugular engorgement, oedema of brisket extending to submandibular region and chronic bloat due to oesophageal compression. gradual weight loss and death.

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220
Q

Describe the skin form of sporadic bovine leukosis.

A

Normally in cattle <3 yo. cutaneous plaques of varying size appear over the neck, back, flank and thighs. lesions can develop rapidly, become covered in a necrotic pale scab and then may regress. peripheral LNs are also enlarged. recurrence of lesions is likely and often will be associated with tumours developing elsewhere eg meninges, heart, abomasum, spleen. weight loss and death related to pathology in internal organs.

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221
Q

How is diagnosis of sporadic bovine leukosis made?

A

Diagnosis of sporadic lymphosarcoma is normally made on clinical signs and post mortem. cattle showing signs of generalised lymphosarcoma should be reported to loal animal health office who may request serology for EBL. There is no serological test for sporadic leukosis as the aetiology is unknown. Biopsy of peripheral LNs or skin lesions is useful. post mortem findings depend on the form of disease but in addition to LNs, tumour masses can be found in a wide variety of organs including heart, abomasum, liver, spleen and CNS.

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222
Q

Describe bovine viral diarrhoea virus? What are the two distinct bioptypes?

A

It is a pestivirus closely related to viruses causing border disease BD in sheep and classical swine fever in pigs. Two distinct forms distinguished by effects on cell culture: cytopathic and non cytopathic (ncp). >9% of uk dairy herds have exposure to BVD and 40% of scottish beef herds show evidence of active infection. Viraemic animals shed virus in nasopharyngeal secretions, urine, aerosol droplets. faeces not a major source of virus excretion. Main transmission is by contact with viraemic animal. Sheep and deer can also act as vectors. Can also be transmitted in fresh or frozen semen of infected bulls.

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223
Q

What are the clinical signs of acute BVD infection?

A

it is seen when previous unexposed antibody negative animal becomes exposed to non cytoopathic BVD virus. Following transient viraemia the animal seroconverts within 3-4 weeks and may remain antibody posivie for years. Many acute infections are subclinical. signs: pyrexia, leucopaenia, dullness, oral/nasal erosions which quickly heal, transient scour, milk drop. Most affected animals recover uneventfully. May temporarily lower immunity to other infectious diseases eg salmonella, IBR, RSV, coccidia.

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224
Q

Describe the different sequelae to acute BDVD infection?

A

In a non pregnant animal - clinical recovery followed by seroconversion and long standing immunity.

Pregnant animal - acute BVD infection during pregnancy in naive cow/heifer can cause various problems associated with transplacental infection of the foetus in utero. Depending on the stage of pregnancy can get: embryonic death, foetal death/abortion, mummmification, congenital defects of CNS and eyes, weak /premature calves, live persistently viraemic calves or live normal seropositive calves.

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225
Q

Describe BVD infection in a pregnant animal <120 days of gestation

A

May lead to birth of live persistently infected PI calf. this is caused by failure of the foetus to recognise virus as foreign due to immune system not being fully functional. <120 days immunotolerant. PI calves are born viraemic and remain so, acting as potent transmitters of BVDV infection.

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226
Q

Describe what occurs when a pregnant animal 90-150 days of gestation is infected with BVD?

A

May lead to congenital abnormalities forming catarats, retinal dysplasia, cerebellar hypoplasia, CNS dysmelination, cerebral cavitation etc. These calves may be born showing ataxia, blindness and are normally antibody positive if sampled before sucking colostrum.

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227
Q

What happens if a pregnant animal is infected >150 days of gestation with BVD

A

Infection >150 days gestation often gives live seropositive calves born at full term. Abortion can occur following infection at any stage of pregnancy but is not common. Colostrally derived antibodies normally disappear in calves by 6 months but can persist for as long as one year.

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228
Q

What is mucosal disease?

A

Can only occur in animas which have been born persistently viraemic following in utero exposure to Ncp BVD in early pregnancy. Mucosal disease occurs when PI animal becomes superinfected with CpBVD virus. The CpBVD virus can arise from genetic assortment of the NcpBVD virus within the PI anima, from transfer of genetic material from a heterologous strain to the NcpBVD strain or can arise as an entirely new strain. most cases occur in 6 month to 2 year age group which may coincide with the waning of passive immunity. Most PI animals die within the first two years of life but a few can survive until much older. PIs are a main source of virus for transmission of disease.

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229
Q

What are the clinical signs of mucosal disease?

A

Acute onset depresison, pyrexia, anorexia. Salivation around muzzle, widespread oral /nasal erosions/ulcers especially on hard palate, gums, dental pad. often mucopurulent nasal discharge. profuse diarrhoea/dysentry with shreds of gut mucosa/blood present in terminal stages. May be interdigital skin erosions/ulcers present and occasionally dermatitis. Rapid weight loss and death within 5-10 days.

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230
Q

How is diagnosis of BVD/ mucosal disease madE?

A

Acute BVD infection - paired acute/convalescent sera 3-4 weeks apart to demonstrate rising titre (ELISA test), hard to interpret in calves< 6mo as maternally derived antibodies still present.
Mucosal disease - Characteristic pm findings - virus isolation from p.m tissues. Take blood sample and test for antibody/antigen. Normally antibody negative, antigen positive on ELISA test. may be low antibody titre along with virus positive due to persistent maternally derived antibodies.
3. Persistent infection - PI calves can often be clinically normal before developing mucosal disease but may commonly be presented as chronic ill thriven or stunted calves. can confirm PI status testing tissue or blood for persistent viraemia. Ear notch testing can be done at any age. IDEXX BVDV serum antigen test used by some labs accurately detects PI calves from 1 month of age in the presence of maternal antibodies. Take two samples 3-4 weeks apart to confirm persistent virus positive status. Newborn calves can also be tested for virus status if sampled before suckling coostrum. Herd screening - to establish BVD status of herd - monitor BVD free herds. Bulk milk and or first lactation screens (dairy only).

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231
Q

What is the treatment of BVD?

A

Acute BDV - symptomatic supportive treatment for enteritis.
Mucosal disease - no effective treatment, will invariably die.
Persistent infection - PI animals should be disposed of as they act as a source of infection. if old enough can attempt salvage slaughter if symptomless.

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232
Q

Is BVD a cause of infertility in bulls?

A

BVD virus can be spread in semen of PI bulls or in bulls experiencing acute BVD with transient viraemia. will lead to low pregnancy rate due to embryonic death or later foetal death/abortion. occasionally infected semen can cause conception and birth of Live PI calf. bulls are tested for BVD before entering AI studs.

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233
Q

What are the different control options for BVD?

A

Do nothing - many herds are endemically infected with BVD and disease is partly controlled by PI calves acting as vaccinators of herd. when most adult animals in herd seropositive then disease losses not so obvious to farmer. Not ideal as ongoing losses likely especially if naive breeding females introduced. Vaccination - 2 inactivated BVD vaccines now available in the UK. initial vaccination 2 doses 3-4 weeks apart before first service followed by boosters at 6 or 12 month intervals, depending on the vaccine used. if all breeding females are vaccinated then this should control disease by preventing acute BVD and production of PI calves. Eradication - BVD eradication is possible following whole herd blood testing and elimination of PI carrier animals. if farmers go for eradication then strict herd biosecurity measures must be maintained to prevent re introduction of disease as herd will soon become naive. scotland is in process of eradicating BVD.

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234
Q

What is bovine neonatal pancytopaenia?

A

It affects calves, causes bleeding from intact skin, injection sites, tagging sites, nose and rectum. Destruction of bone marrow causes pancyotpaenia. Can be associated with use of pregsure BVD vaccine. Rare.

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235
Q

What is necrotic enteritis in beef suckler calves?

A

This disease is seen almost exclusively in spring born suckled calves and normally affects calves in 2-4 month old age goup. Most cases are seen at pasture in june/july. The morbidity is usually low but mortality rates in affected calves are high. disease often recurs in same herd in successive years. common clinical signs are depression and pyrexia in acute stages, diarrhoea often profuse and haemorrhagic then progressing to more scant muco haemorrhagic faeces, tenesmus and abdominal pain, respiratory signs, pale mucous membranes due to anaemia, occasional oral and nasal ulcers.

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236
Q

What are the typical clinical chemistry and gross pathology signs in necrotic enteritis?

A

Anaemia and leucopaenia caused by a severe non regenerative neutropenia. cases exhibiting profound neutropenia carry a poor prognosis. many affected calves have high blood urea levels associated with kidney pathology. The gross pathology - crusting of the nasal mucosa with oral ulceration, oral ulcers often restricted to hard palate, ulcers often overlaid by necrotic debris and secondary fungal infection can be seen in the larynx rumen abomasum and small intestines. the ileum caecum and colon are the areas of the intestinal tract most commonly affected with lesions sometimes extending as far as the rectum. the ulcerative lesions vary frmo small discrete punctate lesions to large linear diptheritic placques overlying peyers patches. The ulcers are often full thickness. Kidneys appear swollen and pale with infarcts present. Lung lesions typical of inhalation pneumonia often seen in association with severe pharyngeal and laryngeal ulcerative lesions. Aetiology remains unclear. Treatment symptomatic and give sulphonamides and fluid therapy.

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237
Q

What is salmonellosis? Which animals does it mainly affect?

A

Salmonellosis is mainly a problem of young calves but any age group can be affected. outbreaks in adult dairy beef and cows are not infrequent. S. typhimurium and S dublin are the most common serotypes causing disease in UK cattle. S dublin most common.

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238
Q

Describe infection of salmonellosis?

A

Faecal oral infection is the most common route of infection. S. Dublin Infection normally arises from exposure to infected purchased animal or from carrier animals in herd. In infected herds cows can become symptomless carriers and excrete at times of stress. Liver fluke damage can predispose cows to excrete, as S dublin will persist in gall bladder/bile ducts. S typhimurium infection normally arises due to contact with infected purchased animal particularly if passed through markets or via contaminated feed stuffs, pasture or water courses. Most outbreaks of salmonellosis occur in winter months.

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239
Q

What are the clinical signs of salmonellosis in calves?

A

Very variable in severity depending on age and immunity, virulence and infecting dose, concurrent disease. often 2-6 week old calves affected. Can be acute septicaemia and death with either serotype. S. dublin may cause pneumonia. Commonly dull, anorexic, pyrexic and have pasty faeces with blood present. Develop more watery foul smelling diarrhoea with shreds of gut lining passed (s. typhimurium). progressive dehydration with tucked up abdomen. High morbidity and mortality can be >60%. Calves that survive can go on to develop chronic ill thrift due to polyarthritis/physitis due to initial septicaemic episode. Extremities may slough following septicaemia.

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240
Q

What are the clinical signs of salmonella infection in adult cattle?

A

Salmonella infection causes enteritis and septicaemia often with abortion if infection occurs in late pregnancy or shedding of the causative organism into milk. S dublin can cause abortion with no signs of enteritis/septicaemia. Severity of clinical signs in outbreak varies considerably in adults. most severe in stressed groups of animals eg newly calved dairy cows, cows in poor body condition, cows in late pregnancy etc. concurrent disease eg BVDV will increase severity. main signs: acute enteritis/dysentery often blood and shreds of mucosa, pyrexia, acute milk drop it lactating, depression/anorexia, septicaemia/dehydration, abortion followed by septic metritis in some cases. Morbidity variable 10-70% depending on virulence of serotype, dose of inoculum, degree of immunity, concurrent stress etc. mortality variable as above. some strains more pathogenic than others.

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241
Q

What is the treatment of salmonellosis?

A

Isolate affected animals if possible to limit spread. Systemic antibiotics - controversial. Efficacy dubious in adult cattle and may prolong excretion if used at insufficient doses. Also potential for emergence of resistant strains. prompt treatment of calves during outbreak may prevent septicaemia and sequelae and clinical impressions suggest a shorter course of disease with higher recovery rate. must check strain sensitivity in vitro as multiple resistance to commonly used antibiotics is widespread. Enrofloxacin, apramycin, florfenicol and clavulanate potentiated amoxycillin are normally effective in vitro. Supportive treatment - NSAIDs, oral or iv fluids, nursing. control of herd outbreak by personal hygiene, raw milk not consumed, isolation pens, do not share feed buckets, foot dips etc.

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242
Q

How can salmonella be prevented on farm?

A

Avoid introducing infected animals: maintain a closed herd quarantine introduced stock for 4 weeks, source new stock from other farms not dealers, avoid shared bulls and communal grazing. Isolate sick animals with dedicatioon isolation boxes. Practice disease security - clean and disinfect buildings between occupancies, provide good drainage and waste removal, maintain good fences to prevent access of neighbouring stock, protect feed stores from vermin including birds, avoid contamination of water sources, only spread slurry on arable land, leave grazing land at least 3 weeks after spreading slurry, insist visitors have clean boots, consider vaccination.

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243
Q

What is winter dysentery?

A

An acute highly contagious diarrhoea that occurs in epizootic fashion in a herd in winter housing period. disease spreads by the faecal oral route. Importance because of production losses. Bovine coronavirus has been demonstrated in the faeces and colonic epithelium of affected cattle and the disease has been reproduced experimentally in susceptible adult cows by exposure to coronavirus isolated from calves.

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244
Q

What are the clinical signs of winter dysentery?

A

Acute explosive watery diarrhoea, often dark brown with flecks of blood and malodorous. not usually pyrexic. Partial anorexia, depression and milk drop up to 50% if lactating. cows may show colic symptoms. may be mild respiratory signs, coughing, naso lacrimal discharge. quickly spreads in herd but outbreak over within 2 weeks.

245
Q

How is diagnosis of winter dysentery made? what is the treatment?

A

It is based on clinical signs and history- rapid spread etc. faecal ELISA and serology for coronavirus possible. Main differential diagnosis include simple indigestion, acute BVD and salmonellosis. Treatment - morbidity is high but mortality is nil so treatment not normally required. most cows recover in 2-3 days. symptomatic treatment may benefit worst cases e.g oral or i/v fluids, kaolin, bismuth salts, spasmolytics. Herd immunity will protect after outbreak for 2-3 years.

246
Q

What is Johnes Disease?

A

Johnes disease - paratuberculosis - is a chronic granuloamtous enteritis of adult ruminants caused by mycobacterium avium subspecies paratuberculosis (MAP). Progressive weight loss and chronic diarrhoea are the main signs in cattle. Diagnosis and control are difficult.

247
Q

How is johnes disease transmitted?

A

Principally by ingestion of the organism in faeces from infected animals, contaminating food, water or teats. infection mainly occurs in neonatal animals up to a few months old but occasionally older animals also become infected. Some evidence for intrauterine infection associated with heavily infected dams. the organism has also been isolated from colostrum, milk and semen. there is usually a long incubation period and clinical disease not usually apparent untill 3-5 years of age although younger cases are possible with a high challenge. Infected animals may shed organisms in the faeces for over a year before clinical signs appear. M paratuberculosis can persist for up to one year on pasture. it is susceptible to sunlight, drying and alkaline soils. Host factors that encourage disease include stress related events such as parturition, transport, poor nutrition and concurrent disease.

248
Q

Describe the pathogenesis of johnes disease

A

After ingestion the organis localises in the ileum and gut associated lymph nodes. it is phagocytosed by macrophages and may multiply intracellularly. depending on the host pathogen balance the animal may become;

  1. Resistant : infection controlled - no clinical disease or faecal shedding of organism.
  2. Intermediate - infection partially controlled - subclinical disease - intermittent/persistent shedder.
  3. clinical: develops clinical disease - heavy shedder.

There is usually a detectable CMI response in resistant animals but this becomes weak in clinical cases. conversely serum antibody responses are poor in resistant and early cases but strong in clinical cases. This suggests a progression over the course of the disease from a CMI to a humoral response, with the latter being regarded as ineffectual against the pathogen.

249
Q

What are the clinical signs of Johnes disease?

A

Usually appear in cattle 2-6 years old with onset often linked ot recent calving. progressive weight loss and emaciation are the major signs and there may also be submandibular oedema and coat depigmentation. this is accompanied by a fall in milk yield. there is no fever or toxaemia and appetite and rumenal activity are usually good although there may be polydipsia. Cattle have soft faeces or diarrhoea that is classically like thick pea soup with no blood mucus or epithelial cell debris and passed without tenesmus. Diarrhoea may be intermittent. Clinical signs may continue for up to several months but eventually the animal becomes terminally emaciated and dehydrated and dies.

250
Q

What diagnostic tests can be used for johnes detection in the faeces?

A

Faecal examination - microscopic examination for clumps of acid fast organisms ZN stain. Usually detects heavy shedders. culture of faeces on mycobactin containing media. Grows very slowly taking up to 3 months or more. modern PCR techniques to detect small quantities in DNNA - rapid and sensitive.

251
Q

What serological tests can be used for johnes detection?

A

These detect antibodies to crude m. paratuberculosis antigen. not all cases have a detectable antibody response. complement fixation test CFT - particularly used for export checks. sensitivity and specificity not good, particularly in subclinical cases. Agar gel immunodiffusion test AGID - regarded as having a higher sensitivity and specificity than the CFt but poor at detecting subclinical cases. Enzyme linked immunodiffusion assay (ELISA) - best option although sensitivity still 50% in subclinical animals.

252
Q

Should biopsy be used to test for johnes disease?

A

Rectal pinch biopsy or scrapings to detect mycobacteria in cells usually have a poor sensitivity and only a minority of cases have rectal lesions. intestinal ilium and ileocaecal or other mesenteric LN biopsies are feasible but largely heroic measures. In practical terms diagnosis is best done using a combination of serology and faecal examination.

253
Q

How is control of Johnes disease implemented?

A

Difficult due to long incubation period, shedding by subclinically infected animals and the imperfect diagnostic technique. Eradication requires a substantial commitment by the farmer, vet and local VIC and is based on identification and removal of infected animals. serology or faecal PCR may be done every 6-12 months with slaughter of positive cases. Control measures can limit losses such as rapid culling of diseased animals, minimise contamination of food water and pasture, avoid spreading yard manure on pasture, separate new born calves from dams at birth and rear by bucket with colostrum, do not ue calves from known infected dams as replacements.

254
Q

Describe dermatophytosis infection (ringworm)

A

Affects value of show/sale animals and value of hide. Caused by trichophyton verrucosum (T mentagrophytes). Comon. Most common 2-7 month calves, in autumn and winter. Spores survive for months/yeras. Transmitted by clinical cases, carrier animals, fomites. incubation period 1 week to 4 weeks, self limiting often 1-4 months. Non pruritic, alopecic lesions, lesionsraised, grey/white with powdery surface. Often roughly circular or oval. Common around periorbital, ears, back, and in adults thorax and limbs. There is infection of keratin of hair and skin, enzymes attack keratin and actively growing hair breaks off. inflammatory reaction often mild.

255
Q

How is diagnosis of ringworm made? What is the treatment and how can it be controlled?

A

Confirmation hair plucks and skin scrapes in paper envelope to laboratory - microscopy, dermatophyte test medium culture > colour change. Definitive Dx - culture and identification. Treatment - will reduce the duration of the disease, decide if treatment needed. Systemic - griseofulvin in feed, not available for cattle in the UK. Sodium iodide 1g/14kg iv. Ringvac vaccine. topical - enilconazole, iodine/glycerine. Control with vaccination (ringvac). Use for prophylaxis which reduces clinical signs or treatment of infected animals. two doses 10-14 days apart from 2 days of age. Disinfection - remains on woods, bricks etc for months/years. clean with high pressure water jets, scrub with hot detergents/disinfectants e.g benzalkonium chloride.

256
Q

Describe infection with Pediculosis (lice)

A

Biting lice - bovicola vovis
Sucking lice - haematopinus euurysternis, linognathus vituli, solenopotes capillatus. Life cycle - 3-6 weeks, entirely on host, eggs attach to hairs, nymphs have several moults to become adult. The survival off host is short, usually anaemia, reduced immunity.

257
Q

What is the treatment of Lice (pediculosis). How can it be controlled?

A

Economic benefit of treating mild infections questionable. may need treatment on welfare grouns. treat all in contact animals. single treatment usually sufficient. Re treatment may be needed with permethrin. Pyrethroid pour ons - eg deltamethrin, aphacypermethrin, permethrin. Endectocides - also treat endoparasites. only eprinex can be used in dairy cows. Pour on or injection - injection not very effective vs biting lice. Control usually achieved by treating all animals at housing e.g ivermectin pour on controls lice and acts as housing anthelmintic dose.

258
Q

Describe infection with chorioptic mange? what is the treatment?

A

Caused by chorioptes bovis surface mite. life cycle 2-3 weeks. lives off epidermal debris. Most common mange mite. Very limited survival off host. transmission by direct contact. Clinical signs - limbs, tail, perineum, udder, neck, flanks, papules and pruritis, self trauma, excoriation and exudation, alopecia, crusts. Diagnosis with clinical exam and skin scrapes. Treatment with ivermectin pour on, or endectocine injection which does not eliminate chorioptes - may be used when skin pathology severe to allow healing then follow up with pour on or use Permethrin pour on & repeat in 4 weeks.

259
Q

Describe infection with sarcoptic mange

A

Sarcoptes scabeie, burronw mange, life cycle 10-17 days. Direct contact or fomites spread, survival off animal only a few days. Head/neck lesions > generalised. Intense pruritis, papular dermatitis, exudate, crusting, self trauma, excoriation, alopecia, thickening, loss of condition, reduced milk. Treatment by ivermectin pour on, injection may be preferred when excess crusting, or permethrin pour on.

260
Q

What is photosensitisation?

A

Photodynamic agent in the skin. irradiation of photodynamic agent causes cell death - non pigmented areas without too much hair covering. necrosis and sloughing of skin occur. may be primary photosensitisation via defective metabolism e.g porphyria or plant origin e.g St. John’s wort, or Secondary photosensitisation due to liver disease, failure to metabolise phylloerythrin (chlorophyll breakdown product), builds up in circulation - photodynamic. Non pigmented skin exposed to sun - head, neck, back flanks and udder - erythema and vesicles, oedema, necrosis - dry sloughing and ulceration, pruritis, pain. Treatment - cool shaded fly free housing topical treatment of lesions, antibiotics for secondary infection, corticosteroids, treat underlying disease - prognosis often poor.

261
Q

What are the common flies which irritate cattle? Why is this a problem?

A

Superficial skin damage caused by non biting species. transmission of disease such as IBK and mastitis. house flies musca domestica, face flies musca autumnalies, head flies hydrotoea irritans (implicated in spread of summer mastitis). Multiple nodules caused by biting flies can also transmit disease eg anthrax, pasteurella, trypanosomosis- haematobia species (horn flies), stomoxys calcitrans (stable flies), tabanid horse flies. Similium blackflies - can cause painful vesicle mass attack can cause acute syndrome with haemorrhage and oedema. Open wounds /lesion son the lower abdomen udder and teats can be caused by bites of flies such as haematobia irritans or feeding of hydrotoea irritans. Hippobosca equina (louse fly) - fly worry and iritation, sucksl bood from the perineal and inguinal regions of cattle. blow fly strike initiated by lucilia sericata or phormia terranovae. Less common than in sheep, larval infestation of soiled skin, especially in warm damp conditions e.g adult cattle dehorned in summer. Warble fly larval infestation by hypoderma bovis or H lineatum is now notifiable in the UK. subcutaneous nodules and cysts along backs of cattle in spring should be regarded with suspision, confirmation obtained by carefully opening swellings.

262
Q

How should fly control be implemented?

A

Insecticide treatments - synthetic pyrethroi ear tags and pour on pyrethroid products. additional methods may be used e.g in dairy housing - baits, larvicides, keep manure dry, compact, covered away from animals, discourages fly breeding and encourages predators/parasites, reduce feed spillage/spoilage, reduce moisture in buildings, biological control. Control of summer mastitis - synthetic pyrethroid ear tags/pour on products, spread in sebum but little hair and few sebaceous glands on teats, use 2 ear tags or more frequent or direct application of pour on products. graze large open fields away from woods and streams. Weekly tar/micropore taple application to teats. prevent teat lesions. Dry cow tubes.

263
Q

What is infectious bovine keratoconjunctivitis?

A

Aetiology: moraxella bovis, mycoplasmas, flies, dust, UV light. Introduced by carrier animals or clinical cases. Variation in severity between and within herds. Uni or bilateral conjunctivitis and chaemosis, discharge clear > purulent. blepharospasm, photophobia, cornea central white cloudy raised lesion, oedema after 6 days > vascularisation + mild anterior uveitis. Loss of vision, reduced appetite and production.

264
Q

What is the treatment of infectious bovine keratoconjunctivitis?

A

Sensitive to most antibiotics. topical - treat both eyes, chlortetracycline (short actinig) or cloxacillin (long acting). Subconjunctival injection - repeat in 48 hours, procaine penicillin. Systemic - oxytetracycline LA, florfenicol, ceftiofur, tilmicosin. In an outbreak - mass treatment with parenteral oxytetracycline, isolate affected cattle if possible, quarantine replacement animals, reduce predisposing factors such as adequate space at feeders, dust/long vegetation. Surgery - third eyelid flap, tarsorrhaphy, conjunctival pedicle flap.

265
Q

What is silage eye?

A

An opthalmitis believed to be associated with listeria monocytogenes recognised in cattle and sheep related to the feeding of big bale silage from hoppers or ring feeers. traditionally it is seen more commonly in cattle than sheep perhaps because they are more regularly fed baled silage. One or both eyes affected. Initially lacrimation, blepharospasm, photophobia, swollen folded iris, miiosis. within 2-3 days - bluish white corneal opacity spreading centrally. White focal aggregations of fibrin may accumulate in the anterior chamber. In advanced cases there is pannus - widespread opacity of the cornea and vascularisation. if left untreated this very painful condition may resolve in 2-3 weeks. Signs at least due partly to an immune response in the anterior uvea.

266
Q

What is the treatment of listerial uveitis?

A

The response to topical treatments is poor. sub conjunctival injection of a combination of oxytetracycline and dexamethasone usually halts the progression of clinical signs when given in the acute stages of the disease. the eye will usually return to normal in a few days to a week depending on the initial severity of the problem.

267
Q

What is ovine infectious keratoconjunctivitis?

A

only of economic importance when heavily pregnant ewes are ffected and pregnancy toxaemia are possible. Caused by mycoplasma conjunctivae - most frequently isolated organism. present in eyes for up to 3 months after recovery. other mycoplasmas may be isolated from cases. chlamydia psittaci has been associated with outbreaks. S

268
Q

Describe the clinical signs of Ovine infectious keratoconjunctivitis?

A

1 - tear staining extending from one or both eyes due to mild conjunctivitis, blinking/blepharospasm/photophoobia. many cases regress spontaneously at this stage.
2- cornea becomes cloudy due to keratitis, pannus and vascularisation spreads from limbus. very irritant, increase lacrimation and blepharospasm, cases may regress spontaneously.
Stage 3- ocular discharge becomes more mucopurulent may be shallow ulceration.
Stage 4- blind, corneal ulceration, anterior uveitis, hypopyon. anterior chamber may rupture resulting in permanent blindness. granulation occurs over a period of several weeks and may leave a corneal scar. temporary blindness when both eyes are badly affected may result in handling difficulties and losses due to misadventure.

269
Q

What is the treatment of ovine infectious keratoconjunctivitis?

A

treatment recommended to prevent risk of permanent blindness. affected animals are separated, ideally housed, single im injection of long acting oxytetracycline is very effective in halting the development of clinical signs or curing in 4 days. Also can do topical application of aureomycin power to the surface of the eye via a puffer used in addition or for mild cases. In lambs - may usee topical chlortetracycline. Purchased rams or replacement breeding stock may introduce the condition into a previously unaffected flock so clinical examination during the quarantine period may demonstrate evidence of disease. prophylactic treatment with parenteral tetracycline will help to reduce any infection but will not eliminate latent M conjunctivae.

270
Q

What is a third eyelid flap? when is it used?

A

For severe ulcer or ruptured anterior chamber. give sedation and topical anaesthesia plus auriculopalpebral block where dorsal border of zygomatic arch meets base of ear. membrana nictitans sutured to loose dorsal bulbar conjunctiva. Alternatively, sutured to dorso temporal upper lid using stents. sutures should not penetrate full thickness of third eyelid and touch cornea. Leave for 2-3 weeks.

271
Q

How is enucleation done? when should it be used?

A

For severe trauma, tumour or panopthalmitis. Ga or sedation with retrobulbar block plus local analgesia of eyelids. Periorbital area clipped and prepped. Eyelids sutured together. Elliptical cut made 0.5cm from eyelid margins. blunt dissect between conjunctiva and eyelids. angularis oculi vein ligated. enter orbit cavity close to bony orbital rim. section all muscular attachments close to the sclera. clamp and ligate optic nerve and vessels.

272
Q

Describe urolithiasis in sheep and why they occur.

A

Partial or complete urethral obstruction is a common condition of intensively reared entire male and castrated lambs fed incorrectly formulated rations and occurs occasionally in mature rams. the most common cause of urolithiasis in male sheep is magnesium ammonium phosphate hexahydrate struvite calculi associated with feeding concentrate rations high in phosphate and magnesium. proteins within the bladder combine with these minerals to form calculi which lodge within the urethra just proximal to the sigmoid flexure or within the vermiform appendix.

273
Q

What is the clinical presentation of urolithiasis in sheep?

A

Separation from other in the group with frequent tail swishing and foot stomping especially in lambs. affected sheep have a wide stance with the pelvic limbs held well bak, frequently stretch and often dog sit. Tenesmus accompanied by painful bleating in lambs and teeth grinding in adults. mucous membranes are congested. Nil or only drops of blood tinged urine are voided rather than a clear continuous flow. preputial hairs often dry compared to wet appearance in normal sheep. Calculi are frequently present on the preputial hairs of normal male sheep but are not indicative of urolithiasis. The firm gritty calculus can often be felt within the vermiform appendix and the diagnosis confirmed following excision with production of a free flow of urine. Rarely does the urinary back pressure cause rupture, rather urine leaks across the taut bladder resulting in uroperitoneum. Rupture of the urethra commonly occurs in cases neglected after a few days with resultant extensive subcutaneous swelling extending from the scrotum cranially to the prepuce. Uraemic state, urinary back pressure/hydronephrosis.

274
Q

What laboratory tests can diagnose Urolithiasis?

A

Concentrations of BUN and creatinine can be increased by many ties the normal range in male sheep with urolithiasis of less than two days duration which recover after excision of the vermiform appendix. Such concentrations are not significantly different from those sheep with a more prolonged urethral obstruction which has resulted in hydronephrosis.

275
Q

How can ultrasonographic examination detect urolithiasis?

A

Diagnostic quality images of the bladder can readily be obtained using a 5.0Mhz sector transducer connected to a real time, B mode ultrasound machine. Examination using a 5.0mhz linear array scanner will readily identify distended bladder and uroperitoneum however the true size of the bladder may not be measured because it may extend to 20cm in diameter. the bladder in normal male sheep is contained within the pelvis therefore the presence of the bladder extending for up to 10cm or more beyond the pelvic brim is abnormal, determination of the actual size of the bladder is not as important. The bladder is clearly visible as an anechoic black area bordered by a bright white line. Urine within the abdominal cavity appears as an anechoic area. the walls of abdominal viscera appear as broad hyperechoic bright white lines/circles displaced dorsally by the urine.

276
Q

What is the treatment of urolithiasis?

A

In mature rams, with the partial complete urethral obstruction most commonly occuring at the vermiform appendix, the blockage is relived during the clinical examination when the penis is extruded and vermiform appendix excised with production of a free flow of urine. catheterisation of the urethra after excision of the vermiform appendix and back flushing, while described in the literature is rarely possible and of doubtful benefit. Surgical correction of urolithiasis caused by blockage proximal to the sigmoid flexure i involves a subischial urethrostomy . Tube cystotomy has been reported to be successful in some breeding rams but requires general anaesthesia, surgical placement of the Foley catheter and hospitalisation. The calculi are reported to dissolve and flushing of the bladder with urine acidifiers is not recommended. Management - urine acidifiers such as ammonium chloride are commonly added to rations. sodium chloride has been adde to rations to promote water intake. provision of roughage promotes saliva production and water intake.

277
Q

Describe urolithiasis in cattle

A

Partial or complete urethral obstruction is very uncommon in cattle. rupture of the urethra is more common than in sheep and the first presenting clinical feature may be a large ventral midline swelling between the scrotum and prepuce. Urolithiasis is more common in yearlings allowing rectal examination which reveals pulsation in urethra and marked bladder distension. Surgery in the standing patient under low extradural block is more succesful than sheep because hydronephrosis does not develop but is a salvage procedure only in cattle near slaughter weight.. there is considerable haemorrhage from the transected penis in the first few days. Pyelonephritis is common following ascending infection with signs apparent after 3-6 weeks but can be controlled by parenteral penicillin.

278
Q

Describe pyelonephritis in cattle

A

It occurs sporadically resulting from ascending infection with cystitis and ureteritis. the common cause is actinomyces renale. pyelonephritis is more common in oder beef cattle, 2-3 months following unassisted calving. A renale able to survive in the environment for months.

279
Q

What are the clinical signs of pyelonephritis in cattle?

A

History of chronic weight loss, poor appetite, fever and poor milk yield over several weeks to months with failure of the beef cows calf to thrive. The cow makes frequent attempts to urinate and the flow rate is uch slower than normal with frequent tail swishing with an arched back maintained for much longer than normal after urination. Flecks of blood and pus at end of voided urine, urine foams due to increased protein concentration. gross staining with pus around tail and perineum more suggestive of chronic endometritis. Grossly thickened ureters palpable on rectal examination and bladder wall may be thickened. Dilation of renal calyces, echogenic flocculent material within the renal pelvis and renal enlargement are suggestive of pyelonephritis. Dipstick reveals evidence of blood and protein in mid stream urine sample and is very useful screen for weight loss/poor condition in adult cattle. Usually euthanased for welfare reasons. Poor treatment response if cow already in poor condition. can atempt treatment for up to 6 weeks with procaine penicillin.

280
Q

What is renal amyloidosis?

A

Rare. Occurs in older cattle causing chronic weight loss, profuse diarrhoea and peripheral oedema resulting from a protein losing nephropathy. Grossly enlarged kidneys may be palpable on rectal examination. there may be evidence of a chronic suppurative disease process leading to amyloidosis.

281
Q

What is bacillary haemoglobinuria (red water)

A

Causes sudden death in cattle and sheep caused by toxins of clostridium haemolyticum. Focal anaerobic areas in liver caused by migrating liver flukes allow spores to germinate with release of toxin. haemogloinuria is rarely witnessed. if seen alive, animals are isolated, arched back, tachypneoic, rectal bleeding and bloody faeces. no treatment. Control in at risk areas is effected by vaccination and routine flukicide treatments.

282
Q

What is babesiosis (red water)

A

BAbesia bigemina and B bovis tick transmitted so geographical and seasonal ocurrence. clinical signs of fever, depression, anorexia, pronounced tachycardia, tachypnoea, anaemia and haemoglobinuria manifest after 1-3 weeks. death follows rapidly in untreated cattle. Treatment with imidocarb.

283
Q

What is postparturient haemoglobinuria?

A

A rare condition of intravascular haemolysis, haemoglobinuria, anaemia and jaundice in high producing multiparous cows thought to be related to hypophosphataemia found in affected cows and herdmates.

284
Q

What is the definition of abortion?

A

The expulsion of a dead or non viable calf before 260 days gestation. The cause can be infectious or non infectious e.g toxins, stress, nutrition, twins. In most abortion investigations, the cause is not confirmed due to the presence of a non infectious cause, submission of inadequate material or the fact that infection occurred some time ago.

285
Q

What is the best approach to an abortion problem?

A

Treat all abortions as infectious until proven otherwise. Isoalte aborter and site of abortion. may be first of an outbreak or isolated. Most herds experience 1 or 2 percent of cows aborting. Owner must inform AHDO of all abortions <271 days under brucellosis order. Blood milk and vaginal swab samples sent with form Bs7 for brucellosis enquiry. History should be taken to include recent purchases, movements, clinical disease, infertility, management, diet etc. The animal should be clinically examinedd, the foetus and placena examined with samples submited for laboratory investigation. A negative serology results fairyly reliably rules out BVD as the cause however cows aborting due to IBR may not have seroconverted at the time of abortion while leptospira and neospora serology may go negative before abortion.

286
Q

Name the different aetiological categories of female infertility

A

Anatomical (hereditary/congenital or acquired), infectious (primary or secondary), functional and managemental. Functional infertility can include anoestrus, sub oestrus, persistent CL, ovarian cysts, ovulation defects, luteal deficiency etc often caused by Nutritional problems, endocrine abnormalities, stress etc. Management related infertility results from poor oestrus detection, poor timing of AI or problems of nutrition and management related stress

287
Q

Describe different times of hereditary/congenital anatomical infertility?

A

Accounts for less than 1 percent of female bovine infertility. Many diagnosed before puberty and culled. Ovaries - agenesis, hypoplasia (white coat colour), freemartins, congenital and parovarian cysts.
Oviducts - aplasia, segmental aplasia, duplication
Uterus, cervix and vagina - uterine diadelphiis, lack of patency, semgental aplasia, infantile vulva, persistent hymen,, freemartinism, lack of endometrial glands, cysts of gartners ducts.

288
Q

What is freemartinism?

A

Placental anastomosis occurs in 90 percent of bovine twins. hormones blood cells and other cells cross, leading to chimerism. toestosterone or male cells lead to masculinisation of female twin. clinical signs may include enlarged clitoris with tuft of hair, vagina 30-1000 per cent normal length and blind, gonads hypoplastic, uterus difficult to palpate, epididymides and vasa deferentia seen on ultrasound, persistent hymen. Diagnosis is based on history external signs, rectal and vaginal exam and blood tests.

289
Q

Name the different types of acquired anatomical infertility

A

Ovary - granulosa cell tumour, ovario-bursal adhesions, oophoritis, ovarian cysts
Oviduct - salpingitis, hydrosalpinx, pyosalpinx
Uterus - adhesions, mucometra, hydrometra, neoplasia, uterine abscesses
Lower genital tarct - fibropapillomata, stenosis, fibrosis.

290
Q

What is the difference between primary and secondary infectious infertility? What are non specific and specific primary infections?

A

Primary - acting directly on the reproductive tract, placenta, foetus. Secondary - systemic diseases, secondary effect on conception/pregnancy. Non specific infections - opportunistic infections in individual cos leading to metritis, endometritis, pyometris, etc caused by streps/saphs, A pyogenes, E. coli. Infections follow the breakdown of normal physical barriers eg following coitus parturition or injury or reduction of the reproductive tracts natural defences eg following metabolic disease, the presence of a persistent CL or devitalised tisue. Specific infectious agents - enzootic,many animals often affected, bacteria, viruses, other microorganisms.

291
Q

Describe how campylobacter causes abortion?

A

Campylobacter foetus var venerealis - n atural habitat is the prepuce, glans penis and distal urethra. Service leads to mechanical transmission. There is no systemic illness. females experience a mild endometritis and cervicitis, with mucopurulent vaginal discharge. Cases present as a repeat breeder which eventually holds, abortion and FRM at 4-7 months or pregnancy survives to term. Herd problems after introduction of new infected bulls. First large number of returns, then abortions. Untreated bulls are usually permanently infected, cows and heifers develop immunity over 3-6 months. In an open herd, problems will then occur in replacements and new bulls will become infected. Females - isolation frmo post service discharges, vaginal mucus agglutination test, C foetus verealis in products of abortion. Males - espeically if bull is for AI - qualitative and bacteriological examination of serum, FAB on preputial washings. Control: AI all stock. Use clean male on clean females. Run clean herd and use infected bull on infected stock. Treatment - females not usually treated, i/u streptomycin will shorten course of disease. Bulls are usually culled or treated systemically plus topically with preputial irrigation, antibiotic cream.

292
Q

How does brucella abortus cause abortions?

A

A zoonoses. Infection is primarily by ingestion, with haematogenous spread at around 6 months gestation to the uterus/placenta. this causes a necrotic placentitis and endometritis. in bulls the infection localizes in the seminal vesicles and testes. Introduced by silent carriers and excreted influids/faeces before and after abortion. cattle normally only abort once but remain infected and excrete as carriers. No systemic disease seen. Only abortion and placental retention. some foetuses are born alive others are dead with signs of bronchopnuemonia. Bulls develop orchitis and epididymitis. In a newly infected her, abortion seen in cows in late pregnancy. Then those earlier in pregnancy. When endemic abortions are seen in clean replacements and home bred heifers. Diagnosis by serology and cultuure, cotyledonary smears.

293
Q

Describe bovine herpes virus and how it causes abortions?

A

Infectious bovine rhinotracheitis (IBR) causes respiratory disease, milk drop and reproductive disease. Non venereal infection at service or AI can lead to repeat breeding or later in gestation to abortion. Infection in late pregnancy may lead to stillborn or non viable calves. Venereal infection at natural service can lead to infectious pustular vulvo vaginitis or epigvag. Virus is shed via respiratory secretions and semen, theb becomes latent int he trigeminal ganglion and can become shed again when the animal is stressed. Any seropositive animal is a biosecurity risk, and this can be a barrier to export or use in an AI stud. Vaccination can be intra nasal or IM with an annual or bi annual booster, often combined with other respiratory pathgens. Seropositive animals cannot be sold to accredited free herds, exported to free countries or used as AI stud bulls. Marker vaccinated animals may be exported to some countries and sold to IBR free herds. Eradiction policies are based on test and cull and can include the use of marker cavvines. eradication schemes and accredited free status are available via commercial health schemes. Infectious pustular vulvo vaginitis is characterized by a sudden onset vulval hyperaemia leading to vesicles and ulcers 48 hours post mating. Males develop similar preputial lesions and mating is interrupted for 2-4 weeks. Epivag seen in africa is similar to IPVV but also leads to epididymitis in bulls which can cause permanent infertility.

294
Q

How does neospora caninum cause abortion?

A

Protozoan of cattle, sheep and goats. definitive hosts are dogs which shed oocysts in their faces. These oocysts are picked up by intermediate hosts - dogs, cattle mice horses and sheep. Verical transmission from cow to calf also occurs. When congenitally infected animals become pregnant, bradyzoite cysts multiply and spread to the placenta and foetus. the consequences may be abortion in the third to 9th month of gestation, premature/stillbirth, a full term calf with neurological signs, a clinically normal infected calf, or rarely a clinically normal uninfected calf. Post natal infection before pregnancy may allow the animal to develop immunity. infection in early pregnancy can lead to later abortion, while infection in late pregnancy can lead to full term, clinically normal, congenitally infected calf. Diagnosis is based on pathoogy with non inflammatory necrotic foci in the CNS, bradzoites in myocardium and liver, inflammatory and necrotic placental lesions and serology. serology indicates exposure but may go negative. positive foetal serology indicates exposure after 17 weeks gestation. No vaccine in the UK or treatment. Control BVD - prevent animal contamination of feed. prevent bovine/canine contact with placenta or abortion tissues. embryo transfer from valuable seropositive cows. Low prevalence herds - cull seropositives or do nothing.

295
Q

What must the daily routine of a dairy cow consist of?

A

Lying down for 12-14 hours, eating for 3-4 hours, drinking for 1 hour, consuming 10-20 meals, spending up to 10 hours ruminating, producing 100-150 litres of saliva, containing 2.5kg bicarbonate.

296
Q

What are the main end products of rumen fermentation?

A

volatile fatty acids VFAs - short chain fatty acids - acetate, butyrate and propionate. High levels in fibre in the ration lead to higher proportion of acetate, the main precursor of milk butterfat. Higher levels of concentrate feeding lead to a higher proportion of propionate - the major precursor of glucose for the cow. Also produced - ammonia, microbial cells, gas many carbon dioxide, methane and hydrogen

297
Q

How is optimal rumen function kept?

A

Keep rumen pH between 6.5-7, low rumen pH will lead to impaired digestion of fibre and may result in ruminal acidosis. ensure optimum cow comfort and health, resulting in good rumination. sufficient protein ERDP must be available to the rumen microbes. sudden dietary changes and excessive quantities of highly fermentable energy.

298
Q

Describe the effect on rumen function of high levels of concentrate?

A

Low levels of fibre >poor rumination > poor saliva production > rumen pH below 6. Decreased acetate, increased propionate and lactic acid. > ruminal acidoosis, poor production and cow health problems. With high forage ration there is high levels of effective long fibre > rumination for 10 hours/day > good saliva production > rumen pH 6.5-7, Increased acetate, decreased propionate.

299
Q

Which factors Affect dry matter intake?

A

Cow factors - body weight, milk yield, stage of lactation, stage of pregnancy, body condition score, cow comfort, health and disease, rumen health. Food factors - digestibility of foodstuffs, in ruminants intakes will increase as the digestibility of the feed increases. concentrates - offering concentrates foods with forage to cows can lead to 3 outcomes - supplementation, substitution or cmplementation. with forages are fed to cattle rumen fill constrains intake, palatability. Mixed forages - will increase intakes by around 5%. TMR diet will increase intakes by 20-30%. Out of parlour feeders increase intakes by 5-10%. Self feed silage systems will reduce intakes by 5-10%. use of electric fence at silage face will reduce intakes 5-10%. The standard DM intake equation for lactating dairy cattle is - 2.5% of live weight plus 10% of milk yield. Cows in mid lactation - 25-30kg DMI/day.

300
Q

How can dry matter intakes be optimised?

A

Ensure optimum rumen health. The TMR ration must be well mixed and highly palatable. The ration should be provided truly ad lib to the cows. this means that enough ration should be provided to the cows that 5-10% is left over at the end of the day. this is then removed before fresh food is offered. trough space should be adequate for all the cows to feed at once. ration must be pushed up on a regular bases, ensure excellent cow comfort, clean fresh water available at all times. Direct correlation between DMi in the day before calving and at day 21 after calving - the higher the DMI prior to calving the higher the DMI in early lactation.

301
Q

What are the protein requirements for a dairy cow?

A

Metabolisable protein is composed of two parts: the microbial protein synthesised from ERDP and NPN and the bypass protein DUP. Optimise rumen microbial protein synthesis by ensuring optimal levels of both energy and protein in the rumen at the same time. Ruminants can also utilise non protein nitrogen to synthesis microbial protein eg urea.

302
Q

Describe fibre in the ration of dairy cattle

A

It is essential as a source of energy to promote rumination, to form the rumen mat to ensure optimum digestion of feeds and stimulate butterfat production, the common laboratory method is to measure neutral detergent fibre (NDF) - the plant cell wall material lignin, cellulose and hemicellulose. which is correlated with rates of digestion and thus DMI. The NDF content of the feedstuff is used to classify feeds as cellulosic or non cellulosic. Just because a feed is high in NDF does not always mean it will stimulate rumination - consider very short chop silage or brewers grains. physical form of the food is critical - stimulation of rumination requires long fibre. it is recommended that long fibre for inclusion in TMR rations should be 2.5-10cm long.

303
Q

How much water does a lactating dairy cow require?

A

2-3 litres of water for every kg of milk produced. for a high yielding dairy cow giving 40litres of water the recommended allowance is 128 litres/day.

304
Q

What is buffer fedeing?

A

Managing high yielding dairy cows at grass is difficult due to the problems with intake constraints. especially a problem with freshly calved cows. one method of trying to ensure maximum DMi of good quality forage is by the use of buffer feeding systems: the buffer feed needs to be highly nutritious to ensure good intakes of energy. thus forages frequently used are maize silage, whole crop silage and good quality grass silages. The buffer must be palatable, fresh food should be fed daily and wastage cleared away. Cows require to be confined with access to buffer only, sot hey eat the buffer. the timing must be correct to allow access to fresh grazing. intakes of grass are higher in the evening due to the higher DM and sugar content of the grass.

305
Q

Describe the different times of concentrates that can be fed to cows

A

Problems associated with over feeding in high yielding cows leading to ruminal acidosis. if concentrate:forage DM ratio exceeds 60:40. concentrates may be purchased as compound feeds, blends or as the raw materials which are fed as part of a TMR.

306
Q

What are the different feeding strategies for dairy cows?

A

Split concentrate feed into three meals a day by feeding a third middal eal. use out of parlour feeders to spread the concentrate load out throughout the day in 10-12 small feeds. total mixed ration - involves mixture of all the separate ingredients of the ration in a mixer wagon - cows therefore receive a mix of slowly and rapidly fermentable feeds 24 hours a day. Traditional method of feeding forage in a trough ad lib then concentrates in the parlour twice daily - limited max amount a cow can eat during milking and risk of Ruminal Ph fluctation.

307
Q

Describe the first time period that the dry period cows can be split into

A
  1. the first month of dry period -f ar off dry period - 2-1 months prior to calving should be viewed as a period to allow the cow to recuperate after calving and get her into body condition score 2.5-3. Fat cows should be slimmed whereas thin cows should be fed to gain body condition.
308
Q

What is the second time period that the dry cows can be split into?

A
  1. transitional period - from 3 weeks before calving to 3 weeks post calving. The dry cow in this period has to cope with increasing nutrient demands from the foetus and increasing requirements for the initiation of milk production all combined with a reduction in DMI. correct nutritional management during this period should involve: the cows should be in the correct body condition score of 2.5-3.0 at calving. Fat cows have depressed DMi and rapidly lose body condition during early lactation. Provide 24 hour access to high quality forage. 2-3kg of forage per cow per day will increase the energy density of ration as DMI falls, allow acclimatisation of rumen to post calving diet, promotes growth of rumen papillae - rapid absorption of VFAs. Maximise DMi to reduce the extent and duration of the drop in DMI at calving. Cows that eat more prior to calving eat more after calving. Provide sufficient palatable long fibre to stimulate good rumination. ensure adequate supplies of protein - both ERDP and DUP.
309
Q

What factors affect milk quality?

A

Milk butterfat and protein affected to large extent. 1) stage of lactation - lactose concentration in milk tends to be stable but butterfat and protein decrease as milk yield increases due do dilution effect. Age - milk quality tends to decrease as the animal gets older. 3. Genetics - channel island breeds have higher milk quality with ayrshires having intermediate quality. 4) disease - various diseases can have major effects on milk quality including mastitis and liver fluke (depresses milk protein levels).

310
Q

How can milk butterfat levels be Increased?

A

increasing the amount of effective long fibre in the ration - will increase butterfat levels. High levels of concentrate feeding will lead to increased propionate production and decreased acetate production in the rumen, leading to a fall in butterfat levels. Rumen pH may be altered by the addition of sodium bicarbonate to buffer the rumen and raise acetate production. Quantities required are high and there are problems with palatibility. 40% of butterfat in the milk does come from dietary fat. inclusion of saturated hard fats will increase butterfat levels, provided their inclusion levels do not exceed 6%. Unsaturated soft fats will actually decrease milk butterfat levels by depressing fibre digestion. Feeding of protected fats that bypass the rumen will also boost butterfat levels. milk butterfat responds very rapidly to dietary changes within days.

311
Q

How may milk protein be increased?

A

Forage changes - maximising DMI during early lactation to minimise the extent of any NEB. Use a mixture of forages/ TMR to stimulate intakes and energy supply. feed higher levels of maize silage. Increased levels of concentrate feeding will supply more energy to the cow. feeding of bypass starch will increase milk protein. Increasing levels of DUP will also increase milk protein production but only if dietary protein is limiting. Controlling body condition score in the dry period to ensure minimise NEB . provision of extra DUP in the dry cow ration may also help.

312
Q

What is SARA? *subacute ruminal acidosis

A

Low milk fat syndrome. Increasing demands for lactation, prolonged NEB in early lactation, high levels of concentrate feeding, increased quantities of rapidly fermentable carbohydrates that result in acid production in the rumen and a consequent fall in rumen pH below the optimum range of 6-7. Loose faeces, with excessive faecel soiling of hindquarters, reduction in milk butterfat gut irritation, reduction in milk yield, reduction in DMI, go off their food, spilling their cud whilst ruminating, increased incidence of nutritional related diseases such as NEB/acetonaemia, LDAs, poor fertility lameness and other per parturient diseases.

313
Q

What are the risk factors for the development of SARA?

A

Inadequate effective long fibre in the ration, overall lack of fibre, lack of effective long fibre, cow chooses not to eat fibre, excessive levels of concentrate feeding particularly starch and sugars, poor nutritional management, poor non existent transitional diet, variable DMI, slug feeding of concentrates in parlour, poor cow comfort.

314
Q

How is SARA diagnosed?

A

Assessment of ration - quantity and quality of effective long fibre, visual assessment of ration in front of cows, use of penn state forage particle separator. using rumen fill, faecal consistency, examination of faeces. Herd assessment - presence of NEB/subclinical ketosis, milk production actual vs predicted/expected. Milk quality - especially milk butterfat levels. rumination - atleast 60% of cows should be chewing their cud whilst resting. cow comfort. incidence of disease e.g lameness, LDAs, fertility records etc. rumen pH measurement - required for the definitive diagnosis of SARA. sample of rumen fluid taken from 12 cows measured using a pH meter or indicator papers. sarah is defined by the presence of a rumen pH of less than or equal to 5.5 in at least 30% of the animals sampled.

315
Q

How is SARA prevented and treated?

A

Feed a suitable transitional diet for 3-4 weeks prior to calving. increase the amount of effective long fibre in the ration. increase DMI to ensure ingestion of sufficient forage. avoid sudden increases in concentrate feeding especially after calving. Review feeding strategies. Reduce sorting of long fibre by cows, improve cow comfort.

316
Q

Describe the aetiology of sub acute ruminal acidosis

A

High yielding dairy cows > increased energy requirements > increased energy density of ration > use of increased levels of concentrate feeding or maize silage > high levels of starch in the diet > rumen pH falls and impaired rumen health > increased lactate and propionate prduction, decreased acetate and butyrate > poor digestion of food, depression in milk butterfat. Decreased forage fibre intakes > reduced chewing and rumination > poor saliva > rumen pH falls.

317
Q

What are the common causes of plant poisoning in cattle and sheep?

A

Poor pasture availability - drought conditions or heavy snow often force animals to graze hedges or toxic pasture weeds. overgrazing/poor pasture management enable the establishment of toxic weeds, forage conservation - most growing toxic plants are avoided because they are unpalatble. however these plants may become palatable without losing their toxicity when they are cut or conserved with forage. accessibility of poisonous plants - many isolatd poisoning cases are associated with dumping of hedge cuttings and garden waste in fields. Fallen and overhanging branches following storms and heavy snow fall may become accessible to inquisitive animals. grazing experience - young animals, animals moved from another area or animals reared on their own often lack the protective behaviour to avoid poisonous plants. environmental effects on toxicity of plants - drought, shade, high temperatures or injudicious use of herbicides may increase the toxicity of some plants. , animal species- some species have different biochemical pathways that make them more or less suspceptible to certain phytotoxins.

318
Q

Describe the clinical signs associated with alkaloid plant poisoning

A

Alkaloid containing plants generally taste bitter and are avoided although individual animals can become addicted to them. Climate soil and other environmental factors can modify the alkaloid content. poisoning is often fatal and in animals that survive recovery is often incomplete. some alkaloids are struturally similar to acetylhcoline, deopamine and serotonin thus induce toxic effects by mimicking or blocking the action of neurotransmitter.s the signs of acute alkaloid poisoning therefore include excess salivation, dilation or constriction of the pupil, vomiting, abdominal pain, diarrhoea, incooordination, convulsions and coma. e.g Yew and laburnum. Pyrrolizidine alkaloids are transformed in the liver to reactive pyrrols which exert their toxic effects in cels, causing necrosis, inhibition of mitosis or vascular damage. Pyrrolizidine alkaloid poisoning usually results in chronic liver disease e.g ragwort. Some alkaloids are teratogeniic eg hemlock and lupin

319
Q

Describe the cyanogenic glycosides and how they cause poisoning

A

Cyanogenic plants eg linseed and cherry laurel contain an enzyme system capable of converting glycosides to hydrocyanic acid HCN. Within the plant the enzymes and glycosides are separated but disruption of plant cells during decomposition or ruminal digestion enables the prooduction of HCN. the highest concentration of cyanogenic glycosides are found in the leave. drying of the plant material does not reduce the potential toxicity but toxic forage loses much of its cyanide content when made into silage. Linseed loses toxicity when boiled. HCN inactivates the cytochrome oxidase system in the mitochondria starving cells of oxygen. clinical signs include dyspnoea, convulsions, muscle tremors and death. animals tolerance to HCN appears to increase with experience. The diagnosis of cyanide poisoning is based on the feeding history clinical signs and non specific post mortem findings of bright red mucosae and a smell of bitter almonds in the rumen. Diagnosis can be supported by analysis of HCN content of liver or muscle tissue. Treatment based on cyanide radicals form complexes with a number of chemicals within tissues. A regime consisting of IV injection of sodium thiosulphate and sodium nitrate has been described but is seldom practical. Large doses of vitamin b12 may enable cobalt to combine with cyanide in the circulation.

320
Q

What effect do the Goitrogenic glycosides have

A

Glucosinolates present in brassica crops and white clover can cause goitre, reduced growth rates and or diarrhoea depending on their composition. sudden onset blindness in cattle and sheep and digestive disturbances in growing cattle grazing on rape are also thought to be associated with glucosinolate poisoning. the highest concentration of these glycosides is present in the seeds of mature plants. Brassica crops contain variable amounts of both glucosinolate and thiocyanate goitrogens. Glucosinolates interfere with thyroid hormone synthesis, while thiocyanates impair uptake of iodine by the thyroid gland. Glucosinolate induced goitre cannot be managed by iodine supplementation, while thiocyanate induced goitre can.

321
Q

What effect do the cardiac glycoside plants have when eaten?

A

Cardiac glycosides eg digitoxin and digitalin present in foxglve, lily of the valley and oleander have a specific action on the mycocardium increasing contractility and slowing the heart rate. Moderate intoxication results in bradycardia, depression, regurgitation and diarrhoeae while larger amounts of toxin cause various cardiac irregularities including bradycardia then tachycardia and dysthythmia. Signs usually develop within 4-12 hours of ingestion of the plant and may persist for 2-3 days. Most deaths occur within 12-14 hours. Plants containing cardiac glycosides do not lose their toxicity w hen dried or boiled. A treatment regime consisting of supportive fluid therapy, atropine and propranolol is described. Oral administration of charcoal and rumenotomy have been reported to be effective.

322
Q

Describe what effect the saponins have when eaten

A

Saponins eg present in ivy are naturally occurring glycosides with the physical properties of soaps. Most saponins found in plants are absorbed very slowly but large quantities can cause gastroenteritis.

323
Q

Describe the effects of bracken poisoning in cattle.

A

The whole plant is toxic. younger plants are most toxic. poisoning when animals are forced to eat bracken, in large amounts over several weeks. contains thiaminase, which causes poisoning in horses. Ptaquiloside, a carcinogenic glycoside present in varying amounts. Causes bone marrow depression - aplastic anaemia, and prunasin - a cyanogenic glycoside deterrent to grazing. In adult animals following long term ingestion there is thrombocytopaenia and neutropenia - acute haemorrhagic disease. In 2-4 month old calves, there is oedema of the throat and nostrils - cell damage and histamine release. Also after exposure over several years - haemangiomas in the bladder wall, association with papilloma virus, intermittent haematuria, cystitis.

324
Q

What are the effects of bracken poisoning in sheep

A

Uncommon bracken poisoning in sheep. Similar haematological effects to those in cattle. Progressive retinal degeneration - bright blindness. 3-4 year old animals, separation from the flock, high head carriage and stepping gait, eyes shine brightly in semi darkness, association with tumours of the jaw. High prevalence of neoplasia - interference with normal immune response.

325
Q

How does nitrate poisoning occur?

A

Plant absorb nitrates from the soil and generally convert them rapidly in to other nitrogenous compouns. Nitrates accumulate in the soil during periods of drought and are taken up by plants in large amounts when the drought ends. Overcast conditions favour plant storage of nitrogens, while in bright light nitrates are converted to amino acids and proteins. some plants eg covers and brassicas may accumulate particularly high concentrations of nitrates. The use of nitrogenous fertilisers cause high nitrate concentrations in plants. roots and stems usually contain more nitrate than leaves. While ingestion of a large amount of nitrates can cause gastroenteritis the min importance of nitrates is as a source of nitrites which are formed in the rumen after ingestion of the nitrate. Nitrite poisoning is most common in cattle, although the disease is seen in other animals.

326
Q

What occurs when many nitrites are absorbed?

A

Absorbed nitrites combine with haemoglobin in the blood to form methaemoglobin which is incapable of transporting oxygen. the clinical signs associated with nitrite poisoning include dyspnoea, characterised by gasping and rapid respiration, tachycarida, muscle tremors and weakness. In severe cases, the oral conjunctival and vulval mucosae appear brown coloured and eventually cyanotic in appearance due to the high blood methaemoglobin content. death from anoxia can occur within a few hours but more usual for a few days to elapse.

327
Q

Describe toxicity with oxalate plants. Which plants contain oxalates?

A

Intake of large amounts of oxalate rich plants eg beet, rhubarb and sorrel results in the ruminal absorption of free oxalate and precipitation of calcium oxalate crystals in submucosal arteries. Free circulating oxalates may damage lung capillaries and cause pulmonary oedema. Continuos ingestion of small amounts of soluble oxalates causes nephrosis due to precipitation of calcium oxalate crystals in the lumen of the renal tubules. Plasma concentration falls and Clincal signs of hypocalcaemia may appear. Most plants contain oxalates in varying amounts. different amounts of oxalates are required to produce toxic effects in different species, sheep being most susceptible. Diagnosis based on history, PM findings of calcium oxalate crystals in the renal tubules and the rumen wall. in short term animals may respond to calcium borogluconate therapy but most relapse or die from acute renal failure.

328
Q

What are photosensitisation?

A

Photosensitisation results from the accumulation of photosensitive metabolites under the skin and their reaction with sunlight to cause necrotic damage. in most cases clinical signs are confined to wool free unpigmented areas of the face, ears and limbs but in some sheep breeds the skin of the midline of the back at the parting of the fleece is also affected. Severely affected animals don’t eat and rapidly loose body condition. skin necrosis, sloughing and regeneration follow.

329
Q

What is primary photosensitisation?

A

Cases of photosensitisation often follow the movement of sheep from poor to lush green pasture such as silage aftermaths, and are associated with failure to adapt to increased amounts of chlorophyll. Certain plants such as St. John’s wort and buckwheat contain photodynamic agents hypericin and fagopyrism that are absorbed and carried systemically to the skin. clinical signs can appear within 2-3 ays of exposure to photosensitising agents.

330
Q

What is hepatogenous photosensitisation??

A

Photosensitisation can occur when the biliary excretion of phylloerythrin a normal degradation product of chlorophyll which is normally excreted in bile is obstructed due to various liver iseases. high levels of phylloerythrin make the skin sensitive to sunlight. h hePatotoxic plants eg bog asphodel and ragwort can cause photosensitisation. in many scottish hill areas annual outbreaks affecting up to 10% lambs occur during the summer, probably associated with the ingestion of bog asphodel.

331
Q

How do proteins, peptides and amino acids cause toxicity?

A

Amanita phalloides, the most toxic mushroom in britain, contains aminotoxins. toxicity symptoms include severe abdominal pain, diarrhoea and eventually coma. mistletoe contains polypeptide viscotoxins which have irritant and necrotising effects. Blue green algae (microcystis) that forms blood on still water, contains peptides that are potent hpatotoxins. the toxins are chemically stable and not inactivated by the usual treatments used for drinking water. Blue green algae are widespread. The amino acid S methylcysteine sulfoxide is converted in the rumen during normal frmentation to dimethyl disulfide. This metabolite causes poor gowth rates and haemolytic anaemia. various amounts of SMCO are found in different brassica crops. The enzyme thiaminase is found amongst others in horsetail and the rhizomes of bracken. Ingestion of large amounts of thes eplants over along period may cause polioencephalomalacia in monogastric animals.

332
Q

Describe rhododendron poisoning in sheep and goats

A

rhododendrons contain andromedotooxin. common toxicity in sheep and goats following heavy snowfall. Andromedotoxin causes hypotension, respiratory depresison, CNS excitation and then depression, excess salivation, green froth at the mouth and nose, attempts to vomit , severe abdominal pain, staggering gait, sternal recumbency, convulsions, dyspnoea.

333
Q

How do tannins cause toxicity?

A

Tannins bind to proteins and produce an astringent reaction in the mouth. oak leaves and acorns contain hydrolysable tannins which are broken down to toxic metabolites in the digestive tract of cattle and sheep. individual cattle and sheep may develop cravings for oak leaves and acorns. unripe acorns brought down after storms are particularly toxic. Initially there is dullness, anorexia, constipation and cessation of urination. later there is persistent diarrhoea and dysentery. dark urine and serous ocular nasal and oral discharges sometimes reported. Post mortem findings include a uraemic smelling carcase, large numbers of acorns in the rumen and intestinal tract, haemorrhagic abomasitis, subcutaneous haemorrhages and oedema especially of the abomasum and perineal area. Treatment consists of the administration of liquid paraffin with milk, mucilage and appetite stimulants. saline purgatives are contra indicated because of kidney damage.

334
Q

How do the brassicas cause poisoning?

A

Brassicas contain several toxic substances - nitrates, photosensitive substances, haemolytic anaemia factors, oxalates, glucosinolates, sulphur and molybdenum. S methylcysteine sulfoxide (SMCO) is converted in the rumen to dimethyl disulfide. Dimethyl disulfide precipitates haemoglobin in RBCs to form heinz bodies. severity of disease is related to the SMCO content of the crop. poor growth rates, severe anemia, sudden death. SMCO increases with the maturity of the crop. Never feed brasicas to store lambs for prolonged periods. provide a pasture run off or supplementary feed. PM findings - jaundice haemoglobinuria, anaemia, congestion of internal organs, dark and swollen kideys. Remove animals from the brassica crop and carefully introduce supplementary feeding.

335
Q

Describe facial eczema in cattle and sheep

A

Causes ill thrift. Due to hepatogenous photosensitisation, in sheep cattle goats and deer. Occasionally seen in the UK. Clinical signs in 3%, production losses in 50%, prevention and control is difficult. Pithomyces chartarum is a saprophytic fungus in mat of leaf litter. In high humidity following a prolonged warm period there is a rapid increase in spore counts. Young spores are most toxic. There is photphobia, swelling of the ears and face, white faced animals most susceptible, restless, seek shade, seepage of serous fluid, skin necrosis and scab formation, ears shrivel and curl at tips. Use pasture fungicide spray to control or give oral zinc oxide in advance of a problem.

336
Q

What is ryegrass staggers?

A

Caused by mycotoxin - lolitrem B. Perennial ryegrass endophyte - acromonium loliae. Resistance to attack by argentine stem weevil. Selection of modern ryegrass cultivars for high levels of A oliae endophyte has inadvertently resulted in an increase incidence of ryegrass stagers. At rest there is fine tremors of the head and neck. when disturbed - head nodding and jerky movements of neck and limbs, wide based swaying stance and high stepping gait, collapse head first when moved, tetanic spasms for several minutes, sudden recovery. Losses associated with misadventure. a few sheep become permanently recumbent. Avoid close grazing of high endophyte ryegrass. supplementary hay or silage feeding.

337
Q

Describe toxicity with fusarium toxicoses?

A

Fusarium spp are active plant pathogens, moulds on stored grain crops in cold and wet weather. Fusarium sp are sometimes saprophytic on pasture - warm and humid weather. Trichothecene toxins - stored grain. Zearalenone - stored grain and growing pasture. Trichothecene toxins are cytotoxic to lymphocytes, cause generalised microvascular haemorrhages. Clinical signs - non specific hepatic and nervous signs, haemorrhagic disorders, necrotic lesions of dermis, oral cavity, GIT liver and kidneys, lowered host resistance to many diseases. Zearalenone - oestrogenic effects, sgns within 3-6 days after feeding mouldy grain, poor fertility, stillbirths, v ulvovaginitis, extreme swelling of vulva.

338
Q

What is ergotism?

A

Claviceps purpurea is a compacted mass of fungus - sclerotium replaces grass seeds and projects from the ear as a dark horn like structure. Ergot poisoning is rae in the UK. Large amounts of claviceps purpurea ergot of rye needed to cause toxicosis. Causes stimulatory and depressive effects on the CNS. Arteriolar, intestinal and uterine smooth muscle constriction - capillary damage, thrombosis, gangrene. There are painful and inflamed extremities, coldness numbness and dry gangrenous lesions int he lower legs, ears and tail, weight loss, painful udders.

339
Q

What is fescue toxicity?

A

Tall fescue endophyte acremonium coenophialum. Symbiotic relationship between plant and endophyte. vasoconstrictor alkaloids effect the extremities during cooler weather. severe pelvic limb lameness 10-14 days after exposure, rapid weight loss, dry skin at or near the coronary b and progressing to hair loss and moist gangrene, distal limb and tip of tail may drop off, hyperthermia in cattle.

340
Q

What is lupinosis?

A

Phompsis leptostromiformis on stems of dead wild lupin plans, more common in humid and overcast weather, hepatotoxins cause weight loss, lethargy, jaundice, hepatogenous photosensitisation.

341
Q

What is aflatoxicosis poisoning?

A

Metabolites produced by aspergillus flavus and other aspergillus spp and penicillium spp. Ubiquitous in stored feed. Associated with poor storage - warm and damp. It is hepatotoxic - causes liver centrilobular necrosis, bile duct hyperplasia, cirrhosis, fatty liver infiltration and immunosuppression. Aflatoxin in milk is a public health concern. Clinical signs include ill thrift, blindness, keratoconjunctivitis,walking in circles and falling, ear twitching, teeth grinding, frothing at the mouth, epistaxis, photosensitive dermatitis, ataxiia, haemorrhagic diarrhoea, recumbency, convulsions and death within 48 hours. Clean grain stores before use and ensure moisture content of grain is less than 13%. Regularly move stored grain. Dilute known contaminated grain with clean feed.

342
Q

What is stachybotryo toxicosis?

A

Stachybotrys spp moulds on moist forage crops - dusty black appearance, trichothecene toxins. non specific clinical signs within 2-3 days of ingestion of contaminated forage - anorexia, fever, muscle tremors, excessive salivation, haemorrhages on nasal and oral mucosae.

343
Q

Describe what occurs when sheep are poisoned with copper - chronic copper toxicosis

A

Very common in sheep, seen occasionally in cattle, chronic and acute poisoning. Chronic - subclinical liver damage, the livers capacity for lysosomal copper storage is exceeded. Lysosomal rupture and release of copper into the peripheral circulation, intravascular haemolysis - reactions between copper and RBC membranes, jaundice, renal and generalised tissue failue. Sudden onset progressivee ataxia, aimless wandering, head pressing , stupor, jaundice, haemogobinuria, rapid shallow respiration, anaemia and methaemoglobin production. In calves - sudden on set dullness and anorexia, pale or jaundiced mucous membranes, ecchymotic haemorrhages, mouth immersed in water bowls, respiratory distress, melena. Ammonium tetrathiomolybdate injections no longer permitted in food producing animals.

344
Q

Describe acute copper poisoning in sheep and cattle

A

Occurs sporadically in sheep and cattle, overdosage of copper supplements causes circulatory copper levels to overwhelm the hepatic capacity for removal and storage. clinical signs seen within 24 hours. Causes generalised oedema, inflammation of the GIT and petechial haemorrhage. clinical signs - sudden onset depression, anorexia, rapid heart and res rates, subnormal temperature, blue green mucoid diarrhoea, collapse and death. liver copper -normal, kidney copper - high.

345
Q

Describe lead poisoning in cattle

A

Young animals more susceptibe than adults. Sources of lead - lead based paints, soil contamination, industrial souces, lead in petrol, metallic lead, linoelum, putty, sprays for fruit trees. In chronic lead toxicity - lead is absorbed through alimentary or respiratory tracts, most is excreted as insoluble complexes in faeces, some is excreted in bile, milk and urine. solubility and availability of inorganic lead is associated with acidity of water or soil. Absorption enhanced by calcium or protein deficient diets, absorbed lead first deposited in liver and kidneys.Re distributed from soft tissues to bone and causes osteoporosis. bone acts as a reservoir until saturated. lead released back to the circulation with chronic disease, pregnancy or poor nutrition. Circulating lead is bound to RBCs. Lead binds to epithelial cells of brain and capillaries. generalised muscle weakness and immunosuppression occurs, young animals most susceptible, lead crosses the placenta.

346
Q

What are the clinical signs of acute lead poisoning in cattle

A

Commonest in calves - apparent blindness, muscle tremors, colic, frothing at the mouth, staggery gait, recumbency, convulsions with bouts of opisthotonus, muscle tremors, facial an ear twitching and hyperaesthesia, death within 12-48 hours of onset of signs. In adult cattle- blindness, aggression, frenzy, head pressing pyrexia, death during convulsions. In subacute poisoning - dullness, inappetence, incoordination, blindness, gait abnormalities, circling, stand immobile for long periods, muscle tremors and hyperaesthesia, ruminal atony and constipation followed by foetid diarrhoea, absence of palpebral eye preservation reflex, death after about 5 days.

347
Q

How is diagnosis of lead poisoning made

A

Blood concentrations - use lithium heparin tubes, elevated in sick animals but concentrations fluctuate, not necessarily correlated with clinical disease, can be used to monitor at risk a nimals, decline rapidly when source of lead is removed, not necessarily usefull. Tissue concentrations - pM or biopsy, kidney, liver. Haematology - normocytic normochromic anaemia in subacute or chronic poisoning.

348
Q

Describe selenium poisoning in sheep

A

Due to excessive supplementation . Acute selenium toxicity - damage to the cardiovascular, respiratory and urinary systems and damage to secondary lymphoid tissue in several organs. Non specific clinical signs - staggering gait, dyspnoea, tympany, colic, diarrhoea, recumbency, cyanosis and death due to respiratory failure within as short a period of 5 hours. Marked kidney tubular degeneration and cast formation. Elevated selenium concentrations in the liver, heart and kidney. A successful treatment regime has not been described. Great caution is therefore required when administering selenium supplements. Chronic selenium poisoning - due to high selenium concentrations in the plants grown on seleniferous soils and seleniferous plants eg milk vetch. Poisoning follows ingestion of plants containing high concentrations of selenium over long periods of time. Brittle hoofs, interference of blood circulation to the extremities. dullnes, ill thrift anaemia, toxic liver damage.

349
Q

What are the major elements and trace elements essential for ruminants?

A

Major - calcium, magnesiu, phosphorus, pottasium, sodium, chloride, sulphur.
trace - copper. cobalt, selenium, iodine, iron, zinc, manganese.

350
Q

Describe what happens when an animal is fed a diet with insufficient levels of a particular element?

A

1 - depletiion - during this phase there is loss of mineral from storage sites eg liver bone but the levels in the bloodstream are normal.

  1. Deficiency - the levels in bloodstream decline.
  2. Dysfunction low levels of mineral lead to a decline in the concentrations or functions of enzymes involved in the metabolism and thus the function is mipaired. animal still appears clinically normal.
  3. Disease - these changes in metabolism lead to detectable clinical abnormalities.
351
Q

Describe the indirect methods used for supplementing mineral deficiencies?

A

Application of mineral fertilisers to pasture - may not work if factors leading to secondary deficiencies are still present then fertilizers may have little effect. Minimising factors that interfere with mineral uptake - this may be feasible in certain circumstances eg soil contamination of forages will reduce copper absorption. Genetic selection - there may be a marked genetic difference between individuals and between breeds in mineral absorption.

352
Q

Describe the direct methods for supplementing Mineral deficiencies?

A

Inclusion in compound feeds - this is most reliable method of ensuring adequate intakes of minreals but may not be economic in some circumstances eg hill grazing. Free access minerals - provision of mierals as blocks, licks and troughs is very convenient but large variation in consumption. Medication of water supply. oral compounds - include drenches or boluses that remain lodged in the GI tract. Injectable compounds - all the animals receive a known amount of mineral at a certain time to provide slow release over prolonged periods.

353
Q

Why does copper deficiency occur?

A

Can occur rarely as a primary deficiency on copper deficient pastures, secondary coper deficiency is more common due to antagonism by sulphur iron and molybdenum in the rumen. This means that between 90-99% of the copper eaten by adult ruminants is assed through the gut unabsorbed.

354
Q

What are the factors influencing the absorption of dietary copper?

A

Sulphur - converted to sulphides in the rumen by rumen flora which then reacts with copper to form insoluble copper sulphicide. Molybdenum - reacts with sulphur in the rumen to form thiomolybdates that irreversibly bind coper and prevent its absorption. molybdenum levels in pasture are affected by soil content, pasture improvement via liming and stage of maturity (increases later in grazing season). Iron - can inhibit copper uptake either directly by the formation of insoluble compounds with copper or via combination with sulphides to form FeS which then binds copper. iron contamination of forages commonly occurs via soil contamination. Differences between feedstuffs - brassicas and cereals tend to be good sources of copper whereas root crops and grazing tends to be poor especially in autumn and winter. Intercurrent disease - GI parasitism can markedly affect copper absorption. Genetics - sheep in particular show marked breed differences in the ability to absorb copper. texels are able to absorb and retain relatively high levels of copper, whereas black face sheep are relatively poor at absorbing copper and are thus more susceptible to deficiency.

355
Q

Describe copper metabolism

A

Liver is the major organ for storage of copper containing 70% of body copper reserves. Caeruloplasmin is the major transport protein for copper and with 80% of copper in the bloodstream bound to caeruloplasmin. Due to their poor absorption, ruminants are designed to cope with constant risk of copper deficiency. Clinical signs of copper deficiency will thus only occur after exhaustion of liver stores followed by decreases in blood copper concentrations and then a fall in copper levels at the essential tissue sites. this process may take between 3-6 months.

356
Q

What are the clinical signs of copper deficiency in Cattle

A

Usually seen in growing animals after weaning (3-12 months), depigmentation - this occurs as greying/brown of the coat in black cattle. Defective keratinisation -can lead to the formation of a thin, dry , sparse hair coat, with a tatty appearance. Bone defects - widening of the epiphyses of the distal limb bones and enlargement of the costochondral junctions. Ill thrift, anaemia only after prolonged periods of deficiency, cardiac hypertrophy leading to sudden death, impaired resistance to infection and immune system dysfunction has all been associated with copper deficiency. Diarrhoea - seen immediately after turnout onto pastures with high molybdenum concentrations and is only associated with molybdenum excess. Infertility - impaired fertility associated with molybdenum excess. Swayback is not seen in calves.

357
Q

What are the clinical signs of copper deficiency in sheep

A
Enzootic ataxia (swayback) - due to severe copper deficiency of pregnant ewes in mid to late gestation it is usually associated with mild winters and can also affect goats and deer. the disease is progressive. Two forms are seen;
Congenital - typical signs include stillbirths, and the birth of weak lambs, neurological signs are seen within a few days of birth and include ataxa, inability to stand, staggering gait and weakness of the hindlimbs. Affected lambs usually bright and alert otherwise. Delayed - occurs in lambs 2-8 weeks of age signs are similar to the congenital form but tend to be less severe. it may be precipitated by gathering or handling. Depigmentation - discolouration of the fleece in dark coloured sheep may be observed. Defective keratinisation - loss of wool cirmp, distortion of the wool fibres and reduction in wool quality may be seen as stringy or steely wool. Osteoporosis and spontaneous fractures may rarely occur in shepe, susceptibility to infection.
358
Q

How can diagnosis of copper deficiency be made?

A

Signs of clinical disease - most non specific. Dietary levels - dietary copper levels useless due to the effects of molybdenum, sulphur and iron. Plasma/serum copper levels - these are suitable for the diagnosis of clinical disease but not for the estimation of body copper reserved. Liver copper levels - liver sample levels give an estimation of body copper reserves and can be used to monitor supplementation. superoxide dismutase - analysis of erythrocyte or liver SOD would give a better diagnosis of deficiency and dysfunction states but is expensive. Response to treatment with copper - may be attempted in cattle but not done in sheep due to risks of copper toxicity. Some recommend the use of caeruloplasmin:copper ratios in the diagnosis of copper deficiency but their use is still controversial.

359
Q

What is the therapy for low copper levels?

A

Oral copper sulphate - oral dosing eight to four weeks prior to lambing traditionally used to prevent swayback. NB sheep are highy susceptible to copper poisoning so supplementation should only be given if clinical disease diagnosed. Copper oxide needles - given orally in a capsule and then lodge in the abomasum to give slow release of copper over a period of 2-3 months. Intra ruminal boluses - provide slow release of copper for up to 6 months. Injectable compounds - vary in respect to speed of absorption from injection site duration of activity, degree of reaction, retention of satisfactory levels in the liver and safety margin and risk of toxicity. (slow absorption, low toxicity risk but tissue reaction). Inclusion in compound feeds - inclusion of copped in concentrate feeds for sheep is banned in the UK, free access minerals, medication of water supply. Indirect methods include application of mineral fertilizers to pasture, minimising molybdenum and iron intakes, and use of genetic selection.

360
Q

How can swayback be treated and prevented in sheep?

A

Although swayback is progressive an the pathology is irreversible it may be worth treating mildly affected lambs to stop progresison of the disease using very small doses of copper. all remaining pregnant ewes should be given copper. all surviving lambs born out of pregnant ewes that have not been given copper should be dosed to prevent cases of delayed swayback. Prevention in subsequent years - house sheep during last 6-8 weeks of pregnancy, provision of supplementary feeding during late pregnancy, copper supplementation of sheep in early pregnancy.

361
Q

Describe selenium/vitamin E deficiency

A

Both selenium and vitamin E play key complimentary but independent roles as cellular anti oxidants. They help protect cells against damage by lipid peroxidases and free radicals where are produced during normal cellular oxidative metabolism. Failure of this protection leads to membrane damage then tissue necrosis. Tissues which have the highest rates of oxidative metabolism are thus most susceptibe to damage, especially muscle - especially skeletal, cardiac and respiratory muscle. The occurrence of clinical disease caused by anti oxidant deficiencies is related to: 1. selenium status, supply of other dietary anti oxidants, supply of dietary oxidants, the main ones are polyunsaturated fatty acids *PUFA, which are found in high levels in young rapidly growing pastures especially in the spring, generation of oxidants via exercise at turnout, infection, toxins. Good correlation between low soil selenium, low pasture selenium and clinical disease. Vitamin E deficiency - vitamin E (tocopherols) is synthesised by plants and levels are high in green pastures (relatively low in root crops). Levels rapidly decline during long term storage and it is destroyed by various treatment methods eg addition of alkali.

362
Q

What are the clinical signs of selenium and or vitamin E deficiency?

A

Congenital - seen as stillbirths, birth of weak calves, lambs that fail to thrive and suckle and usually die within a few days.
Delayed - this is usually seen in calves or lambs at 1-4 months of age. Signs are usually precipitated by exercise eg turnout in the spring or stress such as handling, bad weather. clinical signs vary according to which muscles are affected. Skeletal muscles - stiffness and discomfort, inability to stand, reluctance to move or get up, myoglobinuria. respiratory muscles - respiratory distress, dyspnoea, cardiac muscle. Also ill thrift, poor growth, increased embryonic mortality, impaired immune function - increased susceptibility to disease, in particular mastitis in dairy cows and mortality in lambs, retained foetal membranes in cattle.

363
Q

How is diagnosis of selenium/vitamin E Deficiency made

A

Diagnosis of WMD - creatine kinase - released after onset of muscle damage but levels decline rapidly after a few days. AST - levels may be raised during liver damage so non specific. Levels remain raised for 7-14 days following muscle damage. PM findings - these include white necrotic lesions in the myocardium and skeletal muscles classically the thigh shoulder and diaphragm. soil and pasture levels of selenium - below 0.5mg/kg . Selenium levels in blood and liver - dependent on current daily intake thus are a short term intake. Liver samples may be useful to determine need for supplementation. expensive and rarely performed. Glutathione peroxidase levels in blood - GSHPx is a selenium containing enzyme and is the standard biochemical test for selenium deficiency. as erythrocyte GSHPx levels depend on selenium levels during erythropoiesis and RBCs live for several months, blood GSHPx levels reflect long term selenium status. Vitamin E levels in blood - plasma a -tocopherol levels below 1 umol indicate a significant risk of WMD even if selenium status is adequate.

364
Q

What is the treatment and prevention of selenium deficiency?

A

Direct methods - oral compounds - oral sodium selenate oral dosing using 0.1mg/kg sodium selenate will provide adequate supplementation for 1-3 months. intra ruminal boluses provide slow release of selenium for 6-12 months. injectable compounds - short term supplementation sodium selenate or selenite may be given by injection for up to 3 months. long term supplementation with subcut injections of barium selenate - provide adequate supplementation for 9-12 months. inclusion in compound feeds - selenium and vitamin E frequently added to concentrate rations for feeding to cattle and sheep. free access minerals - can be provided as blocks or licks usually containing salt to improve palatability. intakes are very variable. Indirect methods - treatment of pastures with sodium or barium selenate can be effective for up to 3 years.

365
Q

How can vitamin E deficiency be treated and prevented?

A

Supplementation with vitamin E may be given using selenium combinations or tocovite tablets. treatment may be needed at weekly intervals. Watch for selenium toxicity if giving combined selenium vitamin E preparations. selenium can cross the placenta and both selenium and vitamin E are concentrated in the colostrum, thus supplementation of the dams diet with selenium and vitamin E in late pregnancy will help to ensure good supplies to the newborn calf or lamb.

366
Q

Describe How iodine deficiency occurs?

A

Primary deficiency - low iodine content in the soil occurs predominantly in the west of the uK associated with high rainfall. Secondary deficiency due to goitrogens - act by disruption of iodine metabolism and there are two main types: thiocyanate which act by impairing iodine uptake in the thyroid via competitive inhibition an thus their effects can be overcome by additional iodine, these are found in brassicas and legumes eg white clover. Thiouracil - act by disrupting the iodination of thyroid hormones and prevent the conversion of inactive t4 to active t3. These found in brassica seeds. 3. Deficiencies of other trace elements - selenium required for the conversion of T4 to active T3 and thus selenium deficiency may lead to secondary iodine deficiency states. 4. Environmental factors - factors that increase the basal metabolic rate of animals such as low environmental temperatures, will increase the thyroid hormone production.

367
Q

What are the clinical signs of iodine deficiency?

A

Goitre - this is the classical sign of iodine deficiency - due to compensatory mechanisms invoked by the lack of thyroid hormone production. the enlargement may not always be clinically obvious but can be detected by histopathology in these cases. Stillbirths or birth of weak calves/lamsb - may have goitre and areas of alopecia and subcutaneous oedema. Weak calves/lambs are unwilling to suck and associated perinatal mortality is high. Loss of appetite with poor milk yield and poor wool production in sheep.

368
Q

How is diagnosis of iodine deficiency made?

A

soil and pasture iodine levels - iodine deficient areas usually known but the role of goitrogens in many cases means that soil and pasture levels are not particularly useful. Goitre - readily diagnosed on clinical exam and PM.Thyroid histopath - gold standard. thyroid iodine levels - will decrease markedly. Iodine levels in blood urine and milk - plasma inorganic iodine measures current daily iodine intake (short term) and is thus susceptible to changes in feed intakes/inappetance etc. Iodine levelsin milk and urine reflect dietary intakes. the normal range for plasma inorganic iodine in cattle is 105-287. Thyroid hormone levels - t4 levels reflect the thyroid and iodine status of the animal and thus are useful in the diagnosis of deficiency. care must be taken in interpretation of values as there is natural variation in t4 levels according to stage of lactation - levels are much lower in early lactation, season etc. t4 levels will be high in cases of iodine deficiency secondary to thiouracil goitrogens as they prevent conversion of T4 to T3.

369
Q

How is iodine deficiency treated and prevented?

A

Direct methods - oral compounds such as oral iodine salts - oral dosing using potassium iodide may be performed but this is relatively short acting. iodine poisoning is a potential risk. Intra ruminal boluses. These boluses provide slow release of iodine for 6mths. painting of 5% tincture of iodine on the flank skin fold once a week in cattle. injectable compounds - long term supplementation - intramuscular injections of iodised poppy seed oil provide adequate supplementation for up to 2 years. inclusion in compound feeds - in concentrate rations, kept seaweed. free access minerals - usually containing salt to improve palatability. medication of water supply, application of iodine fertilisers to pasture - poor uptake by herbage,

370
Q

What is the UK national average incidence of mastitis?

A

40 cases per 100 cows per year.

371
Q

Describe the causes of mastitis

A

Mastitis is a complex disease with a number of factors contributing to influence the level of mastitis in a herd including environment, management, udder physiology and cow health. Low incidence of mastitis in suckler cows. The major pathogens are contagious and environmental. Contagious - transferred to the teat and establish a colony at the teat end. They then grow up through the teat canal and into the udder. Environmental pathogens - enter the udder by propulsion through the teat canal (during milking, by capillary action, insertion of antibiotic tubes, insertion of teat cannula etc) and by passive penetration f the teat canal immediately after milking.

372
Q

Describe the difference between contagious and environmental pathogens involved in mastitis

A

Contagious - cow (udder teat r skin), transmitted during milking from cow to cow, the bacteria has adhesive properties, control measures include milking routine, post milking teat dip, dry cow therapy, SCC tend to be high, bactoscan tend to be low. Includes - staph aureus, strep agalactiae, strep dysgalactiae, mycoplasma, corynebacterium b ovis, coagulase negative, staphylococci.
Environmental pathogens - transmitted between milking from environment, no bacterial adhesive properties, main control measures include environmental hygiene, pre milking teat dip, optimising teat end defences, maximising immune response. SCC tends to be low (except with strep uberis) and bactoscan tends to be high. Includes - E Coli, streptococcus uberis, pseudomonas aeruginosa, other coliforms, bacillus cereus, yeasts and moulds, pasteurella.

373
Q

Describe the natural defence mechanisms which work against the entry and establishment of pathogens in the udder

A

The teat skin may become compromised by cuts, chaps, warts etc. Teat canal barrier - teat canal is lined with keratinised epithelium which secreted keratin into the canal to form a solid seal and prevent bacterial entry. Genetic factors - large pendulous udders and cone shaped teats are more prone to mastitis as are cows that have short or wide teat canals. Defences within the udder - even if bacteria have managed to penetrate the teat canal defences, there are a number of other mechanisms to remove bacteria from the udder;
Intrinsic defence mechanisms - lactoferrin is an iron binding protein that is present in relatively high concentrations during the dry period, and prevents the growth of bacteria by removing iron from udder secretions. Lactoperoxidase is an enzyme that is bacteriostatic on gram positive bacteria and bacteriocidal on gram negative bacteria. Normal milking has a flushing effect removing bacteria from the udder (3xday milking). Inducible defence mechanisms - the mechanisms whereby the inflammatory response recognises the presence of bacteria in the udder and acts via variety of mechanisms to eliminate the bacteria - eg migration of WBCs into the udder.

374
Q

Describe the mastitis which is caused by staph aureus (a contagious pathogen)

A

The primary reservoir is the udder but can persist on teat skin, has strong adhesive properties, a cow shedding infection in her milk can infect the next 6-8 cows to be milked by the same cluster. Majority of Staph aureus produce B lactamase. three disease syndromes are recognised; Peracute gangrenous mastiits, acute mastitis and chronic mastitis. In peracute gangrenous mastitis - cows have a high temperature, with heat pain redness and swelling, the cow is systemically ill and will become recumbent with severe depression. The udder is cold and clammy developing a blue black discolouration and secretion is reddish brown/watery. Cows which recover usually slough the affected quarter and require to be culled. acute mastitis of staph aureus is similar to other forms of acute mastitis with clots in milk. Chronic mastitis - staph aureus is notoriously difficult to treat leading to formation of chronic infections with extensive fibrosis and induration of the udder. reasons include poor antibiotic penetration due to extensive fibrosis, production of B lactamase by the majority of staph aureus strains, persistence of bacteria within macrophages and other cell types, development of L forms, capsules and bacterial dormancy, that renders the bacteria insensitive to antibiotic treatments.

375
Q

Describe mastitis that occurs with coagulase negative staphylococci? (contagious)

A

This applies to a group of bacteria including staph chromogenes, staph hyicus, staph simulans, steph epidermidis, staph hominis, staph xylosus. They commonly colonise the teat end and teat canal and may only be a sample contaminant if the correct sampling procedure has not been performed. however these bacteria may invade the udder under certain circumstances leading to high SCC and clinical mastitis during early lactation.

376
Q

Describe how strep agalactiae causes mastitis? (contagious)

A

It is highly contagious and is readily transmitted between cows during the milking process. it is usually brought into the herd via purchase of milking cows or via the relief milkers hands. it is primarily an infection of the udder although it can colonise the teat canal and teat skin. milk from infected quarters contains massive amounts of bacteria up to 10^8 per ml. response to antibiotic therapy is good - blitz therapy can eliminate infection from the herd.

377
Q

How does strep dysgalactiae cause mastitis? (contagious)

A

This survives well in the environment and thus has some of the properties of an environmental pathogen. it is commonly found on the teat skin, especially if the skin is damaged. it commonly infects dry cows, prepartum heifers and even calves.

378
Q

Describe mastitis caused by mycoplasma? (contagious)

A

Rare in the UK. caused by mycoplasma bovis and mycoplasma californicu. it usually occurs as a sudden onset condition with multiple quarters involved. The udder is hard with enlarged mammary lymph nodes. the mammary secretions vary from watery with sandy material present to thick colostrum like material. mycoplasma mastitis is highly contagious and can spread rapidly within infected herds. Although the bacteria have good sensitivity in vitro clinical response is poor and most cows have to be culled. strict hygiene is essential.

379
Q

Describe mastitis caused by corynebacterium bovis? (contagious)

A

This bacterium was thought to be a teat end commensal but has been associated with subclinical mastitis and high SCC especially with poor milking teat disinfection.

380
Q

Describe the types of mastitis that may occur when infected with E. coli ( an environmental pathogen)

A

Various environmental factors such as poor housing and poor hygiene lead to the multiplication of E. coli and thus an increased incidence of coliform mastiits. Peracute mastitis caused by E. coli classically occurs in early lactation - 60% of cases occur in the first 88 weeks of lactation and presents as a life threatening condition. initially the cow may be anorexic and pyrexic with diarrhoea and the udder and milk may appear normal. The condition rapidly progresses and the quarter becomes hard hot swollen and painful with a yellow watery secretion. the temperature becomes subnormal and the cow becomes dehydrated and endotoxaemic due to the release of endotoxins. the condition may be fatal. in contrast to peracute mastitis caused by staph aureus, gangrene rarely develops and non fatal cases will completely recover. subclinical mastitis can also occur when the only changes detectable are an increase in SCC and bacterial numbers in the milk. chronic recurrent mastitis may occur in cows with a poor immune response to E. coli as a sequel to acute coliform mastitis although clinical coliform mastitis is clasically described as a one off evnt. Coliform infection during the dry period - can become established during dry period, remain dormant in the udder and cause clinical mastitis in early lactation.

381
Q

Describe how klebsiella, pseudomonas and other coliforms can cause mastitis (environmental pathogens)

A

Klebsiella is associated with damp sawdust bedding causing peracute coliform mastitis. pseudomonas aeruginosa - associated with contaminated water and outbreaks associated with contaminated udder wash, teat dip and dry cow tubes. the clinical signs vary from peracute endotoxic mastitis to chronic recurrent cases. udder secretions may be blue/green in colour. response to treatment is poor. Other coliforms such as enterobacter aerogenes and citrobacter cause sporadic disease.

382
Q

How can strep uberis cause mastitis?

A

Widespread in the environment especially in straw yarsd which may contain up to 10^6 bacteria per gram of straw bedding. it is also widespread on the skin of the cow but relatively rare in faeces. outbreaks can occur in cows at pasture especially in alte summer, presumably by transmission from the skin of the cow via the lying area to the teat. It is a very common new infection of the dry period. the clinical signs of strep uberis infection vary from subclinical infections to acute cases with a hard hot swollen painful quarters pyrexia and systemic illness in the cow. certain strains of strep uberis are highly resistant to phagocytosis by WBC in the udder and develop into chronic recurrent cases.

383
Q

How can bacillus mastitis arise?

A

Classically associated with infected brewers grains (Draff) and may produce an acute mastitis with udder secretions resembling port wine. B licheniformis has been associated with fermenting waste silage left beside feed troughs which cows then lie on. B licheniformis has been associated with fermenting waste silage left beside feed troughs which cows then lie on.

384
Q

How do yeasts and moulds and other pathogens cause mastitis?

A

Candida and Aspergillus are common environmental organisms an cause mastitis due to contamination of water used for udder wash or dirty udders. Other mastitis organisms include leptospira borgpetersenii serovar hardjo type hardjobovis - the cause of milk drop syndrome and tuberculosis

385
Q

What are the clinical signs of mastitis?

A

Not all cases of mastitis have obvious changes in the milk or the udder. the presence of severe cases of peracute mastitis eg staph aureus or E. coli tend to represent the tip of the iceberg, and the approximate incidence of mastitis cases is fatal 1% to severe 29% to mild 70%. Normal milk contains approximately 2.6% casein, 2.8% butterfat, 4.6% lactose and has a ph of 6.7. in mastitis: decreased caesin, lactose and butterfat, total proteins, calcium phosphorus, total milk yield, stability and keeping quality. Increased - RBcs, wbcs, sodium, chloride, bacteria, pH, milk conductivity. SCC and bacteria are raised in subclinical mastitis and are detectable prior to clinical signs. changes in the milk may be detectable especially if foremilking is practicsed. mastitis can lead to changes from caseous lumps to clots in the milk to watery secretions. although some changes may be classical eg yellow watery secretion in coliform mastitis, it is not consistently possible to determine the organism producing mastitis from clinical signs alone. Changes in the udder are detectable as hot painful swollen quarters, systemic illness in the cow may be seen especially in mastitis caused by staph aureus, strep uberis and coliforms.

386
Q

What are the different methods of detection of mastitis?

A

Subclinical mastitis may be detected by the use of somatic cell counts and bactoscan results. Clinical mastitis is detected by: foremilking palpation and observation of the udder, change in the behaviour of the cows( only severe masitits), ambic in line mastitis detectors - filters detect any clots in the milk which clog the filter. they will not detect watery milk changes and must be checked regularly. checking the milk/sock filter at the end of milking - a retrospective measure as the sock is checked at the end of milking. the presence of clots /faecal contamination indicates mastitis or poor pre milking teat preparation.

387
Q

What is somatic cell count SCC and how is it used to detect mastitis?

A

The SCC is the number of cells present in the milk and is normally made up of a combination of epithelial cells and white blood cells. in resposne to inflammation of the udder, WBCs enter the udder to combat the infection and the SCC rises. measurement of SCC is perforemd by - automatic electronic methods (fossomatic method) or california mastitis test - crudely estimates SCc via a gelling reaction with a detergent reagent. Can help identify individual quarters with high SCC. Only detects relatively high SCC over 400,000/ml. Cell counts can either be performed on bulk milk SCC presented as monthly, three monthly and annual averages or individual cow SCC. Below 200,000/mlml indicate healthy udder status.

388
Q

What are the penalties/premiums for different Somatic cell counts in milk?

A

Premium - 400,001 -10.0ppl

389
Q

What factors affect the somatic cell count?

A

Clinical and subclinical mastitis - raised SCC
Mastitis organism - contagious pathogens such as staph and strep bacteria tend to give high SCC whereas coliforms tend to be eliminated rapidly and thus give low SCC.
Testing method - poor agitation of bulk tank prior to sampling can give high results. Age of animal - older cows tend to have higher cell counts due to prior infections. Stage of lactation - due to a concentration effect with lower yields. Seasonal and diurnal variations - cell counts may fluctuate due to seasonal calving patterns (groups of cows being dried off and at afternoon milking). Milking frequency - three times daily milking have lower SCC. stress and management factors can lead to variations in SCC.

390
Q

What is bactoscan and how is it use to detect mastitis?

A

Bactoscan measures the total number of bacteria present in a milk sample. Bactoscan is quicker and more reliable than total bacteria count. Bactoscan is 3-4 times the TBC value.

391
Q

What are the penalties/premiums for bactoscan levels?

A

Premium 500,000 -5ppl.

392
Q

What are the potential sources of bacteria in the milk?

A

mastitis pathogens from the udder - the numbers of bacteria excreted frmo mastitis quarters can be over 100,000,000/ml, especially if strep agalactiae and strep uberis. environmental contamination - poor washing of teats prior to milking will lead to bacteria entering the milk as well as predisposing to mastitis. Dirty milking plant - poor cleaning of the milking equipment after use. Poor refrigeration of milk - should be immediately cooled to 4 degrees as soon as possible after milking to prevent bacterial multiplication.

393
Q

Describe aseptic milk sampling technique for taking samples for bacteriology in monitoring of mastitis

A

Wear clean gloves, wash gross contamination from the teat, dry, pre dip, allowing 30 seconds contact time, dry , strip foremilk to remove teat canal contaminant bacteria, clean and disinfect teat by scrubbing with swab containing 70% alcohol, repeat until swab is clean, dry, collect sample, holding collection tube as horizontally as possible to prevent it entering the tube, do not touch the rim of the sample pot with the teat or your fingers, label with cow number, quarter, date and farm identity, store at 4 degrees until transported to laboratory.

394
Q

What is the five point plan in controlling mastitis?

A
  1. regular milking machine maintenance
  2. post milking teat disinfection
  3. Dry cow therapy
  4. Prompt treatment and recording of all clinical cases
  5. Culling chronic mastitis cases.
395
Q

how does the milking machine have an effect on the incidence of mastitis?

A

It acts as a fomite - can spread infection
Causes damage to the teat end - high teat end vacuum and overmilking may damage the end of the teat and can be assessed by looking at the teat ends for damage (teat scoring.) Colonisation of the teat canal - the keratin in the teat canal acts as a type of blotting paper, soaking up bacteria and is then removed by the milk flow. Impact forces - impact forces are a reverse flow of milk back up against the teat end due to liner slip which can lead to the propulsion of bacteria into the udder. Overmilking.

396
Q

What are the most important control measures for the milking machine to reduce its involvement in mastitis?

A

Liners - most liners have a lifespan of 2500 milkings or 6 months and must be replaced after this. Routine specialist testing every 6 months - Static testing is carried out when no cows are being milked, it involves checking the vacuum levels, regulator function, pulsation system and general plant maintenance. Dynamic testing - carried out during milking- Involves checking the vacuum levels and fluctuations during milking.

397
Q

What is the purpose of post milking teat disinfection? (post dips)

A

Performed for three major reasons:
Removal of contagious mastitis pathogens from the teat skin
Removal of bacteria from teat sores - a potential reservoir for mastitis pathogens.
Improving teat skin quality - emollients are added to post dips up to a concentration of 10% and act to improve teat condition. Post milking teat disinfection has no effect on existing infections.

398
Q

What are the reasons for pre milking teat disinfection?

A

Used as a control measure against environmental mastitis pathogens by;
Disinfecting the teat, and reducing superficial teat contamination
Reducing the number of bacteria in the bulk milk lowering bactoscan results, reduces the incidence of environmental mastitis. Teats should be foremilked, washed and drier prior to application of pre dip. the teats should be coated in pre dip, allowed a minimum of 30 seconds contact time and then wiped off. Teat disinfection may be applied by dipping with excellent coverage or spraying - will give good coverage of the teat and use approximately 15ml disinfectant solution per cow, if applied too quickly then poor teat coverage may result. Automatic teat disinfection systems - at the exit of the parlour, tend to give poor teat coverage.

399
Q

Compare pre and post milking teat disinfection

A

Pre dips - used at housing and high risk periods, rapid speed of action, effective against environmental pathogens, limited effect on SCC, decreases bactoscan.

Post dips - used all year round, not important speed of action as left on, effective against contagious pathogens, decreases SCC if used with other control measures, no effect on bactoscan.

400
Q

What are the main aims of dry cow therapy?

A

The treatment and cure of existing infections for example staph aureus. Prevention of new infections - summer mastitis, coliform mastitis. Prevention of new infections due to environmental pathogens in particular E. coli and strep uberis has become more important.

401
Q

What must you take into consideration when choosing dry cow therapy?

A

Duration of action, persistence of activity during the dry period - particularly important in the control of new infections especially in the last 2 weeks of the dry period. Residues - the balance to the longer persistence of effective concentrations in the udder is that these can lead to longer residues. If the farm does not know the exact calving dates then antibiotic failures may result. Type of bacteria involved - the most common subclinical infections that require treatment in the dry period are staph aureus, strep uberis, w whereas the most common infections that may become established during the dry cow period are strep uberis and E. coli. Complete cure of subclinical infections - bacteriological cure rates can be as low as 30% in the treatment of chronic recurrent cases of mastitis especially chronic staph aureus and strep uberis. Improved cure rates at drying off may be achieved by use of parenteral antibiotics for 3-4 days procaine penicillin, clavulanic acid, potentiated amoxycillin, tylosin at the same time as the dry cow tube. Cows should be dried off abruptly - not milked once a day and the dry cow tube inserted using strict asepsis - scrubbing the teat end with 70% alcohol prior to insertion to prevent the introduction of bacteria into the udder.

402
Q

Describe the different types of dry cow therapy available?

A

1- antibiotic dry cow therapy; cloxacillin cephalonium, framycetin, penethamate, penicillin.

  1. External teat sealants - dry flex - a polymer based teat dip that dries to give a physical seal around the teat. to ensure uninterrupted coverage they should be applied twice weekly. this lack of adherence and need for re application is a major problem. can be used on organic farms.
  2. Internal teat sealants - an inert paste containing 65% bismuth subnitrate that remains in the base of the teat cistern and teat canal preventing the introduction of new bacterial infections during the dry period. it contains no antibiotics and thus will have no effect on existing intramammary infections. Should be infused using strict assepsis. Orbeseal should be used only in cows with an ICscc below 200,000 in the last three months of lactation. cows with high ICSCC will probably have subclinical mastitis and should be treated with antibiotic dry cow therapy. can be used on organic farms.
403
Q

when Should cases of mastitis be culled?

A

Culling is one method of removing cows with high SCC or recurrent mastitis from the herd. current recommendations suggest that cows which have had three or more outbreaks of mastitis in the same quarter in the same lactation ( or 5 cases of mastitis in all quarters in the same lactation ) and a high SCC ( over 500,000) for three months should be culled as they will probably never be cured. Should also take into consideration factors such as cow health, age and mastitis. Staph aureus and strep uberis are difficult to treat but strep agalactiae treatment will be successful.

404
Q

How do you know when a case of mastitis is a returning case or is a new case?

A

If a case of mastitis clears up but recurs in the same quarter more than a week after remission of clinical signs then it is defined as a new case of mastitis. Under 7 days and it is a continuing case of mastitis.

405
Q

Describe the different types of intrammamary antibiotic lactating cow therapy

A

Amoxycillin clavulanic acid - broad spectrum, licensed for use with synulox injection. Ceftquinome - broad spectrum, can use with injection. Framycetin, pirlimycin - lisenced for treatment of subclinical mastitis - withdrawal 5 days. The milk withdrawal times are between 48-84 hours except pirsue which has a very long withdrawal - 5 days. all products should be administered using strict asepsis to prevention the introduction of bacteria into the udder and should be combined with regular stripping of the udder to remove bacteria and debris.

406
Q

Describe grate I - mild mastitis - milk changes only - TREATMENT?

A

Choice of antibiotic will depend on organism involved. strep spp do not produce B lactamase but almost all staph aureus isolates will. consider parenteral antibiotic therapy if Intramammary treatment alone is not achieving good cure rates. The response of strep agalactiae to antibiotic therapy is very good and is sensitive to almost any antibiotic. It can be eliminated from herds by the use of blitz therapy combined with other measures against contagious pathogens to prevent spread and re infection.

407
Q

What are the possible reasons for failure of antibiotic therapy?

A

Delay in the detection and treatment of cases of mastitis, establishment of chronic infections especially staph aureus and strep uberis, constant reinfection of quarter due to teat end damage, teat scores etc, inappropriate antibiotic usage, duration of treatment too short mastitis caused by organisms non responsive to antibiotics eg yeast.

408
Q

Name the different treatments that are available for parenteral antibiotic therapy for the treatment of mastitis?

A

Penicillin - effective vs strep spp no activity vs G- and B-lactamase.
Amoxycillin clavulanic acid - road spectrum
Cefquinome - only cephalosporin with good udder penetration, broad spectrum.
Trimethoprim - brooad sectrum, resistance, cheap, good udder penetration
Framycetin - aminoglycoside good G- activity, poor udder penetration
Tylosin - excellent udder penetration (ion trap) G+ activity only
Fluoroquinalones - good udder penetration, expensive, broad spectrum. Medical worries concerning resistance.

409
Q

What Parenteral NSAIDs can be given for the treatment of mastitis?

A

Flunixin, Ketoprofen, tolfenamic acid, meloxicam. These are the only NSAIDs licensed for use in lactating cattle. good for the resolution of pyrexia, pain and treatment of endotoxaemia in coliform mastitis.

410
Q

What are the causes of severe systemic mastitis?

A

USual causes are Coliforms and staph aureus, and sometimes strep uberis and summer mastitis. aggressive treatment required.

411
Q

Describe the factors in the milking routine which play a major role in contagious mastitis?

A

Milker hygiene wearing of disposable gloves with frequent rinsing in disinfectant, foremilking aids in early detection of mastitis, teat preparation - teats should be clean and dry prior to attachment of the cluster, communal udder cloths spread infection and should never be use, pre dipping helps to reduce the incidence of environmental mastitis, attachment of cluster, milking and automatic cluster removal. Over milking increases the incidence of mastitis and leads to teat end damage, post milking teat disinfection helps in control of contagious mastitis. Milking order - ideal milking order is to milk the most susceptible cows first and milk cows with high ICSCC and mastitis cows last, to reduce the spread of infection. Cows are to remain standing for 30 mins after milking to allow teat canal to close.

412
Q

Describe the cause of summer mastits?

A

It is a disease of dry cows and heifers but may even occur in rudimentary udders of young heifers, bulls and steers and occurs at grass during summer months. Bacterial causes include arcanobacterium pyogenes, peptostreptococcus indolicus, streptococcus dysgalactiae as well as a variety of other bacteria including microaerophiilic cocci, bacteriodes melaninogenicus and fusobacterium necrophorum have been implicated. The major factor in the transmission of infection is thought to be the head fly (hydrotea irritans) these flies live in bushes and trees and can only fly during dry conditions and low win speeds. cases tend to be associated with problem fields.

413
Q

What are the clinical signs of summer mastitis?

A

Affected quarter is swollen, hard painful and hot with an enlarged teat. the udder secretion is thick and clotted with foul smelling green yellow pus, severely affected animals are pyrexic, stiff and lame due to the painful quarter. oedema may extend around the udder and up inside the leg. affected animals may abort and may die if prompt treatment is not administered. even after prompt treatment the affected quarter is permanently damaged.

414
Q

How should summer mastitis be treated?

A

Parenteral antibiotic injections (procaine penicillin potentiated sulphonamides or tylosin), intrammmary antibiotics, NSAID injections to reduce pyrexia, swelling and pain, stripping of the udder manually as often as practical. Remove from the other cows as is a potential source of infection.

415
Q

how is summer mastitis conrolled?

A

Reduce exposure keep cows away from susceptible fields, application of fly tags ,pour ons and spray usually synthetic pyrethroids. Sealing of teat canal using micropore/adhesive tape and external teat sealants, dry cow therapy.

416
Q

Describe the approach to an individual case of coliform mastitis

A

Thorough clinical examination, especially udder, rectal, vaginal. Full DDx as for downer cow. common clinical findings include severe depression, recumbency, subnormal rectal temperature, diarrhoea, hard quarter with yellow watery secretions and signs of endotoxaemia. Fluid therapy - endotoxaemia results in an initial vasoconstriction followed by dilation, hypovolaemia, reduced cardiac output and inadequate tissue perfusion. A 700 kg cow that is clinically 7.5% dehydrated requires over 50 litres of isotonic fluid to restore the circulating blood volume. Give either orally, IV (most give 10-15 litres of non sterile isotonic saline quickly via the jugular vein using a garden weedkiller spray pump and repeat this every 6- hours, or intravenous hypertonic fluids - rapid infusionn of 3 litres of hypertonic 7.2% sodium chloride after which the cow will drink up to 40 litres of warm water. Give NSAIDS to reduce pyrexia, counteract endotoxaemia and reduce pain. Antibiotics - treat using broad spectrum antibiotics at high dose rates. Calcium borogluconate - many cases of coliform mastitis are also hypocalcaemic. Quarter stripping ad oxytocin - regular stripping of affected quarters is essential to remove inflammatory products from the udder and should be performed as often as practical. oxytocin may assist in milk let down. Cow should be provided with a comfortable lying area with plentiful supply of food and water. other supportive therapy including multivitamin injections and intravenous glucose.

417
Q

Describe your approach to a herd with a high incidence of mastitis?

A

The initial investigation should concentrate on identification of the problem, this involves data collection - examination of mastitis records such as percentage of herd affected, recurrence rate, milking cow tube usage, seasonal variation with environmental pathogens. Bulk tank analysis - high SCC and high bactoscan. Clinical inspection - inspection and management of cows with mastitis, bacteriology of clinical cases, high ICSCC cows before treatment, treatments (lactating and dry cow Intramammary tubes) teat scoring - hyperkeratosis/teat end eversion/teat skin condition. Farm inspection - milking routine, farm environment - housing, cleanliness, milking machine maintenance and operation, treatment of mastitis, biosecurity. This all should lead to the identification of the predominant pathogen causing the mastitis and control measures can be directed towards this.

418
Q

How can environmental mastitis pathogens be controlled?

A

the control of environmental pathogens is based upon improving environmental hygiene, reducing the level of contamination at the teat end, optimising teat end defences and improving the immune response of the cow. The udder is most susceptible to new infections around calving and at dying off. Environmental hygiene - clean dry cool, cubicles must be correct size, comfrotable, straw can predispose to strep uberis, sawdust can predispose to coliform mastitis, sand is very good, straw yards - bedding wetness, ened to apply fresh bedding frequently, clean out every 4-6 weeks at least to prevent heating, calving boxes often neglected, must be clean and dry, regular scraping of rear of cubicles, passage ways etc. Ventilation needs to be adequate to prevent condensation/high humidity. Dietary influences - high concentrate feeding will give loose dung. High stocking rates lead to increased faecal soiling and high humidity. Reducing contamination at the teat end - cleaning and drying of udders prior to cluster attachment, pre milking teat disinfection, post dipping and loafing time after milking to prevent cows immediately lying after milking, aseptic infusion of intramammary tubes. Milking machine maintenance, teat damage, good teat seal to prevent the introduction of bacteria especially during dry period, genetic influences. Immune response of cow - stress predisposes to infection, milk fever, ystocia, nutrition when dry, vaccination to prevent coliform mastitis reduces the severity of clinical signs.

419
Q

What normally causes a high SCC in herds? How can high SCC be approached?

A

Usualy due to subclinical mastitis caused by contagious pathogens or strep uberis. Farm inspection - implementation of the 6 point plan especially milking machine maintenance. Identification of high SCC cows, identification of mastitis pathogens involved - bacteriology from 10 high cell count cows, or bulk tank bacteriology. Blitz therapy for strep agalactiae, strep dysgalactiae suggestive of poor teat condition so may require use of higher concentration of emollients in post dip, C bovis is suggestive of poor post milking teat disinfection. Action for high cell count cows - early dry cow therapy - treatment with lactating cow intramammary or parenteral antibiotics prior to drying off to enhance bacteriological cure rate. Culling - permanent and expensive method and decision should b e taken on basis of multiple ICSCC, bacteriology, chances of cure. Treatment during lactation - treat early and aggressively to ensure good cure rates. Milk high cell count cows last as a separate group if possible. Discarding milk from high ICSCC cows can be witheld from the bulk tank.

420
Q

Where does a high bactoscan result normally arise from?

A

Pathogens from udder, environmental contamination, dirty milking plant and poor refrigeration of milk.

421
Q

What methods can be used for bulk tank analysis

A

Bactoscan - total number of bacteria in sample, total bacteria count - measures number of viable bacteria, thermoduric count - bacteria that withstand pasteurisation over 63 and thus high levels are indicative of a wash up problem. coliform counts - level of environmental contamination. Psychoroph indicator value - found in dust, grow best at low temperatures - indicator of poor pre milking teat disinfection. bacterial differential counts - bacteriology to determine the presence of staph aureus, caogulase negative staphylcocci, strep spp. Bactoscan should be below 20,000, TBC below 5000, thermoduric count below 175, coliform count below 20, psychotroph indicator value below 30, total staphs below 200, staph aureus below 10

422
Q

What is papillomatosis?

A

Bovine papillomavirus - of which there are several strains. two main types - flat or rice grain fibropapiillomas seldom of clinical significance, more florid type or projecting fibropapillomas can cause problems if teats badly affected as interfere with milking. Treatment/prevention - most seen in heifers and often resolve before they enter the milking herd. if herd immunity is not good then may get spread of warts at milking time due to virus transmission on hands and utensils. minimise this risk by milking parlour hygiene.

423
Q

What is herpes mamillitis?

A

Caused by bovine herpes virus 2 - Normally seen in autumn/winter months, in naive herd will spread rapidly through all ages of cows but more often outbreaks are seen in susceptible heifers when entering milking herd. Initially widespread vesicles form on teats and base of udder which rupture to give painful ulcerative lesions. these ulcerative lesions become covered in dried serum exudate which forms thick brown scabs. healing takes 2-3 weeks. Symptomatic treatment of skin lesions with antiseptic udder creams and iodine based teat dips may help. milk affected cos last and disinfect clusters carefully to try and minimise spread. cows may be hard to milk due to painful teats and may get secondary mastitis if lesions affect teat orifice.

424
Q

What is pseudocowpox?

A

A parapox virus closely related to those causing orf in sheep and papular stomatitis. Can be zoonotic. common in dairy cows seen at all times of the year. immunity is short lived. often have endemic infection in herds. occasionally can get more severe widespread outbreaks in naive herds. initial erythematous and oedematous painful lesions appear on teats which soon become raised orange papules and then small dark red scabs. Vesicles rare. the scabs will be shed after 10-12 days leaving the classical raised horseshoe or ring lesion which is pathognomonic for pseudocowpox. Complete healing may take 4-5 weeks. The virus can cause localised painful nodules on the hands and arms of in contact humans. Symptomatic treatment only - the lesions do not usually cause any problems to cows unless on the teat orifice predispose to mastitis. good milking parlour hygiene may limit spread.

425
Q

What is udder impetigo/necrotic dermatitis?

A

Severe infection of the udder with staphylococci, can give rise to multiple small pustular lesions which can sometimes spread onto the teats. controlled by improving environmental hygiene and topical treatment of skin lesions with antibacterial washes. necrotic dermatitis (udder rot) can be see in the udder skin where it lies tight against the medial thigh and occasionally in the ventral midline immediately cranial to the udder. treatment is symptomatic with topical antibacterial creams and debridement.

426
Q

What is udder oedema?

A

Mainly a problem in peri parturient heifers - the exact cause is unknown but it is a physiological phenomenon related to nutrition - high concentrate Na or K excess, circulatory disturbance of udder vessels and possibly with some hereditary component. In severe cases there is massive oedema of udder and teats extending along the ventral midline, most cases resolve soon after calving when milking is initiated but in severe cases treatment may be required. milking can be started pre calving or calving can be induced with corticosteroids. Diuretic injections eg frusemide will aid in the elimination of oedema.

427
Q

What is photosensitisation and how can it affect the teats?

A

Cows suffering from photosensitisation will usually develop painful swollen teat skin in the acute stages. this may lead to peeling and sloughing of the teat skin before healing occurs. local or systemic anti inflammatory treatment along with housing out of direct sunlight will lead to rapid recovery unless photosensitisation is secondary to other disease.

428
Q

What are teat chaps?

A

Normally horizontal cracks in the teat skin which can cause discomforrt when being milked or suckled. they act as a good reservoir for contagious mastitis pathogens. Teat chaps can be caused by badly fitting teat cup liners and poor environmental conditions along with extreme cold temperatures. in beef cows lesions can start with aggressive suckling by old calves prior to weaning then fly bite damage will exacerbate the lesions. in dairy cows teat dips containing glycerine or lanolin will help prevent chaps and in beef cows fly control and weaning calves will prevent problems.

429
Q

What are milking machine induced lesions of the teat?

A

Malfunctioning milking machines can lead to a herd problem of teat end lesions which can predispose cows to mastitis. Damage can be as a result of incorrect vacuum pressure liner slip or overmilking. a common lesion is hyperkeratosis caused by prolapse/eversion of the streak canal lining which can then become traumatised and infected. teat end scoring can be used as a way of monitoring milking machine function. Secondary infection of teat ends with fusibacterium necrophorium leads to dark scabby lesions known as blackspot.

430
Q

Describe the different types of treatment for teat lacerations

A

Usually caused by teats being stood on. most teat injuries can be treated conservatively - injuries which do not involve the teat cistern should be cleaned thoroughly with mild antiseptic solution and any loose or devitalised skin trimmed off using a scalpel blade or sharp scissors. healing by second intention will occur and if the cow will not tolerate being milked a sterile teat cannula can be inserted to allow milk to be drained at milking time. strict attention to hygiene must be observed when using canulae as there is a high risk of mastitis developing. Surgical repair of teat injuries is rarely successful and most wounds break down due to secondary infection.full thickness teat lacerations where the teat cistern has been breached will require surgical repair otherwise a leaking fistula will develop. Cow should be sedated and cast before anaesthetising the teat with a ring block. Must be cleaned and debrided. fine absorbable suture material on an atraumatic needle should be used for the mucosa and submucosal layers. the teat skin can be sutured with fine monofil nylon or repaired with stainless steel staples. A teat cannula can be used to avoid milking until healing is complete.

431
Q

What are blind quarters and how can they be treated?

A

Congenital obstruction - occasionally newly calved heifers are presented with blind quarters. if milk can be felt filling the teat cistern then all that may be required is to open the teat orifice which is sometimes non patent. this is done with a sterile needle or teat knife. Placement of a sterile plastic teat cannula for a few days might be required to prevent the teat orifice healing up. Infusion of intramammary antibiotic may be sensible to reduce the risk of mastitis at this time. If no milk can be felt then this suggests a membranous obstruction at the base of the gland cistern - attempts to break this down should be avoided as unlikely to be successful and will lead to infection of the gland or worse. these quarters are best left well alone.

432
Q

What are teat peas?

A

Most are caused by prolierative granulation tissue, mucosal injury or fibrosis secondary to teat trauma. these are small fibrous lesiosn which can be free in the teat lumen or attached by a stalk to the mucosal lining. they can cause obstruction to milk flow by blocking the opening to the streak canal. usually they can be removed by enlarging the teat orifice with a teat knife then manipulating and squeezing it out. large or fixed lesions may required cutting up within the teat lumen before removal. the teat lining can be desensitised by placing a tourniquet around the base of the teat hten infusing 10ml of lignocaine into the teat cistern. strict hygiene and minimum trauma should be observed if possible. infusion of antibiotic/corticosteroid Intramammary tubes is advisable for a few days to reduce risk of post surgical mastitis and inflammation. if good surgical conditions are possible then teat peas can be removed surgically following a vertical incision into the teat lumen.

433
Q

What are pencil obstructions of the teat?

A

These lesions may follow diffuse teat trauma leading to chronic granulomatous reaction of the teat mucosa. Milk will only flow in very small amounts and a firm pencil like obstruction can be palpate in the teat cistern. Prognosis for these lesions is guarded and interference with teat knives will only worsen the lesion. in very valuable cows surgical repair using silicone cannula implants has been described.

434
Q

What is a vertical fissure of the hoof wall? (sandcrack)

A

There is loss of continuity of horn fibres of the palmar/plantar hoof wall extending for a variable distance from the coronet towards the bottom half of the hoof wall. sandcracks result from damage to the periople and underlying coronary band. Factors contributing to this condition may include excessive drying out of the horn during dry summer months, sudden excessive pressure such as jumpiing/galloping and faulty nutrition. In the UK, sandcrack is seen more commonly in galloway breeds and its crosses. The front feet are more often affecteed. the lesion varies from a small vertical crack near the coronet to a large jagged uneven fissure on the anterior wall. many beef cattle have sandcracks in their hooves but are not lame. There is often sudden onset of severe lameness when impacted material leads to pus formation and pressure on the sensitive laminae of the wall. Careful hoof paring of the sandcrack releases pus. Foot paring of the palmar hoof wall presents numerous practical difficulties because it involves extending the carpus and distal limb joints rather than the usual method of flexing to permit paring of the sole. dirt is often packed deep into the sandcrack near the sensitive laminae. remove sufficient under run horn by cutting out a shallow V to release pus. neither antibiotics nor a bandage is necessary afterwars. there are no specific control measures.

435
Q

Describe a horizontal fissure of the hoof wall (thimbling)?

A

Poor horn production during a severe toxaemic condition such as coliform mastitis or metritis appears as a horizontal fissure in the hoof horn of all eight digits. As this defect in the wall grows down to about two thirds of its length three to four month later, it weakens and may separate from the healthy horn proximally. the corium remains intact distal to the horizontal fracture holding the distal hoof horn attached at the toe. this fissure moves when weight is taken tensing the corium still attached distally causing variable pain and lameness. Material can occasionally become impacted in the fissure causing abscesses. All claws of all four feet are affected with variable lameness depending upon the amount of material impacted in the horizontal fissure. Typical appearance affecting all eight digits, most noticeable at the toes. Careful hoof paring is necessary only when the cow is lame to remove all under run horn and impacted material, best achieved with hoof shears, but the hoof capsule may be still attached at the toe. No specific control measures except prompt treatment of toxic conditions.

436
Q

What is a white line abscess?

A

An abscess arises following bacterial entry into the white line area, usually found in the lateral claw of the hind foot on the abaxial border close to the junction with the heel. the condition is more common in dairy cows that spend long periods standig/walking on poorly maintained surfaces. Inflammation of the laminae/corium weakens the white line. separation of the white line, caused by torsional forces as cattle turn sharp corners, allows impaction with small stones and dirt. entry of bacteria with multiplication forms an abscess which may extend to the white line and discharge at the coronary band in neglected cases. Affected cattle often present with sudden severe lameness of the affected leg with only the toe touching the ground. careful foot paring reveals separation and impaction of the white line with dirt leading to an abscess which is under pressure and may spurt pus upon release. Care must be taken not to expose the sensitive corium. There is a marked improvement in locomotion within two days. A white line abscess that has ascended to involve the coronet can be differentiated from septic pedal arthritis by the small area of the abaxial coronary band affected and not the whole coronet. The abscess is confirmed upon release of pus. release pus by careful foot paring with removal of all under run horn. there is no requirement to bandage the foot or any n eed for antibiotic therapy. more thorough investigation is necessary when lesions cause considerable heel swelling. Maintain all roads, tracks and the area infront of the silage face. Correct space allocation 25cm per cow at self feeding silage face. design movement/flow of cattle to avoid sharp corners.

437
Q

What is interdigital white line abscesses?

A

Interdigital skin hyperplasia refers to excess epidermal and hypodermal tissue occupying part or all of the interdigital space. used to be common in hind feet of hereford bulls. some association with corkscrew claws. Aetiology - probably hereditary. usually appears as a protuberance of skin at the front of the interdigital space. interdigital skin hyperplasia does not cause lameness unless it becomes so large that excoriation leads to superficial infection. Diagnosis confirmed by careful examination of the interdigital space and foot paring to ensure other potential causes of lameness are not overlooked. prompt topical antibiotic treatment of superficial infection and debridement of any under run tissue. excision of the growth under intravenous regional anaesthesia and application of a pressure bandage to the affected area is not a simple procedure and is rarely indicated. recurrence after surgical debridement is common.

438
Q

What is chronic necrotic pododermatitis?

A

Slurry heel is a very common condition affecting the feet of almost all housed dairy cows during the late winter months. new horn growth affects the weight bearing function of the hoof which predisposes to corium damage, sole ulcer and white line disease. Prolonged exposure to slurry during the winter housing period is an important factor in the aetiology of slurry heel. The role of dichelobacter nodosus infection has also been suggested. On its own slurry heel dos not cause lameness. there is necrosis of the horn of the heel and heel/sole area varying frmo small blackish pi tter areas of the horn up to black cracks of penetrating deeply towards the corium of the heel/sole area. Slurry heel causes overgrowth of the soft horn of the heel and sole. Cut away necrotic horn where necessary to restore normal foot shape, spray with oxytetracycline aerosol. Improve slurry management in dairy herds - regular use of a formalin footbath has been recommended.

439
Q

What is a sole ulcer?

A

A specific circumscribed lesion of the sole at the sole/heel junction nearer to the axial than abaxial wall affecting dairy cows and occasionally beef bulls. never seen in growing cattle and rarely beef cows. the highest prevalence occurs during late winter after cattle have been housed for several months. sole ulcer affects the lateral digits often involving both hind feet. Pressure damage to the corium is caused by compression at the posterior axial border of the pedal bone. build up of new horn consequent to slurry heel is an important factor. Often sudden onset severe lameness. Affectedd cattle may stand with toe of affected digit on the edge of the cubicle standing. When walking, the cow may abduct the leg to bear weight on the unaffected medial claw and cows are reported to kick backwards before placing the affected foot on the ground. there is much new overgrown soft horn on the lateral claw containing obvious sole haemorrhage. this overlying flap of horn often obscures the area of ulceration. further paring often following a black necrotic horn crack will lead to sole ulcer site. the sole ulcer may present with or without protrusion of granulation tissue. the treatment is caused by pressure to corium, so the sole should be rendered concave to reduce this pressure by ccareful foot paring. all underrun horn is removed which may expose an ulcer. remove granulation tissue level with the sole using a scalpel blade. there is no requirement to use local anaesthetic because this granulation tissue does not contain a nerve supply. Apply a pressure bandage over the site of the sole ulcer. apply a wooden shoe or similar to the sound claw. if deep infectio, amputate digit. Always check other hind lib lateral claw first for signs of an ulcer.

440
Q

Describe the clinical presentation of septic pedal arthritis?

A

Septic pedal arthritis occurs sporadically in all ages of cattle following deep penetration of the distal interphalangeal joints by nails and other metal objects but is encountered most commonly following extension from sole ulcer lesions in the lateral hind claw of dairy cows. Infection of the distal interphalangeal joint rarely arises from interdigital infection such as foul of the foot. Affected cattle show 10/10 lameness with marked muscle atrophy of the afected limb after 7-10 days. there is a history of poor milk yield and general body condition loss due to reduced grazing/feeding. there is marked swelling of the drainage lymph node which may be five to ten times its normal size although the popliteal lymph node is difficult to palpate. the foot is hot, swollen and very painful. there is marked swelling above the coronary band on the abaxial aspect extending to the bulb of the heel but discharging sinuses are uncommon except for neglected cases. Rupture of the deep digital flexor tendon where it inserts onto the caudal aspect of the navicular bone may result in the toe not contacting the ground. Swelling may extend above the fetlock joint which suggests infection of the deep flexor tendon sheath and a guarded prognosis.

441
Q

What is the treatment of septic pedal arthritis

A

Further antibiotic therapy is useless in cattle with infection of the distal inter phalangeal joint. Digit amputation under IV regional anaesthesia gives good results. IV injection with an NSAID such as Flunixin is recommended prior to amputation.

442
Q

Describe the procedure of digital amputation in cattle

A

The animal is restrained and the affected leg lifted and secured. in an adult dairy cow weighing 600-700kgs 25-30mls of 2 percent lignocaine solution is injected into a superficial vein after application of a tourniquet either above the hock or below the carpus. a calving rope can be used for this purpose. the recurrent metatarsal vein runs on the craniolateral aspect of the mid third metatarsal region and is readily palpable. insertion of needle into distended superficial vein releases 5-10mls of blood under pressure, blood flow then quickly reduces to the occasional drop if the tourniquet is tight enough. Analgesia is effective within two minutes and is tested by needle pricking the coronary band. The interdigital skin incision is extended for the full length of the interdigital space for a depth of approximately 25mm at the cranial margin extending to 40mm at the most caudal extent. A length of embryotomy wire is introduced into the incision and the digit is removed through the proximal region of the second phalynx by rapid sawing action (distal P1 is recommended bysome). the deep flexor tendon sheath is carefully examined for evidence of ascending infection which usually manifests as heat, pain and swelling extending to the mid third metatarsal region. If infected a section of the deep flexor tendon is excised. Topical antibiotic spray is applied to the wound. a Melolin dressing is applied to the wound and pressure applied using cotton bandages over a large amount of cotton wool. a course of parenteral antibiotics such as procaine penicillin is administered in most cases. the dressing is removed two to three days later and the granulating wound sprayed with oxytetracycline aerosol.

443
Q

What is digital dermatitis?

A

An infectious contagious disease causing severe lameness in adult dairy cattle. Unproven but widely accepted to be a spirochaete. related to prolonged exposure to slurry. Lameness is variable. weight is borne at the toe leading to excessive growth at the heel bulbs. hind feet lesions more common than front feet and are more prevalent during early lactation. the feet are frequently encrusted with faeces above the level of the fetlock joint and must be first removed to expose the skin. the early lesion is a moist area of skin approx 2-5 xm in diameter above the cleft of the bulbs of the heel. there is erosion of superficial skin with a yellow/green Diphtheritic membrane covering the lesion. There may b e considerable skin hyperplasia forming hairy warts (papillomatous digital dermatitis) extending 2-3 cm from the skin surface. Thoroughly clean lesion and apply topical oxytetracycline aerosol. repeat treatments frequently necessary. daily footbaths containing either lincomycin or tylosin are frequently used to control herd outbreaks. Formalin or copper sulphate footbaths have no effect on the transmission or development of this condition.

444
Q

What is superfoul?

A

A peracute form of interdigital necrobacillosis with suggested synergism with the causal agents of digital dermatitis. There is very sudden onset of severe lameness. the lesion starts as a swelling and widening of the interdigital space with extensive tissue necrosis which if left untreated for 12-24 hours can rapidly progress to involve the navicular bursa, flexor tendon sheath and distal interphalangeal joint. the foot is very swollen and the cow is 10/10 lame. Diagnosis is confirmed following clinical examination of sudden severe lameness involving interdigital space and deeper tissues affecting a number of cow. Immediate actin important. under IVRA debride the lesion and pack with 2-4 500mg clindamycin tablets. apply bandage. treat cow with 20mls of tylosin injected intramuscularly twice daily for at least 3 days. administer flunixin or ketoprofen. isolate cow in well bedded straw pen. cull severely affected cattle. Quarantine all cattle introduced into the herd. Reduce environmental contamination and increase bedding in cubicles Disinfectant footbaths containing formalin or copper sulphate are reported to provide good control.

445
Q

Describe how a fracture of the pedal bone presents?

A

Seen in older dairy cows presenting with sudden onset foreleg lameness. sudden contact with concrete or hard ground often during bulling activity is the most comon cause. the cow presents with severe lameness of a medial claw of a front foot and adopts a characteristic crossed leg stance with the weight borne on the sound lateral claw. careful examination of the foot is essential to eliminate other more common causes. the fracture site is readily identified by radiography but this is rarely undertaken in practice. a wooden block applied to the sound claw relieves lameness and the prognosis is very good.

446
Q

how can infection be reduced to reduce herd lameness in cows?

A

All lame cows examined ASAP for appropriate treatment. Prompt and effective treatment. reduce spread of infectious conditions in particular digital dermatitis and superfoul by reducing the amount of infectious agent in the environment eg slurry management and the spread of infection by regular footbathing. Biosecurity - there are still a number of closed herds with no digital dermatitis and so the biggest risk factor for them is buying in animals with digital dermatitis. check animals before purchase, quarantine and prophylactic foot bathing may all be necessary.

447
Q

Why is regular hoof trimming important in all cows?

A

Routine hoof trimming aim is to remove any overgrowth and so restore the foot to its correct shape and weight bearing position. primarily overgrowth occurs in two areas - the toe which results in rotation of the pedal bone and the sole especially of the lateral claw of the hindlimb. These processes may result in discomfort to the cow and predispose her to sole ulcers and other conditions. routine foot trimming at least once a year has been shown to result in less lameness as well as improved gait and locomotion scores.

448
Q

How does foot bathing have a role in the control of infectious conditions causing lameness?

A

Important mainly in digital dermatitis and foul. This is for the treatment of existing infections but also the control and prevention of these conditions. correct foot bath design is crucial to make sure that the cows are treated effectively. the usual recommendations are to place the foot bath after the exit of the parlour but far enough away that it does not obstruct cow flow. It is crucial to get the feet clean first to allow good penetration of the chemical by hosing them down in parlour or using a prebath containing water to wash the feet before the disinfectant footbath.

449
Q

Describe the two main types of chemicals used in footbaths?

A

Antibiotic footbaths containing oxytetracycline,tylosin or lincospectin - used for the treatment of acute raw digital dermatitis lesions, however they are expensive, off license and so require a 7 day milk withhold and cause severe problems if the cows drink the solution. Best for reducing active digital dermatitis infection or strategically through the winter every 4-6 weeks.
Chemical disinfectant footbaths containing 3-5% formalin, 5% copper sulphate, 5% zinc sulphate, peracetic acid. th ese are used on a regular basis eg every milking every afternoon milking or 5 times a week as a control measure to disinfect the cows feet to prevent new infections and the spread of infection within the herd. Formalin must NOT be used on acute digital dermatitis lesions as very painful.

450
Q

What animal factors influence the development of lameness?

A

Calving - the majority of lameness cases occur 2-4 months after calving which is thought to be due to a combination of reduced horn growth at calving and increased movement of the pedal bone in the hoof due to general ligament relaxation at calving. this makes calving a high risk period for the development of lameness. strategies to minimise this risk include housing fresh calvers in straw yards for 4-6 weeks after calving, minimising stress at calving by mixing heifers with dry cows for the last 3 weeks of pregnancy and the use of correct transition dry cow diets. Seasonal factors - housing, wet weather, poaching of fields, training of heifers to use cubicles, heifer bullying, leading to inadequate lying times, heifer management - separate grouping, nutrition to reduce stress, genetics - selection for conformational traits, stress, exercise often advocated to promote horn wear and growth.

451
Q

What environmental factors are important in herd lameness?

A

Cow comfort - lack of lying time by poorly designed or poorly maintained cubicles or insufficient numbers. Excessive standing times or standing for long perioods. cubicle bedding - inadequate bedding and hock sores. Correct maintenance and bedding of straw yards. Building should be designed with cows behaviour in mind to reduce stress and avoid making sharp turns. Concrete surfaces must be properly maintained as damaged and pitted surfaces lead to loose stones and so white line disease. Rubber flooring - due to the problems with concrete there is a recent trend to fit rubber flooring to areas where cows stand but then cows may end up lying on rubber passageways instead of cubicles. poor cow tracks can result in more white line disease due to stone penetration. slurry disposal systems - rapid and efficient removal of slurry from passageways. wet conditions result in sftening of the horn and sllurry pooling will pathe the cows feet in muck which will predipose to digital dermatitis.

452
Q

How can nutrition predispose cows to lameness?

A

The main risk factor for lameness is subclinical rumen acidosis due to high levels of concentrate feeding, insufficient long fibre, sudden changes in the diet which results in increased levels of solar haemorrhage and sole ulcers. the exact mechanism is still debated but not thought to be the same as in equine laminitis. Pododermatitis asceptica diffusa is used instead now. Results in sinking of the pedal bone in the foot with subsequent pinching between the bone and horn of the sole and the developmeent of bruising and sole ulcers. Aim to reduce coriosis is by avoiding the sudden introduction of concentrates, spreading concentrate feeds throughout the day and good youngstock nutrition to avoid subclinical acidosis and sole haemorrhages in heifers. micro macro element deficiences - biotin deficiency by the rumen - reduction in lameness due to claw horn disease by supplementation with 20mg /cow/day biotin in the diet.

453
Q

What is acetonaemia?

A

A metabolic disease of high yielding milking cows associated with an inadequate supply of energy to sustain the high milk yields. The majority of dairy cattle are in NEB in early lactation, resulting in subclinical acetonaemia which has profound effects on cow heath, productivity and future fertility.

454
Q

What is fatty liver syndrome?

A

This term is used to describe the mobilisation of fat that frequently occurs around calving and during the first month of lactation in high yielding dairy cows. this is thought to be a normal occurence in high yielding dairy cattle which may have up to 20% fat in t he liver in the immediate peri parturient period. however if the negative energy balance is severe and prolonged then more than 20% fat may be deposited in the liver which can interfere with liver function and result in exacerbation of energy problems and the development of acetonaemia which may lead to fat cow syndrome.

455
Q

How does acetonaemia arise?

A

If gluconeogenesis from propionate in the liver is not working effectively, excess acetyl coA is converted into ketone bodies (acetoacetate, B hydroxybutyrate and acetate).
Acetate and butyrate > acetyl co A
if energy stable > fat deposition or energy via TCA cycle, need oxaloacetate.
Energy deficit > ketone bodies as no oxaloacetate is present. Primary Acetonaemia may occur during early lactation in high yielding dairy cows when the cow cannot consume enough energy to supply her glucose requirements. secondary Acetonaemia occurs secondary to diseases that depress food intake.

456
Q

What are the risk factors that influence the occurrence of acetonaemia?

A

Inadequate enregy content of the ration for high yielding dairy cows, inadequate intake of the diet, secondary acetonaemia due to Inappetance following a primary disease e.g LDA, excessive intakes of ketogenic food eg silage with high levels of butyric acid, poor rumen function including sudden changes in diet and excessive levels of concentrate feeding.

457
Q

What are the clinical signs of acetonaemia?

A

Usually occurs within the first month of calving, but may occur at other times if the energy deficit is severe. as all cows are fed as part of a group it is important to realise that a case of primary clinical acetonaemia represents the tip of the iceberg. there are two forms of clinical acetonaemia: wasting form - with the cow losing body condition over a period of days or weeks, loss of appetite with refusal to eat concentrate feeds and a sudden drop in milk yield. the faeces are often dark fir with a waxy appearnce. TPR is usually normal. Nervous form: a small number of cases of clinical ketosis will develop neurological signs due to a hypoglycaemic encephalopathy. signs vary from the animal being a bit jumpy to a frenzied delirium. there may be head pressing, circling, wandering, licking at any object, salivation and depressed appetite. signs are intermittent.

458
Q

How is diagnosis of clinical acetonaemia made?

A

Usually occurs in high yielding dairy cows in the first month after calving. check for possible primary diseases. Biochemistry - acetonaemia is characterised by hypoglycaemia, mobilisation of body fat and the accumulation of ketone bodies. Low plasma glucose levels below 3mmol/l indicate disorders of energy metabolism but values may be normal during periods of NEB. mobilisation of body fat - elevated NEFA levels (over 0.7mmol/l) indicate increased levels of fat mobilisation and provide supporting evidence for NEB. Ketone bodies - acetone, acetoacetate and bhydroxybutyrate are the three principal ketone bodies that are produced. Levels of B hydroxybutyrate in the serum/plasma. Cases of clinical acetonaemia have blood BHB levels of over 3mmol/l. Cowside tests can utilise milk (rotheras test - nitroprusside reagent) or urine.

459
Q

What is the approach to an individual case of acetonaemia?

A

Restoration of blood glucose levels - use 400ml of 40% glucose IV. this only lasts for 2-4 hours. oral administration of glucose precursors such as propylene glycol or glycerine twice daily by drench. Glucocoticoid hormone therapy that stimulates gluconeogenesis reducing the levels of ketone bodies and depresses milk yield reducing energy requirements. Other therapies such as vitamin B12 - essential for the metabolism of propionate and thus some people drench cows with cobalt to promote vit b12 synthesis. multivitamin injections also used. Correction of predisposing causes - causes of secondary ketosis such as LDAs, metritis etc must be treated.

460
Q

What are the consequences of subclinical acetonaemia/NEB in early lactation?

A

Reduced milk production, reduced milk quality in particular depression of milk protein production, increased incidence of clinical disease including LDA, metritis, RFM and mastitis. Imunosuppression, leading to increased susceptibility to mastitis, metritis etc. REduced fertility.

461
Q

How is diagnosis of NEB in early lactation made?

A

Diagnosis of clinical disease - prevention of disease is always better than cure. loss of body condition score. the target is to have no body condition loss in early lactation. losses of over 3/4unit in the first month of lactation are bad news. Milk production records - failure to reach predicted peak yields or reduced persistency. Milk quality - NEB in early lactation may result in depression of milk protein due to long term NEB, increase in milk butterfat due to increase levels of VFAs for butterfat synthesis

462
Q

What is fat cow syndrome?

A

This is the extreme manifestation of NEB and fat mobilisation in early lactation and occurs due to excessive body condition score in fat dry cows prior to calving body condition score >4.0. This results in a depressed DMI at calving and these cows thus enter a state of severe NEB in early lactation. Fat is then deposited in massive quantities in the liver leading to disruption of liver function. Clinical signs are fat dry cows with rapid body condition loss in early lactation, reduced appetite or anorexia which exacerbates the body condition loss, reduced milk yields, development of metabolic diseases which are unresponsive to conventional therapy, high mortality rates.

463
Q

How can negative energy balance/acetonaemia/fat cow syndrome in early lactation be prevented?

A

Cows should calve at condition score 2.5-3. Avoid excessive body condition. tranitional cow management in the late dry period is importat. Provision of good quality forage to cows in late dry period/early lactation and use of diets that increase levels of insulin and thus levels of propionate production by the feeding of high quality concentrates. Ensure that protein and energy supply in the diet is balanced. do not overestimate the energy contribution from the forages available. this may be a problem for high yielding early lactation cows that are grazing grass. balance rations for cows requirements of mineral trace elements and vitamins. Maximise dry matter intake in the late dry period. any changes in diet should be made gradually. group cows according to nutritional requirements. avoid overcrowding and stress to cows particularly the freshly calved cows. Heifer management allow adequate feeding space, avoid excessive stress. minimise factors disturbing rumen flora eg sudden changes in diet, do not overfeed concentrates, resulting in SARA. Ensure excellent cow comfort, regular monitoring of nutritional status including body condition score of cows, faecal consistency, metabolic profiles etc. medication with sodium monensin improves proprionate production in the rumen.

464
Q

What is ovine pregnancy toxaemia?

A

metabolic disease in low ground flocks in the last month of pregnancy. Rapid growth of foetus in late pregnancy results in a marked increase in glucose requirements of the uterus. the predisposing factors for the development of pregnancy toxaemia are; last month of gestation, ewe carrying two or more lambs, prolonged period of energy shortage, ewes in poor condition score but may occur in Overfat ewes, older ewes, precipitated by stress - adverse weather, housing, handling etc.

465
Q

What are the clinical signs of ovine pregnancy toxaemia?

A

Initially isolation from remainder of flock and refusal to feed, easy to catch, dull and depressed, neurological signs then progress due to the development of hypoglycaemic encephalopathy- apparent blindness, hyperaesthesia, head pressing, star gazing, teeth grining. progression to a profound depression and recumbency. Characterised by high mortality rate. Affected ewes frequently abort. Diagnosis is made on clinical signs and history - confirmation of diagnosis is by serum B - oh butyrate levels over 3.0mmol/l. post mortem examination will reveal fatty infiltration of the liver.

466
Q

What is the treatment of ovine pregnancy toxaemia?

A

Response to treatment tends to be poor with approx 50-70% mortality rates usually quoted. Treatment must be instigated early. 160ml oral electrolyte and glucose solution orally 4 times daily or 50ml proylene glycol. 100ml of 40% glucose IV as well as clacium if required. supportive therapy - concentrate feeds and water, good bedding and shelter, if the ewe is more than 136 days pregnant induction of parturition within 48 hours can be performed using 16mg dexamethasone.

467
Q

What is milk fever? How does it arise?

A

99% of calcium is stored in the skeleton, so only 10g is available in extracellular calcium pool. Daily dietary requirement of a cow will rapidly increase at the onset of lactation (approx 1.7-2.3g of calcium is required for each litre of colostrum, milk is 1.1g per litre). An adult cow is losing 20-50g of calcium per day via the milk as well as endogenous losses of 10g in faeces and 0.5-2g in urine, blood calcium must be kept under tight control via PTH, calcitriol and calcitonin - maintain the normal concentration of calcium in the blood by absorption of calcium from the gut and or mobilisation from t he skeleton. These processes take 2-3 days to become fully active, and if they fail Hypocalcaemia will occur.

468
Q

When do the clinical signs of milk fever develop? what are the factors which affect the speed and extent of the response to PTH?

A

Age - older cows respond more slowly and thus are more prone to milk fever. oestrogens are potent inhibitors of bone resorption. hypomagnesaemia may interfere with the release of PTH, the ability of PTh to act on its target tissues, hydroxylation of vitamin D in the liver. Calcium intake during the dry period - low calcium levels stimulate PTH secretion and thus mobilisation of calcium from bone and absorption from the gut. Acid base status of the animal - metabolic alkalosis predisposes cows to milk fever. nutritional factors - depressed dry matter intakes in cows at calving and digestive upsets will reduce calcium absorption from the gut. Channel island breeds more susceptible to milk fever.

469
Q

What are the clinical signs of milk fever?

A

occur around parturition and are progressive over a period of 10-24 hours. loss of appetite, dullness, lethargy, normal or slightly depressed rectal temperature, initial hypersensitivity and hyperaesthesia with grinding and muscle tremors, stiffness of legs, straight hocks and paddling of feet when standing, cows will be reluctant to move with incoordination and ataxia. progression to recumbency with cow initially in sternal with a lateral kink in the neck then progressing to the head and resting on the shoulder. Dilated pupils, increased heart rate, reduced PLR, gut stasis, rumen bloat and constipation, severe depression. cows become comatose in lateral recumbency, very weak and with elevated heart rate. eventually ruminal tympany/paralysis of respiratory muscles > death. other potential complications include uterine inertia leading to dystocia/stillbirth, prolapse of the uterus and musculoskeletal damage. Most cows have history of recent or imminent calving. usually high yielding. Intravenous administration of calcium borogluconate will produce a clinical response within minutes.

470
Q

What blood measurements can be taken to diagnose milk fever?

A

Blood calcium levels - normal total calcium levels are 2.2-2.6 but fall around calving in most cows. clinical signs occur if serum calcium levels fall below 1.5mmol/l. Blood phosphorous levels - hypophosphataemia frequently seen during milk fever, may fall below 1.0mmol/l in the majority of cases. blood magnesium levels - normally increase at calving and most cases of milk fever have a slight hypermagnesaemia above 1.25mmol/l. Hypomagnesaemia durig the dry period may result in milk fever due to the critical need for magnesium in milk homeostasis.

471
Q

What is the treatment approach to an individual case of milk fever

A

will normally have been given calcium borogluconate by subcut injection by farmer. poor absorption of subcut fluid due to impaired peripheral blood circulation in cases of milk fever. Take blood sample for measurement of calcium,magnesium and phosphorous levels. administration of 400ml of 40% calcium borogluconate solution by slow intravenous injection via the jugular vein using a flutter valve, which will provide 12g calcium. some also administer 400ml calcium borogluconate subcutaneously at the same time as the IV injection to prevent relapses occuring. do not over treat. removal of calf and restriction of milking for 24 hours to prevent calcium withdrawal. TLC - should be propped in sternal recumbency and good nursing management is essential. If blood sample reveals hypomagnesaemia this should be treated with 400ml of 25% magnesium sulphate administered providing 9.25g magnesium subcutaneously. Hypophosphataemia should also be treated with phosphorous supplementation.

472
Q

How is a herd problem of milk fever approached/treated?

A

Forage component of the diet - usually potassium or calcium content. change forage being fed to dry cows. magnesium supplementation - low dietary magnesium may be a factor. Magnesium chloride will also lower the DCAB of the diet. Prophylactic administration of calcium - cows known to be at risk of milk fever can be given calcium just before calving using drenches, gels, and boluses. Vitamin D3 injections - administration of 250mg vitamin D or alfacalcidol prior to calving. Measures to prevent calcium withdrawal include - no pre calving milking, removal of calf at birth, withdrawal of calf colostrum by hand if required, no milking out for 3-4 days after calving. check cow for mastitis twice daily.

473
Q

How can milk fever be prevented?

A

Manipulation of the dry cow diet is the most cost effective method of controlling the incidence of hypocalcaemia. there are two very different approaches available:
1. dietary calcium restriction during the dry period - the traditional method of preventing milk fever. limit to less than 50g per head per day. Magnesium levels should be above 40g per day. or 2. Manipulation of the dietary cation anion balance DCAB - metabolic alkalosis predisposes cows to milk fever as the raised pH prevents PTH from acting on its receptor, thus blocking the mechanisms of PTh dependent calcium mobilisation from the bone and renal production of calcitriol. Lowering the pHH stops this lack of response to PTH and releases cations mainly calcium from the bone. therefore the difference between number of cation and anion particles absorbed from the diet determines the acid base balance of the blood and thus has a large influence over the calcium homeostasis - termed the DCAB.

474
Q

How is DCAB reduced? (Dietary cation anion balance)

A

DCAB = (Na+ and K+) minus (Cl- and S-). sodium potassium sulphate and chloride ions exert the strongest effects on acid base balance and are refferred to as strong ions. Reduce DCAB to betweel -100 to -200mEq/kg DM by increasing Cl- and S- and reducing Cations Na+ and K+ thus enducing a mild metabolic acidosis. Grass silage and grass has a high positive DCAB. anionic salts are commonly used to reduce DCAB but most are potentially harmful and can depress dry matter intakes as are unpalatable. blood pH is strongly buffered and will remain unchanged on DCAB adjusted diets. urine pH is a useful measure of the success of a negative DCAB ration and should fall to between 5.5-6.5 if the ration is sucessful. due to problems with implementing a full DCAB approach many farms use a partical approach which empirically attempts to reduce the DCAB value of the transitional cow diet. The aim is to use predominantly low potassium forages such as maize silage, wholecrop wheat or straw and increase the anions using magnesium chloride in feed or water. there are a number of DCAB mineral mixes that are added empirically to the diet.

475
Q

What is ovine hypocalcaemia? (parturient paresis)

A

Hypocalcaemia is commonly seen in ewes in late pregnancy in the last 6 weeks of gestation and may occur sporadically in early lactation. it is more common in older sheep and ewes in any body condition may be affected. It is frequently associated with sterssful husbandry events. Clinical signs are due to muscular paralysis and are similar to those observed in milk fever in cattle. ewes have a rapid respiratory rate with a passive reflux of ruminal contents down the nose. treatment for a 70kg ewe is by the administration of 20.40mls of warm 40% calcium borogluonate b y slow IV injection and 50-100mls subcut. Feeding of diets containing adequate levels of calcium but not excessive quantities that will suppress the homeostatic calcium mechanisms. recommended calcium intakes are 5-10g calcium per day for ewes in late pregnancy. avoidance of stressful husbandry conditions.

476
Q

What is hypomagnesaemia? Why does it occur?

A

Magnesium is an essential mineral necessary as a co factor for a range of enymess vital in every major metabolic pathway. the majority of magnesium is found in bone with 30-440% in soft tissues and less than 1% in the extracellular fluid. There are no specific homeostatic control mechanisms for the regulation of magnesium levels. the amount and concentration of magnesium in ECF is dependent on ; absorption of magnesium from GI tract mainly rumen and omasum, requirement for magnesium for milk production, tissues and endogenous losses, the maintenance requirements are relatively constant and lactation markedly increases the needs. excretion by kidneys - excess dietary magnesium is removed via urine.

477
Q

What factors affect the availability of magnesium to the cow?

A

How much is eaten, how much is absorbed from the gut and transport of magnesium from the gut to tissues. factors influencing the availability of magnesium to the cow include: soil levels, pasture species - generally legumes weeds and herbs contain more magnesium than grasses. Cold weather and potassium fertilisers have been linked with reduced uptake of magnesium by grass species. daily dry matter intake regulates the daily intake of magnesium. High levels of potassium disrupt absorption of magnesium and also decrease the levels of sodium in the rumen. Application of potash fertilisers will increase the potassium content of the herbage. sodium is required to carry magnesium across the rumen wall thus sodium deficiency leads to poor absorption of magnesium from the diet. rumen ph - magnesium solubility declines rapidly as rumen pH rises above 6.5 ammonia - high levels inhibit magnesium absorption either directly or indirectly by raising ruminal pH. spring grass has high levels of ERDP and non protein nitrogen from use of nitrogenous fertiliser. Dietary energy - magnesium absorption is reduced when energy levels int he rumen are reduced and adding fermentable carbohydrates to ration can increase absorption. some fats combine with magnesium to form an insoluble soap. lush spring pastures are low in fibre which increases the rate of passage of material through the rumen leading to insufficient time for the absorption. Some evidence that particular cattle breeds are better at absorbing magnesium. Stress leads to release of adrenaline and noradrenaline which cause a decrease in plasma magnesium levels. particular stressful events include turnout onto spring grass and cold wet weather. High levels of insulin will also lead to a rapid fall in plasma magnesium levels this may be triggered by high plasma potassium concentrations or the mobilisation of body fat during periods of energy deficiency.

478
Q

When will hypomagnesaemia occur?

A

If intake and absorption of magnesium is less than the demands of lactation and metabolism for magnesium. the onset of clinical signs is related to the concentration of magnesium in the CSF, which only begin to fall at low blood magnesium concentrations. a vicious circle then occurs due to the stress and release of catecholamines resulting in severe clinical signs and tetany.

479
Q

What are the clinical signs of hypomagnesaemia?

A

peracute - sudden death with disturbed soil around the feet of the animal indicating paddling.
Acute - initial apprehension, nervousness and hyperaesthesia with high head carriage, twitching of muscles and incoordination. There is rapid progression with collapse into lateral recumbency and convulsions leading to coma and death. progression into convulsions may be precipitated by stress eg response to noise, touch, herding, restraint. 30% will die, although spontaneous recovery can occur. relapses common even after treatment. majority of the rest of group may be affected subclinically. subclinical/chronic - this form often goes unrecognised. Cows may appear slightly nervous reluctant to be milked or herded with depression of DMI. the other main symptom of subclinical hypomagnesaemia in dry cows is hypocalcaemia.

480
Q

What is milk tetany in calves?

A

Calves absorb magnesium very efficiently from the intestine, however this falls rapidly by 2 months of age, thus calves that are reared for prolonged periods on whole milk diets without magnesium supplementation are prone to developing acute hypomagnesaemia.

481
Q

How is diagnosis of hypomagnaesaemia made?

A

history - occurs in lactating cows at grass during spring and autumn and in suckler cows with calves at foot with no supplmentation. usually acute onset with signs of hyperaesthesia and convulsions. The normal reference range for plasma in healthy cows is over 0.8mmol/l. any levels below this indicate subclinical hypomagnesaemia and a risk of developing acute hypomagnesaemia. Blood magnesium levels rise rapidly after death and there are no specific lesions present at post mortem. diagnosis depends on magnesium levels in the CF - below 0.6mmol in CSF in freshly dead animals are indicative of hypomagnesaemia. In the urine - kidney will stop excreting magnesium thus no magnesium in urine. In aqueous humor - in freshly dead animals, magnesium levels in aqeuous humor below 0.25mmol/l are indicative of hypomagnesaemia. Magnesium levels in vitreous humour are stable for 48 hours post mortem and levels below 0.55mol/l are diagnostic. Calcium/magnesium ratio in bone is used to diagnose milk tetany in calves.

482
Q

What is the treatment approach to an inddividual case of acute hypomagnesaemia

A

Any sudden stimulus may precipitate fatal convulsions. take a blood sample prior to treatment for measurement of calcium magnesium and phosphorous levels in case further confirmation of diagnosis is required. administration of 400ml of 40% calcium borogluconate, 5% magnesium hypophosphite solution by slow IV injection. Administration of 400ml 25% magnesium sulphate by subcut injection. Control of seizures - pentobarbitone, xylazine or ACP - none are licensed in cattle IV. Cow should be kept quiet in lateral recubency for 15 minutes to allow treatments to take effect. ensure adequate dietary intakes to prevent relapses. the administration of magnesium injection will only increase plasma levels for 6-12 hours. blood sampling of a group of atleast 5 cows should be performed to check the herd magnesium status.

483
Q

How can magnesium be supplemented in the diet?

A

Inclusion in the concentrate rations - most common. total diet should contain 2.5g/kg DM magnesium. usual target is to use max of 60g magnesium oxide per cow per day. Medication of water supply - with soluble magnesium salts. will help DCAB manipulation for milk fever control. All other water sources must be excluded to ensure adequate intakes, the medicated water is unpalatable and depresses water intake, this method provides insufficient daily magnesium especially in high yielding cows, variations in water intake. Mineral supplements - magnesiums alts and minerals are unpalatable and thus ad lib minerals are not satisfactory bt can be incorportaed into TMR feeds. dusting/spraying off pastures - may be dusted during high rsk periods with finely ground calcined magnesite every 10-14 days. it relies on coating the leaves of grass with calcined magnesite dust. Intraruminal boluses.

484
Q

What is ovine hypomagnesaemia? How is it treated and controlled?

A

Hypomagnesaemia in sheep nearly always occurs after lambing in ewes rearing twins at peak lactation. clinical signs are similar to those in cows. it frequently presents as sudden death in adult ewes. serum magnesium concentrations below 0.6mmol/l confirm the diagnosis. investigation of hypomagnesaeima as a cause of sudden death can be confirmed by fresh CSF and urine magnesium concentrations below 0.6mmol/l or fresh aqueous humour magnesium concentration below 0.4mmol/l within 12 hours of death. Treatment involves 20mls of warm 20% calcium borogluconate and magnesium solution invtravenously and 50mls of 25% magnesium sulphate subcutaneously. provide extra magnesium to ensure intakes of 7g magnesium per ewe per day. the most reliable way to perform this is with ewes in lactation at grass via concentrates. magnesium boluses are available. reduce stress. provision of extra forage to increase magnesium absorption

485
Q

What is a ‘downer cow’?

A

Been down for more than 24 hours, cow is not suffering from hypocalcaemia, no obvious condition eg mastitis, toxaemia or injury, animal is in sternal recumbency, usually related to calving (half of all downer cows develop within 24 hours after calving). The downer cow has a multifactorial primary aetiology and the most comon causes are related to dystocia and milk fever.

486
Q

What are the possible primary causes for ‘downer cows’?

A

Traumatic - pelvic fractures, sacroiliac luxation/subluxation, rupture of the gastrocnemius tendon, dystocia - ruptured uterus, internal haemorrhage, exhaustion.
Neurological - obturator paralysis usually following dystocia, sciatic paralysis following dystocia, prolonged recumbency, struggling to rise. peripheral nerve paralysis - peroneal and tibial paralysis due to trauma/recumbency. General neurological conditions - BSE, botulism, tetanus.
Metabolic - hypocalcaemia, hypomagnesaemia fat cow syndrome, rumen acidosis..
Toxaemia- acute coliform mastitis, acute metritis, RDA/volvulus, Peritonitis, traumatic reticulitis.
Pressure damage develops due to the prolonged weight of the cow on the hindquarters. recumbency in one position for greater than 6 hours reuslts in ischaemic necrosis and muscle damage, and this may become irreversible after 12 hours of recumbency in the same position. This is why prompt treatment of recumbent cows is essential to prevent these associated secondary complications.

487
Q

Describe the pathogenesis of downer cow syndrome?

A

Metabolic disorders, toxaemia, pre and post partum injuries > sternal recumbency > compression of soft tissues (contraction of functional muscles > muscle damage and haemorrhage) > mechanical venous constriction in the upper half of hind limbs > venous congestion and thrombosis, oedema of tissues.

488
Q

What history should you take when approaching a downer cow?

A

How long has the animal been recumbent, when did the cow calve, were there any problems related to calving, was any assistance required and if so what degree of assistance, did the cow rise after calving, have any treatments been given previously by the farmer eg calcium, is the cow trying to get up, an she move around, where did she become recumbent, eg concrete floors, slippery surfaces, what degree of nursing has been provided?

489
Q

Describe the clinical examination of a downer cow

A

The usual downer cow will be bright and alert with normal TPR. they will usually eat and drink normally, with normal urinatin and defecation. prognosis will be good for cows that are bright and alert with repeated attempts to rise. cows that cannot maintain sternal recumbency and fall into lateral recumbency and are depressed or hyperaesthetic have a poor prognosis. Position of the cow and limbs - most downer cows will be in sternal recumbency but the position of the ind limbs may also indicate potential causes: abduction of hind limbs is indicative of obturator paralysis, frog legged cows with parxial flexion of both hind limbs usually indicative of obturator/tibial nerve paralysis. prognosis usually good. animals which will remain in sternal recumbency on one side only even when turned onto the other side, generally have a poorer prognosis due to the development of pressure damage. Cows that immediately fall into lateral recumbency have a poor prognosis. Inability to either flex or extend the hind limbs indicates severe nerve or pelvic damage with very poor prognosis. Position of the lower limb - flexion of the hock/extension of the digits indicates tibial parlysis or hyperextension of the hock/flexion of the digits indicates peroneal damage. Severe swelling of upper musculature of hind limbs - is indicative of pressure damage and Ischaemic necrosis of the muscles and thus poor prognosis. A standard full clinical examination, all four quarters of the udder should be examined, vaginal examination, rectal examination for pelvic fractures, crepitus, dislocation etc, neurological examination to check for senstaion, deep pain sensation of distal limb, manipulation of hind limbs to check for crepitus, swelling, ability to move the limb, muscle damage and pain. Cows that make repeated attempts to rise and can move them selves about are often called crawlers. They have a good prognosis.

490
Q

How is diagnosis of primary cause made in a downer cow? What biochemistry must be done?

A

Metabolic disease - a blood sample for calcium, magnesium and phosphate levels will determine if hypocalcaemia/hypomagnesaemia has been treated effectively. energy status - may be a concern in fat cow syndrome or where the nursing of the cow has been inadequate leading to poor food intakes. IF fat cow syndrome is suspected liver enzymes AST, GLDH and GGT may indicate the degree of liver damage

491
Q

How can assessment of muscle damage be made in a downer cow?

A

Tests for muscle damage are not utilised for diagnostic purposes - as by the time a cow has been down for a couple of days there will be some degree of muscle damage. their value lies as prognostic indicators - and AST and myoglobin appear to be most reliable.
Creatinine kinase - released by damaged muscle cells and levels can reach over 10,000. Short half life and remains elevated for only 1-2 days, indicative of ongoing acute muscle damage.
Aspartate amino transferase - not muscle specific as levels may be raised following liver damage. it will remain elevated for 1-2 weeks following muscle damage.
Myoglobin levels - can be measured in both serum and urine and also gives an indication of the degree of muscle damage. not readily available as a lab test

492
Q

What treatment should be given to Downer cows?

A

TLC - dry clean comfortable bed, to prevent further pressure damage, clean to prevent mastitis and non slip to aid attempts to rise. turning of cow every 3 hours to prevent pressure damage, provision of good quality food, provision of ad lib water. Treatment of underlying disease - eg intravenous calcium borogluconate, if milk fever is complicated by Hypomagnesaemia or Hypophosphataemia then these should also be corrected. mastitis and other toxaemic conditions must also be treated. Anti inflammatory drugs - to reduce pain and tissue damage as well as improving demeanour and appetite. either NSAIDS flunixin or corticosteroids may be used.
Assistance in rising - briefly to assist the diagnosis or as a form of physiotherapy to improve the circulation to the hind limbs and encourage the cow to rise. Use hobbles or soft rope on hind legs for obturator paralysis. the use of hp clamps may be used only once to assist diagnosis but can cause severe damage if misused. cow nets - supportive harness and inflatable bags are all used to varying degrees usually used to lift the cow for 1/2 hour 3 times a day. water flotation tanks are expensive but have been bought by agricultural farmer groups for hire.

493
Q

What is the normal gestation length of a cow?

A

280-285 days, but there is significant between breed and within breed variations. continental breeds such as Charolais tend to have longer gestation than dairy breeds.

494
Q

Why does twinning occur in cows?

A

Cows are classically considered monotocous but twinning can occur in 1-4% of cow births. twinning increases with maternal age, very uncommon in heifers. identical twins are very rare in natural breeding - most are a result of double ovulation. 80% of twin pregnancies are bicornueal, 20% unicornueal. bicornueal twins are more successful than unicornual with less dystocia and better birth weights.

495
Q

Which horn are most singleton pregnancies in?

A

2/3 in RHS, 1/3 in LHS. Rare for CL and foetus not to be ipsilateral.

496
Q

What are placntomes?

A

Placental cotyledons attach to maternal caruncles to form placentomes - which develop in the non gravid and gravid horns. around 120 in total. arrange din 4 longitudnal rows in each horn. formed by villi containing capillaries growing from the allantochorion into the crypts of the maternal uterine caruncles.

497
Q

Describe the development of the foetal fluids during gestation

A

Initially there is some fusion of the allantoamnion and allantochorion causing allantoic fluid to be pushed to the extremities of the allantochorion and the amniotic fluid to lie centrally. as the volume of allantoic fluid increases the allantoanion and allantochorion separate. at 2-4 month there is a rapid increase in volume of allantoic fluid. at 3-4 months there is a rapid increase in volume of amniotic fluid. at the end of 6 moths - the length of foetus > width of amnion so that foetus lies in anterior presentation (95%) or posterior presentation (5%) from now onwards. 6-8 months - rapid increase in volume of allantoic fluids. at term - amniotic fluid volume 5-8 litres, allantoic fluid volume 14-16L.

498
Q

What is the source of progesterone during pregnancy?

A

Major source of progesterone until day 150+ is the corpus luteum. loss of the corpus luteum up until this time will terminate the pregnancy - can abort with prostaglandin injection up to 120-150 days. Beyond day 150+ the corpus luteum isn’t the sole source of progesterone which is now produced by the ovarian stroma, the placenta and adrenals. Loss of the copus luteum beyond day 150+ won’t necessarily terminate the pregnancy. combination of PG and corticosteroid injection needed to abort.

499
Q

How can induction of abortion/parturition be done in a cow?

A

Induction of parturition may be indicated where the pregnancy is going over term or the dams wellbeing is threatened by the pregnancy. misalliance can lead to unwanted pregnancy in young beef heifers. cow /heifer close to or over normal gestation - inject short acting corticosteroid eg dexamethasone or PGF2a. parturition normally occurs within 48-72 hours. Cow /heifer between 150-270 days of gestation - PGF2a alone will not reliably cause abortion at this stage of pregnacy. best option is a combination of dexamethasone and PGF2a injections - abortion should occur within 5 days. Cow /heifer <150 days of gestation - injection of PGF2a should terminate unwanted pregnancy up to 120-150 days of gestation but is not 100% reliable. abortion or return to oestrus should be seen within 3-5 days. Wait until at least 7 days after service to terminate misalliance pregnancies to ensure responsive CL is present.

500
Q

At what stage of a pregnancy is it most likely to be lost?

A

Fertilisation rates are high around 85-95%, however early embryonic mortality before day 19 is very common - around 30%. Late embryonic mortality day 19 to day 40 losses are around 10%. if either fretilization does not take place or EEM occurs before day 19 then maternal recognition of pregnancy does not occur. In this instance the cow wil return to oestrus 18-24 days later, therefore no abnormal interoestrus interval will be observed. LEM results in delayed luteolysis, high progesterone concentartions at day 21 and a return to oestrus at day 25 plus after insemination.

501
Q

How does the cow recognise she is pregnant?

A

Cow must recognise she is pregnant by day 16 to prevent luteolysis. interferon - tau is secreted from the blastocyst >15mm diameter normally by 15 until around day 20. interferon tau has antiluteolytic properties as it inhibits oxytocin receptor expression in the endometrium which prevents prostaglandin production by the endometrium and therefore prevents luteolysis.

502
Q

What are the possible reasons for a loss of pregnancy around fertilisation?

A

Average loss 10-15%. Reasons - poorly timed AI, delayed ovulation, hostile uterine environment, blocked oviduct/bursal adhesions.
Early embryonic death day 1-16- 20% – Genetic defecct, poor quality follicles/ova, endometritis, hormonal environment, lack of BtP1 production, heat stress, infectious agents.
Late embryonic death day 17-40 - same as for early embryonic death as well as management stress.
Fetal death/abortion - 40-270 days - 5% - many infectious and non infectious causes.

503
Q

What is mummification?

A

Foetal death in utero, persistence of corpus luteum, cervix remains closed, uterine contractions are absent. Mummification can only take place when foetus dies well before time of expulsion or removal. it is a time consuming process.
Papyraceous mummification - may occur in any breed, after foetal death all foetal fluids are slowly reabsorbed ie amniotic, allantoic intra and extra cellular. foetues becomes a dried friable contorted mas surrounded by parchment like membranes.
Haematic mummification - said to be more common than papyraceous, associated principally with channel island breeds, caused by autosomal recessive gene, affected foetus homozygous recessive for this trait, occurs at 3-8 months gestation. haemorrhage from Placentomes between endometrium and chorion follows foetal death. blood degenerates into a viscous brown material. Diagnosis of mummification - usually made during late pregnancy/beyond term, time of calving approaches - no imminent signs seen, general health of dam is unaffected. If uterus is over pelvic brim and not able to be retracted the blood sample for oestrone sulphate or pregnancy specific protein B will confirm absence of viable foetus.

504
Q

What happens when luteal regression after mummification occurs?

A

Causes spontaneous expulsion:
into the posterior tract from where it can manually be removed, or total expulsion less usual. OEstrus may follow luteal regresison. If luteal regression occurs and cervix dilates but mummy remains in utero then maceration follows.

505
Q

What is the treatment of mummification?

A

Injection with PGF2a can be tried to lyse CL and cause expulsion of mummy. not always effective. in Most cases the mummified calf may be pushed into cervix/vagina but require manual assistance to remove. if PGF2a treatment fails then cow may need culled for infertility.

506
Q

What is foetal maceration?

A

it can occur in all breeds of catlte, it is a sequel to foetal death in utero without expulsion. following foetal death the corpus luteum regresses and parturient process begins, but fails to run its complete course. bacteria enter the dilated cervix and by putrifaction and autolysis the soft tissues regress until a compact mass of bones remain. Clinical signs - dam clinically well, discharge from vulva, examination per rectum reveals uterus small for dates, hard foetal parts palpable, bony remnants and lack of a viable pregnancy demonstrable using u/s.

507
Q

What is the treatment for foetal maceration?

A

Rarely attempted. uterus may be manually emptied of larger bones but smaller ones may remain and are attached to or embedded within the endometrium where they cause residual chronic inflammation and act as an intra uterine contraceptive device.

508
Q

What causes pyometra?

A

Most cases follow parturition and endometritis. can be a sequel to early pregnancy loss when corpus luteum persists, cervix remains closed, cows remains anoestrus.

509
Q

What causes pre partum metritis and emphysema? (rotten calf)

A

Most commonly encountered in the peri partum period notably cases of neglected dystocia. Uterine infection by gas producing bacteria which usually gain access via the cervix. uterine contents provide an ideal medium for bacterial growth. A dead foetus in utero can be emphysematous without initially causing maternal ill health. bacteraemia/toxaemia renders the dam acutely ill, the condition may be rapidly fatal. Can be depressed, signs of dehydration/toxaemia, foetid vaginal discharge, occasional straining etc. Diagnosis is confirmed by vaginal examination. removal of emphysematous rotten calf can be difficult and time consuming. ideally use lots of lubricant and remove calf intact by traction. partial fetotomy may be required but may be hard to remove all of calf as can be dry and clamped in uterine horns. C section may be preferable in some cases. aggressive antibiotic and supportive treatment may be required (NSAID and fluids).

510
Q

What is hydroamnios?

A

much rare than hydrallantois. condition is characterised by gradual accumulation of excess volume of amniotic fluid around mid-late trimester, caused by foetal abnormality impairing ability to swallow fluids. various foetal abnormalities have been associated with hydramnios including bulldog calves, brachygnathia, hydrocephaly etc. Variable abdominal distension depending on volume of amniotic fluid. may not be noticed prior to full term. may be apparent when delivering an abnormal calf that there is excessive fluid when amnion ruptures. induction of calving/abortion is rarely required so most cases go to term.

511
Q

What is hydraallantois?

A

Hydrops allantois is the most common cause of dropsy of the foetal membranes and is seen sporadically in last trimester of gestation. condition is caused by abnormal placental function and normally the foetus is normal. there can be abnormal adventitious placental tissue, reduced numbers of abnormally large placentomes and other placental abnormalities. Can be a fairly sudden onset of severe abdominal distension in the last trimester associated with massive volume of allantoid fluid up to 250 litres. cow has distended pear shaped abdomen when viewed from rear. Fluid accumulation can be rapid and lead to decreased appetite, weakness and recumbency. rupture of prepubic tendon and ventral abdominal musculature can occur due to sheer weight of uterine contents. Death can occur due to compression of abdominal organs and cardiovascular failure.

512
Q

What is the treatment for hydrallantois?

A

When cow is presented recumbent and weak due to excess abdominal distension then the prognosis is poor and humane destruction should be considered. if identified earlier then the aim is to monitor the wellbeing of the cow and induce parturition as soon as the cow deteriorates. some cases will go full term but may require assistance at calving due to uterine atony. Emergency C section can be attempted as a last resort. uterine wall my be thin friable and sudden release of allantoic fluid can lead to hypovolaemic shock. administration of hypertonic saline prior to surgery and post op iv fluids. Retention of foetal membranes and metritis are likely.

513
Q

What is hydrocephalus?

A

Arises because of interference with normal circulation of CSF and is usually secondary to cranio facial deformities. sporadic and unknown aetiology.

514
Q

What is feotal anasarca?

A

Grossly oversized foetus may be aborted up to 3 x normal birth weight. excessive subcutaneous fluid distorting whole body will cause dystocia problems. caused by an autosomal recessive gene. mild hydrallantois and oedema of the foetal membranes may accompany foetal anasarca.

515
Q

What is foetal ascites?

A

Gross accumulation of fluid, chiefly within the body cavities, may occur in any breed, may be the only abnormality but often associated with others especially achondroplasia. will often cause dystocia with calf getting stuck at shoulders as abdomen too distended to enter pelvis. Partial fetotomy can allow puncture of diaphragm and drainage of fluid via thorax or incision of abdomen. c section may be indicafed.

516
Q

What is schistosoma refluxus?

A

Foetus is presented with 4 feet or intestines at vagina of dam and may require partial embryotomy or c section to deliver.

517
Q

Describe when the uterus is involved in a ventral hernia?

A

Due to muscle weakness, debility, trauma, rupture associated with hydrallantois. ventral herniae arise lateral to the linea alba although they appear to be in midline. only a heavily gravid uterus will enter a ventral hernia. clinical signs - progressively larger swelling apparently in midline, swelling greatest between hind limbs from where it extends forwards. differentiate from haematoma, abscess and prep partum oedema. Treatment - cull if severe concurrent injuries present. if not aim to treat the animal conservatively until calving if humanely posible. will need assisted at calving.

518
Q

Describe a prolapse of the vagina & cervix?

A

This occurs as a sporadic problem in late pregnancy most commonly in fat multiparous beef cows. Aetiology is a combination of overcondition, abnormal relaxation of pelvic ligaments associated with increased oestrogen levels and other unknown factors. Clinical signs vary from very mild to complete prolapse exposing the cervix and vagina. mild cases show only when cow is lying and return to nomral position when standing. in severe cases the entire vagina prolapses, the cervix is opened and associated rectal prolapse may be present due to straining. inability to micturate as bladder often involved in prolapse. prolapsed tissues become severely congested and traumatised. rarely the prolapse ruptures dorsally.

519
Q

What are the treatment options of a prolapse?

A

Very slight and only occurs when close to calving - keep under observation until calves when problem will self cure post partum. if very severe and badly traumatised infected may need salvage slaughter- if very close to calving a C section might salvage a valuable calf. Most cases can be replaced and retained until calving - give caudal epidural analgesia, clean prolapsed tissue, lubricate and replac prolapse by steady manual pressure, drainage of urine via a needle/catheter by puncturing vaginal wall in some cases, check replacement correct and no damage done, give antibiotic and NSAId cover if vaginitis is present.

520
Q

What sutures can be used in retaining the prolapse?

A

The suures should be non absorbale material, placed deeply in the perivulval tissue in order to avoid tearing if straining occurs when the epidural wears off and should not interfere with urination. Buhners suture is a modified purse string suture which is best tolerated and least traumatic. use 6mm nylon tape as suture material and purpose designed mneedle. mattress sutures or toggles may be placed across the upper 2/3s of the vulva but both these methods traumatise the vaginal mucosa and will cause tissue irritation/infection.

521
Q

Describe a vaginal/uterine tear in a cow

A

Normally associated with dystocia, excessive traction, large calves. rarely uterine tear can occur during first or second stage labour and go undetected. Always check for tears in vagina/cervix after calving. may be associated with profuse post calving arterial haemorrhage from the vulva. usually tears occur in dorsal/lateral vagina /cervix. urgent if profuse bleeding present. identify tear and site of bleeding vessel using clean hand, clamp end of vessels using artery forceps and leave in place for 2-3 days. give antibiotic cover for 3-4 days. Usually impossible to stitch vaginal/cervical tears. will heal by second intention. if large uterine tear identified salvage slaughter should be considered or can attempt to repair via laparotomy. Avoid foeto/maternal disproportion, Overfat cows at calving and excessive traction at calving. if Vulvar relaxation is poor an episiotomy may help to avoid uncontrolled tear.

522
Q

Describe a uterine prolapse in a cow?

A

Normally associated with delivery of a large calf prolonged parturition/straining. hypocalcaemia often present. usually occurs within hours of calf being delivered. large mass of everted uterus protrudes from the vulva. placenta may still be attached to uterine caruncles. cow often down due to exhaustion, shock, hypocalcaemia, pelvic nerve damage. may be up walking around with uterus hanging down from vulva. Give iv calcium borogluconate if hypocalcamiea. if cow down, place in sternal recumbency with hind legs pulled back. Give caudal epidural anaestheic. clean uterus and remove placenta if possible. replace using firm manual pressure starting at cervical portion. if very swollen/oedematous can reduce oedema using firm presure with arms around mass beefore replacing. ensure uterus is fully inverted to tpi of the horn when replacing to reduce risk of recurrence. insert antibiotic pessaries and give antibiotic cover 3-4 days. Single injection of iv short acting corticosteroid will help reduce oedema/inflamation. Stitching vulva not necessary if uterus properly replaced. If cow standing with uterine prolapse, support weight of uterus with clean sheet/feed bag and replace in standing position if possible. prognosis is good in uncomplicated cases. occasion death due to shock or internal haemorrhage due to rupture of uterine artery caused by stretching of broad ligaments.

523
Q

What are the important evens in normal post partum period?

A
  1. uterine involutiion
  2. regeneration of endometrium
  3. elimination of bacterial contamination of uterus
  4. Return of cyclical ovarian activity.
524
Q

Describe uterine involution post partum?

A

Reduction in size occurs in a decreasing log scale. uterine contractions continue for a few days which aids in the feotal membrane expulsion. time for complete changes of involution is four to 6 weeks. palpable changes after 20-25 days imperciple so can assess at three weeks post calving checks. with increasing parity involuted uterus feels larger. cervix constricts rapidly post parutm within 12-24 hours may nto be able to pass hand through to uterus. mean diameter - 2 days pp =15 cm, 30 days ppp 7-8cm, 60 days pp -5-6cm. beyond 25 days pp diameter of previouos gravid horn should be less than that of cervix. prostaglandins released from uterine caruncles have a role in controlling uterine invlutin. PGFM (PGF2a metabolite) levels raised until 10-200 ay spp. positive correlation between PGFM concentrations and diametter of involuting horn.

525
Q

What factors affect normal involution of the uterus?

A

Parity, retained placenta, uterine infection, twins, hypocalcaemia, selenium deficiency, suckling frequency, dystocia, climate - heat stress, hydrops.

526
Q

Describe the normal discharge in cows LOCHIA?

A

normal cows have pp discharge for 7-10 days due to sloughing of surface tissue from uterine caruncles. this discharge is referre to as lochia. lochial discharge usually is reddish brown and odourless. volume varies within individuals and whether primaparous or multiparous. NB normal lochia not derived from foetal membranes as they should separate from caruncles and be expelled within 24 hours. Lochia derived from remains of foetal fluids, blood, shreds of foetal membranes but mainly from sloughed surfaces of caruncles. complete regeneration of caruncular epithelium normally achieved by 25 days pp. caruncles gradually shrink as involution progersses.

527
Q

Describe how bacterial contamination of the uterus post partum occus?

A

At calving and immediately pp vulva is relaxed and cervix open so opportunity for environmental bacteria to colonise uterus - importance of calving in clean surroundings. common bacteria isolated from pp uterus include actinomyces pyogenes, E. coli, fusibacterium necrophorum staphyloccoci, streptococci. Normally this contamination is rapidly eliminated by phagocytosis by leucocytes uterine contractions and sloughing of caruncular tissue and secretory IgG in uterine secretions. 90% of uteri swabbed within 15 days post calving have bacterial contamination but this is reduced to around 9% by 46-60 days pp. early resumption of PP cyclicity aids in elimination of any persistent bacterial contaminatoin. More alkaline uterine pH at oestrus not fabourable for bacterial growth also get increased blood supply and nuetrophil influx during oestrogen dominated phase of cycle. failure to eliminate peri parturient bacterial contamination may lead to the development of metritis which may have serious detrimental effects on subsequent fertility.

528
Q

What is post partum metritis?

A

Contaminant bacteria fail to be eliminated from the uterus du to either overwhelming degree of bacterial contamination or impaired natural uterine defence mechanisms. ixed bacterial infection probably occurs in acute metritis. evidence of synergy between gram positive bacteria eg A pyogenes and gram negative anaerobes eg bacteroides spp and fusbacterium which can lead to chronic endometritis. bacteriodes spp produce substances that inhibit leucocyte function and fusibacterium produces leucotoxin.

529
Q

Describe puerperal metritis?

A

Puerperal metritis is an animal with an abnormally enlarged uterus and a fetid watery red brown uterine discharge associated with signs of systemic illness and fever >29.5 degrees C within 21 days after parturition. Normally occurs in the first week post calving often following dystocia/assisted delivery. often associated with retained foetal membranes. clinical signs are anorexia, milk drop, pyrexia, increased HR, congested MM. usually foul smelling vulval discharge. Treat with broad spectrum antibiotics eg cephalosprins such as ceftiofur for three to five days If toxic shock present give i/v fluids and NSAID flunixin IV. Removal of RFM may be contraindicated as increases uterine trauma and toxin absorbtion. Prostaglandin injection may be beneficial when calved 10-14 days. Often may develop secondary ketosis, hypocalcamemia and displaced abomasum. may develop clinical or subclinical endometritis, salpingitis or adhesions. occasionally bacteraemic spread from uterus leads to endocarditis/pulmonary abscessation.

530
Q

What is clinical metritis?

A

Animals that are not systemically ill but have an abnormally enlarged uterus and a purulent uterine discharge detectable in the vagina, within 21 days post partum .

531
Q

What is clinical endometritis?

A

Characterised by the presence of purulent uterine discharge detectable in the vagina 21 days ore more after parturition. there is no systemic illness. predisposing factors include dystocia/assisted calving , RFM, dirty calving environment, premature calving - twins, induced calving, delay in return of pp cyclicity, over fat at calving /fatty liver syndrome, nutritional deficiency eg selenium. Consequences - extended calving - conception interval in affected cows due to delay in return to cyclicity or deliberate delay in rebreeding plus reduced conception rates due to hostile uterine environment causing semen/embryo death. Evident at three to four weeks post calving by persistent purulent vulval discharge. often evidence of tacky discharge stuck to tail below vulva. may be seen following oestrus when cervix opens. manual vaginal examination revels partially open cervix and purulent discharge. rectal palpation normally reveals one or both uterine horns enlarged, but may be little palpable abnormality in mild or chronic cases. Ultrasound is useful to diagose distension of the horn.

532
Q

What is the treatment of endometritis?

A

Prostaglandin injection - best treatment for clinical endometritis and treatment of choice for pyometra. Requires responsive CL for optimum effect, cow comes into oestrus therefore get beneficial effect of oestrogen dominant phase of cycle. can repeat treatments in 10-14 days in cases of persistent vulval discharge.
2Intra uterine antibiotics - pessaries or washouts. pessaries have insufficient concentrations of antibiotic administered, some of which may not be active in anaerobic environment. Metricre washout is preferable. can try antibiotic wash out 12-24 hours after AI in repeat breeder cows if suspect low grade endometritis. Antiseptic wash out - irritant to endometrium and cause PGF2a release which may have curative effect.

533
Q

What is subclinical endometritis?

A

Can be defined as endometrial inflammation of the uterus usually determined by cytology in the absence of purulent material in the vagina. unlike mares cows will rarely have uterine biopsies carried out routinely so will rarely e confirmed.

534
Q

What is a pyometra?

A

Defined as the accumulation of purulent material within the uterine lumen in the presence of a persistent corpus luteum and a closed cervix. will palpate distended uterine horn which must be distinguished from pregnancy as could develop after service. with pyometra uterine wall is often thicker and no membrane slip or cotyledons /foetus is palpable. can confirm using ultrasound scan. vaginal examination may reveal thick purulent cervical discharge but normally cervix is closed. treatment with PGF2a injection is effective with luteolysis being followed by return to oestrus and evacuation of the uterus.

535
Q

What are retained foetal membranes?

A

Partial or complete retention of foetal membranes beyond 12 hours post partum. effectively this means failure of normal third stage labour. normally in around 3-10% of cows. failure of normal separation of feotal cotyledonary villi from maternal caruncles or primary uterine inertia. physiological processes controlling separation of placenta begin weeks pre partum. Normal separation requires: prepartum maturation of the placenta with hormonal changes involved, Intrapartum detachment by uterine pressure contractions, anaemia of cotyledonary villi after foetal expulsion, reduction in size of uterine caruncles post partum. Factors predisposing to RFM are - premature parturition, immature Placentomes not physiologically prepared for separation eg twin births, late abortions, induced births, oedema of chorionic villi caused by trauma - eg dystocia, caesarian following uterine torsion. Pathological inflammation eg placentitis caused by abortion agent such as bacillus licheniformis. Uterine inertia - due to hypocalcaemia, hypselenaemia, hydrops, twins. there is a putrid placenta hanging out from the vulva, but may be retained in cervix/vagina and not obvious from the outside. may be straining in attempt to pass placenta. usually no systemic illness unless peurperal metritis develops.

536
Q

What is the treatment for retained foetal membranes?

A

Spontaneous expulsion may occur in 5-10 days with no treatment. May develop acute puerperal metritis - RFM decreases uterine phagocytic function. studies have shown no effect on fertility following RFM unless associated with metritis. Manual removal probably contraindicated unless comes away with gentle manual traction. best time to attempt manual removal is 3-5 days pp. definitely contraindicated if associated with metritis as causes trauma to endometrium which which may increase toxin absorption and decrease phagocytic function.
Ecbolic drugs: oxytocin, PGF2a, calcium salts, oestrogens have all been tried in the immediate pp period with varying results. unlikely to be effective other than in ases of primary uterine inertia as have no effect on cases caused by defective separation of chroionic vili.
Intrauterine antibiotics/pessaries - doubtful benefit as MIC probably not achieved. may reduce risk of metritis developing. if puerperal metritis present appropriate systemic antibiotics will be needed.

537
Q

What is cystic ovarian disease?

A

Varies between 5-10%. most develop 20-60 days pp. often in 2nd and 3rd lactation high yielding cows. leads to financial loss associated with extended calving-conception 20-60days increase in affected cows, caused by delay or disruption in normal post partum cyclicity. There is a fluid filled structure >2.5cm diameter present for > ten days on one or both ovaries in the absence of a corpus luteum. cysts can be further classified as follicular which are thin walled and non progesterone producing, or luteinised/luteal which have thicker walls, progesterone producing.

538
Q

Describe why cystic ovarian disease occurs?

A

Cysts form due to failure in LH surge around time of normal ovulation or failure of follicle to respond to LH. Follicles fail to ovulate and instead of becoming atretic continues to grow and forms cysts. cystic follicles initially produce oestradiol which suppresses further follicular development in the ovaries and then they enter an oestrogen inactive phase during which time the cyst can persist for many weeks. many cysts which form in early pp period regress spontaneously without any treatment.

539
Q

What are the possible reasons for the failure of the LH surge which causes cysts to form?

A

stress - causes cortisol release which can interfere with hypothalamus/pituitary interaction and block or delay normal LH surge or may alter LH receptor activity at follicular level. stress hard to define eg movement/transport, change of diet, high yield, rapid liveweight loss, energy stress (NEB) is thought to play a significant role. Metritis/endometritis - endotoxin production from uterus can cause cortisol release which may interfere with ovulation. Other possible predisposing factors - B carotene deficiency in high concentrate diets, plant based oestrogens in the diet other dietary deficiencies.

540
Q

What are the clinical signs of cystic ovarian disease?

A

Follicular cysts - anoestrus or occasionally nymphomaniacal behaviour eg irregular or recurrent oestrus behaviour. luteinised cysts: anoestrus. most cysts are associated with anoestrus and are only detected on routine pp checks or when cow examined for failure to show oestrus. Hard to define type of cyst on rectal palpation. if thick/firm walled then likely to be a luteinised cyst. rectal palpation plus milk/blood progesterone analysis may increase accuracy of diagnosis. follicular cyst low milk progesterone, luteal cyst high milk progesterone >2ng/ml. Progesterone output varies over time with cysts and may be undetected CL producing progesterone. follicular and luteinised cysts can be differentiated on the basis of morphology with reasonable accuracy using ultrasound.

541
Q

What is the treatment for cystic ovarian disease?

A

Treatment is indicated to reduce delay in calving - 1st service/conception in cystic cows. Not worth treating cysts found <30 days pp. 1. Gonadotrophin releasing hormone induces an LH surge which causes luteinisation of cysts and possibly ovulation of any mature follicles present at ovaries. successful treatment should give a rise in plasma progesterone to luteal levels within 7 days of treatment. 80% of cows in oestrus within 30 days of treatment. Cure time may be reduced if PGF2a given 7-14 days after GnRH treatment if oestrus has not yet occurred. Human chorionic gonadotrophin - LH agonist action causes luteinisation of cyst and regression. oestrus variable within 20-30 days post treatment. Repeated treament may cause anaphylaxis. giving PGF2a 7-10 days after HCG will give more predictable onset of oestrus. Progesterone - PRID/CIDIR inserted in vagina for 10-12 days then removed. mechanism not clear - causes atresia of cyst by suppression of LH and FSH support through progesterone negative feedback. oestrus normally occurs within 2-3 days of PRID/CIDR removal along with ovulation of new dominant follicle. Cows can be inseminated at this induced oestrus although conception rates may be lower. Prostaglandin F2a - can use PG alone if confident of diagnosis of a luteal cyst. Non luteinised cyst will not respond. if correct diagnosis PG treatment gives excellent cure rate of luteal cysts with oestrus within three to five days normally. Manual rupture not recommended due to traumatic damage/haemorrhage in ovary following rupture which may cause bursal adhesions. It positive luteal cyst use PG. if positive follicular cyst use PRid/CIDR for 10-12 days or GnRH injection. If unsure of cyst type use GnRH + PG in 7-14 days if not sen in oestrus or insert PRID cidr for 1-12 days with injection of PG at removal.

542
Q

Describe the return to normal cyclicity post partum in cows

A

During pregnancy and for a short period follwing parturition, cows are normaly acylic. 90% dairy cows resume cyclicity by 50 days pp. 70% of beef cows cyclic by 50 days pp. 5% may go anoestrus having resumed cyclicity. Throughout pregnancy waves of follicles develop and become atretic in the ovaries - ovulation is inhibited by high progesterone levels during pregnancy giving negative feedback on hypothalamus. following parturition, FSH induced waves of follicular growth are soon accompanied by ovulation and return of regular cyclicity. The first dominant follicle can normally be detected by 7-20 days pp in dairy and beef cows. In dairy cows 1st pp ovulation normally within 20-30 days. in beef cows 1st pp ovulation normally within 20-60 days. Difference is due to beef cows often not ovulating first dominant follicle to appear. first pp ovulation often not accompanied by oestrus behaviour - silent heat.

543
Q

What controls the time of the first pp ovulation?

A

Follicular growth and ovulation controlled by hypothalamus/anterior pituitary. FSH present in sufficient amounts to stimulate waves of follicular growth by 10-20 days, but ovulation of the dominant follicle requires sufficient LH pulse frequency. LH pulse frequency is controlled via a GnRH pulse generator in the hypothalamus. If dominant follicle fails to ovulate it will become atretic or occasionally become cystic. delay in pp ovulation in beef cows c/f dairy cows due to delay in sufficient LH pulse frequency. Any factors causing interference with GnRH /LH output in early pp period can influence pp anoestrus period. several factors have been identified that can cause extended anoestrus.

544
Q

What factors can cause extended anoestrus?

A

1- nutritional effects - inadequate energy intake in late pregnancy/early pp period can cause extended anoestrus due to suppression of LH pulse frequency. Body condition score at calving highly negatively correlated to pp anoestrus period. Negative energy balance in the early pp period affects levels of circulating insulin and growth hormone which can have direct detrimental effect son early follicular growth and oocyte uality. minimise effects by calving in good BCS and minimising early lactation LWL. Specific trace element deficiency may also be involved especially sulphur and molybdenum induced copper deficiency. Suckling effects - greater impact from natural suckling than milking therefore more effect in beef cows. frequency and duration of suckling affects LH output via opioid release interfering with GnRH output in hypothalamus. temporary calf separation in beef cows may increase LH pulse frequency and shorten pp anoestrus. Seasonal effects - first dominant follicle appear 20 days pp in spring and7 days pp in autumn. Delayed uterine involution due to assisted calvings, RFM, metritis etc can cause delayed involution which may delay resumption of cyclicity. Cystic ovarian disease - cysts form due to failure of ovulation of early dominant follicles and this can delay next wave of follicular development. persistent corpus luteum - usually found along with uterine infection/pyometra as this can lead to a failure of endometrial PGF2a release, treat with PG injection.

545
Q

How is diagnosis of nutritional anoestrus made?

A

Most cows presented for examination as anoestrus will be cycling normally and have not been observed in oestrus due to poor heat detection/poor heat expression. to diagnose true anoestrus need to either palpate two small hard ovaries with no CL or large follicles with similar rectal findings in 10-14 days. Have two low progesterone values in milk or blood recorded 10 days apart. with knowledge of history of LWL/bcs etc can often diagnose anoestrus on the basis of rectal palpation of two small hard ovaries.

546
Q

What is the treatment of nutritional anoestrus?

A

Sort out management, nutrition etc. Progesterone releasing devices - give short term progesterone treatment 9-12 days to mimic luteal phase. get LH surge on withdrawal and ovulation anoestrus in most cases within 2-3 days of implant removal. if deep anoestrus or early pp may need 400-600 iu PMSG injection at progesterone withdrawal to ensure ovulation and oestrus. GnRH injection - single dose of GnRH > 55 pp will give oestrus in most acyclic cows within 23 days. onset of oestrus very variable as depends on stage of follicular wave present and whether dom follicle presents on ovaries. if follicle capable of ovulation present then ovulation normally occurs in response to LH surge and a corpus luteum is formed. oestrus will occur following natural or induced regression of the CL.

547
Q

How can GnRH on the day of service enhance fertility?

A

Treatment with GnRH at the time of insemination has been shown to improve pregnancy rates in some studies. the mechanism is not clear but may be due to improved timing of ovulation relative to insemination. some cows may have delayed ovulation relative to standing oestrus. The GnRH injection induces an LH surge ensuring ovulation occurs synchronous with the insemination. GnRH given at oestrus has also been shown to improve subsequent luteal function.

548
Q

How does giving GnRH at day 11-12 post service enhance fertility?

A

After service cow must recognise it is pregnant by day 16 to prevet luteolysis. bovine trophoblast protein is secreted from embryos >15mm diameter normally by day 15 until about day 20. bTP-1 has antiluteolytic properties as it inhibits oxytocin receptor expession in the endometrium which prevents PG pulse release required for luteolysis. oestradiol increases OTR expression. it is crucial that embryo signals its presnce by day 16 of the cycle. small slow developing embryo may be lost due to luteolysis starting before sufficient bTP-1 is produced to prevent PG release from endometrium. GnRH causes LH release > luteinisation of large 2nd wave follicles + ovulation and formation of accessory CLs. this reduces oestradiol secretion from 2nd wave follicles which normally increases oxytocin receptor expression and boosts progesterone levels. this reducs change of early luteolysis if embryo is late to produce BTP-1. Can be given to all cows at day 11 post AI or more economically can be targetted on cows that return for a second or third service.

549
Q

Describe the ovsynch/intercept regime for improving submission rates

A

In herds with poor heat detection and submission rates a combination of GnRH and prostaglandin injections can be used to synchronise dairy cows for fixed time AI. pregnancy rates may be poor with this regime but all cows can achieve first service on target. Day 0 - 2.5mlGnRH, Day 7 - prostaglandin injection, day 9- 2.5ml GnRH, day 10 - AI 72 hours post PG or at observed heat if earlier.

550
Q

What is a repeat breeder cow? Why does this occur?

A

A cow that fails to become pregnant following three or more consecutive serves at normal oestrus intervals. Due to pure chance, genetics. undiagnosed pathology such as hostile uterine environment for sperm, blocked oviduct/salpingitis, delayed ovulation, bursal adhesions, cervical non patency, embryo dies on entry to uterus or at hatching, failure of sufficient btp-1 production from embryo leading to failure of maternal recognition of pregnancy. timing of AI, environment etc.

551
Q

Describe the clinical approach to repeat breeder cows?

A

Examine on day of oestrus when due for service.
Vaginal examination - check for clear mucus/normal cervix. if cloudy/purulent mucous, do not serve, use antibiotic uterine wash out and serve at next oestrus or short cycle using PG 10 days later. Rectal examination: palpate cervix, uterus, oviducts, ovaries/bursae. If no abnormalities - AI on 2 consecutive days, or give 2.5ml GnRH and AI 6-7 hours later.

552
Q

What is abortion?

A

The expulsion of a dead or non viable calf before 260days of gestation. the cause can be infectious or non infectious e.g toxins, stress, nutrition, twins. in most abortion investigations the cause is not confirmed due to the presence of a non infectious cause, the submission of inadequate material or the fact that the infection occured some time ago.

553
Q

How should you approach an abortion problem? what steps should you take?

A

Treat all abortions as infectious unless proven otherwise. the client should be advised to isolate the aborter and site of abortion and to retain the products of abortion. a single abortion may be an isolated incident or the first of an outbreak so all abortions should ideally be investigated. Most herds experience 1 or 2 percent of cows aborting, if 5 percent or more abort a thorough investigation is required. under brucellosis order, the owner must inform AHDO of all abortions <271 days. In practice, they should inform an LVI at their vet practice who contacts the AHDO. the AHDO informs the vet if a brucellosis enquiry is required (usually in sucklers and dry cows). blood milk and vaginal swabs are sent with form BS7. the Form bs26 is served to prohibit movement and allow the disposal of aborted material. A history should be taken to include recent purchases, movements, clinical disease, infertility, management, diet etc. the affected animal should be clinically examined, the foetus and placenta examined and samples submitted for laboratory investigation. These should consist of the whole foetus, placenta with cotyledons, lesions and nrmal tissue and possibly a maternal blood sample. if the whole foetus cannot be submitted, these samples should be taken - foetal stomach contents, pleural or peritoneal fluid, liver, lung, thymus and blood. maternal serology is often unreliable, a negative result fairly reliably rules out BVD as the cause however cows aborting due to IBR may not have seroconverted at the time of the abortion, while leptospira and neospora serology may go negative before abortion even if they are the cause. A positive neospora serology result has been correlated with an increased chance of abortion. paired serology may be useful, particularly for IBR.

554
Q

Describe hereditary/congenital anatomical infertility in cows?

A

Accounts for less than 1 percent of female bovine infertility. many cases are diagnosed before or at puberty and are culled. only valuable heifers may be investigated. Ovaries - agenesis, hypoplasia, freemartins, congenital and paraovarian cysts. Oviducts - aplasia, segmental aplasia, duplication. Uterus, cervix and vagina - uterine diadelphis, lack of patency, segmental aplasia including uterus unicornis and persistent hymen, infantile vulva, freemartinism, lack of endometrial glands, cysts of gartners ducts.

555
Q

What is a freemartin?

A

Placental anastomosis occurs in up to 90percent of bovine twins. hormones blood cells and other cells cross the placenta leading to chimerism. testosterone or male cells lead to masculinisation of female twin. clinical signs may include an enlarged clitoris with tuft of hair, vagina 30 percent normal length and blind, gonads hypoplastic, uterus difficult to palpate, epididymides and vasa deferentia seen on ultrasound, persistent hymen. Diagnosis is based on history, external signs, rectal and vaginal exam and blood tets.

556
Q

Name the different causes of acquired anatomical infertility?

A

Ovary - granulosa cell tumour, ovario bursal adhesions, oophoritis, ovarian cysts. Oviduct - salpingitis, hydrosalpinx/pyosalpinx, uterus - adhesions, mucometra/hydrometra, neoplasia (primary eg carcinoma, secondary e.g lymphosarcoma), uterine absesses.

557
Q

Describe the difference between infectious primary infertility and secondary infertility?

A

Primary -acting directly on reproductive tract, placenta or foetus. econdary - are systemic diseases which have a secondary effect on conception/pregnancy. Primariy infectious fertility may be non specific - which are opportunistic infections in individual cows leading to metritis, endometritis, yometra, salpingitis etc caused by streps/staphs, A pyogenes, E. coli etc. infections follow the breakdown of normal physical barriers for example following coitus parturition or injury and the reduction of the reproductive tracts natural defences following metabolic disease , the presence of a persistent CL. Specific infections - enzootic, many animals often affected, bacteria viruses or other micro organisms cause infertility.

558
Q

Describe how campylobacter causes infertility?

A

the natural habitat is the prepuce, glans penis and distal urethra. service leads to mechanical transmission. there is no systemic illness, females experience a mild endometritis and cervicitis, with mucopurulent vaginal discharges. Cases present as a repeat breeder which eventually holds, abortion and RFm may occur at 4-7 months or pregnancy may survive to term. It is a herd problem after introduction of new infected bull. first large number of returns, then abortions. if untreated bulls are usually permanently infected, cows and heifers develop immunity over 3-6 months. in an open herd problems will then occur in replacements and new bulls will become infected. Isolation from post service discharges, vaginal mucous agglutination test, C foetus venerealis in products of abortion. Test m ales - especially if bull is for AI, qualitative and bacteriological examination of semen, FAB on preputial washings/scrapings, virgin heifer test. Control - AI all stock, or AI infected stock and use a clean male on clean females or run clean herd, and use infected bull on infected stock. Treatment - females not normally treated, I/u streptomycin will shorten the course of disease, bulls are usually culled or treated systemically plus topically with preputial irrigation, and antibiotic cream.

559
Q

Describe how brucella abortus causes abortions in cows

A

Infection is primarily by ingestion with haematogenous spread at around 6 months gestation to the uerus/placenta. this causes a necrotic placentitis and endometritis. in bulls the infection localizes in the seminal vesicles and testes. It is introduced by silent carriers and excreted in fluids/faeces before and after abortion. cattle normally only abort once but remain infected and excrete as carriers. there is no systemic disease, abortion and placental retention occurs. some foetuses are born alive, others are dead with signs of bronchopneumonia. bulls develop orchitis and Epididymitis. in a newly infected herd, abortion seen in cows in late pregnancy then those earlier in pregnancy. when endeimc, abortions are seen in clean replacements and home bred heifers. Diagnosiis by serology and culture of milk, vaginal swabs, foetus, cotyledonary smears.

560
Q

How does bovine herpes virus 1 cause abortion in catlte?

A

Infectious bovine rhinotracheitis causes respiratory disease, milk drop and reproductive disease. non venereal infection at service or AI can lead to repeta breeding or later in gestation to abortion. infection in late pregnancy may lead to stillborn or non viable calves. venereal infection at natural service can lead to infectious pustular vulvo vaginitis, or at AI can lead to repeat breeding and endometritis. many females with reproductive IBR problems experience no respiratory signs. virus is shed via respiratory secretions and semen then becomes latent in the trigeminal ganglion and can be shed again when the animal is stressed. any seropositive animal is a biosecurity risk and this can be a be a barrier to export or use in an AI stud. Vaccination can be intra nasal or IM with an annual or biannual booster often combined with other respiratory pathogens. seropositive animals cannot be sold to accredited free herds, exported to free countries or used as AI stud bulls or for semen export. marker vaccines have been developed allowing the differentiation of wild and vaccine positives with a blood test. marker vaccinated animals may be exported to some countries and sold to IBR free herds. eradication polcies are based on test and cull and can include the use of marker vaccines. eradication schemes and accredited free status are available via commercial health schemes. infectious pustular vulvo vaginitis is characterized by sudden onset vulvar hyperaemia leading to vesicles and ulcers 48 hours post mating. this leads to pain, anorexia and pyrexia, preventing further service. males develop similar preputial lesions and mating is interuppted for 2-4 weeks.

561
Q

How does neospora caninum cause abortion in cows?

A

A protozoan. the definitive hosts are dogs which shed oocysts in their faeces. these oocysts are picked up by intermediate hosts. vertical transmission from cow to calf also occurs which seems to be the major route of infection of cattle. when congenitally infected animals become pregnant, bradyzoite cysts multiply and spread to the placenta and foetus. the consequences may be abortion in the third to ninth month of gestation, premature birth/stillbirth, a full term calf with neurological signs, a clinically normal infected calf, or rarely a clinically normal uninfected calf. Postnatal infection before pregnancy may allow the animal to develop immunity. infection in early pregnancy can lead to later abortion while infection in late pregnancy can lead to a full term clinically normal congenitally infected calf. Diagnosis is based on pathology (non inflammatory necrotic foci in CNS, bradyzoites in myocardium and liver, inflammatory and necrotic placental lesions and serology (positive maternal serology indicates exposure but may go negative, positive foetal serology indicates exposures after 17 weeks gestation. No vaccine in the UK. Prevent animal contamination of feed, prevent bovine/canine contact with placenta or abortion issues, embryo transfer from valuable seropostive cows. low prevalence herds - cull seropositives or do nothing.

562
Q

Describe what happens in rupture of the uterus in a ewe and how it can be corrected?

A

Ewe presents in shock, odontopresis, painful expression, may show frequent abdominal straining, blood at vulva, fast shallow abdominal breathing, rapid pulse. in such cases excessive manual interference of a breech presentation would be obvious. an explorative laparaotomy/c section under high extradural block reveals the uterine tear. repair is possible except when the tear extends close to the cervix.

563
Q

What analgesia should be given to a ewe to under go C section underation?

A

Intravenous NSAId such as ketoprofen is given prior to surgery. antibiotics should also be given at this stage. C section performed after infiltration of the left flank incision site with 2 percent lignocaine solution although efficacy of this method is questioned. distal paravertebral anaesthesia is more effective and is best administered in the standing sheep but may not be as easy to identify bony landmarks as in cattle. Excellent analgesia of flank for C section can be achieved after lumbosacral (high) extradural injection of 4mg/kg of 2 percent lignocaine. This is recommended when there is considerable trauma to the posterior reproductive tract, vaginal prolapse during first stage labour, a foetal monster in utero or likelihood of adhesions from previous elective surgeries. xylazine injected into the extradural space at sccrococcygeal site affords analgesia of the flank approximately 30 minutes after injection. too great a delay for on farm use.

564
Q

Describe how surgery is complete for a C section on a ewe?

A

The ewe is positioned in right lateral recumbency. a large area of the left flank is shaved, under no circumstances should the wool ever be plucked frmo the skin. a Plastic disposable drape is fenetrated and held in position with clips into the fleece. surgery is performed through a left flank incision midway between the last rib and the wing of the ileum commencing 10-15cm below the level of the transverse processes of the lumbar vertebrae. a 15cm incision is made through the skin, external abdominal oblique muscle, internal abdominal oblique muscle using a scalpel blade. the transversus muscle and closely adherent peritoneum are grasped with forceps and raised before a small nick is made and subsequently extended. Care is necessary at this stage to avoid puncturing an underlying viscus especially if the ewe is bloated or shows tenesmus. Care is necessary when exteriorising the gravid uterine horn because of its thin wall and often friable nature. the left horn is always chosen in a multigravid uterus. the abdominal wound can be packed with sterile guaze swabs prior to the incision being made in the greater curvature in an attempt to prevent leakage of uterine fluids into the abdomen. The incision is made starting 6-8cm from the tip of the uterine horn at the level of the fetlock joints and extended towards the cervix as necessary using scissors. the uterine incision is normally extended over the lambs tail head. when the lamb in the left uterine horn is presented in anterior presentation it will be delivered hind legs first. if present, lambs in antierior presentation within the right uterine horn are delivered head first. it is easier to use your right hand to manipulate the lamsb head within the right uterine horn. The uterine incision is closed with a connel suture of 7 metric chromic catgut or equivalent suture material. the suture line is carefully checked for leakage of uterine contents. the peritoneum and transverse abdominal muscles are closed with a continuous suture of 7 metric chromic catgut. The skin incision is close with interrupted horizontal mattress sutures of 6 metric monofilament nylon or similar.

565
Q

Describe a vaginal prolapse in a ewe. why do vaginal prolapses occur?

A

The diameter of a vaginal prolapse varies from an area of dorsal vaginal wall of approximately 8cm up to 20cm when the prolapse may contain urinary bladder, uterine horn or both these structures. preparturient vaginal prolapse occurs in mature ewes during the last month of gestation with an incidence around 1 percent. Many factors are implicated in vaginal prolapse including excess body condition, multigravid uterus, high fibre diets particularly those containing root crops, limited exercise in housed ewes, lameness leading to prolonged periods in sternal recumbency, steep fields, and subclinical hypocalcaemia. Short docked tails have been implicated in vaginal prolapse but the condition also occurs in mountain breeds with undocked tails.

566
Q

Describe the clinical presentation of a ewe with a vaginal prolapse

A

Ewes with vaginal prolapse may show many behaviour signs consistent with first stage labour including isolation from the remainder of the flock, failure to come forward for concentrate feeding, periods spent in lateral recumbency with repeated short duration forceful abdominal contractions and associated vocalisation. frequent attempts to urinate with no urine voided, is often noted when the ewe raises herself. Neither cervical mucus plug nor foetal membranes are visible at the vulva instead a red spherical prolapse measuring 8 to 20 cm is present. A full clinical examination of ewes with vaginal prolapse must be undertaken as clinical signs indicating toxaemia, inappetence, reduced ruminal contractions , raised pulse and congested mucous membranes may be consistent with foetal death and impending abortion. Fetal movement can be reliably demonstrated in near term sheep using transabdominal real time B mode ultrasound machines with a 5MHz sector transducer if there is doubt regarding the viability of the foetuses.

567
Q

What is the treatment of a vaginal prolapse?

A

Needle decompression of the displaced bladder throught he prolapsed vaginal wall because effective caudal analgesia allows emptying by raising the prolapse relative to the vulva in the standing ewe thereby reducing the fold in the neck of the bladder at which point urine flows from the urethral orifice. Plastic retention devices cause considerable discomfort with irritation and secondary infection of the vaginal mucosa resulting in frequent tenesmus. harnesses and trusses are very useful when farmers detect the prolapse early and there is little superficial trauma/contamination but they may prove difficult to fit and give rise to pressure sores if too tight. Detection of first stage albour can become problematic.

568
Q

Describe how to give a sacrococcygeal extradural injection in a ewe

A

The area over the tail head is clipped and surgically prepared. the first intercoccygeal space can be identified by digital palpatioon during slight vertical movement of the tail and a 25mm 20 guage needle directed at 10 to 20 degrees to the vertebral column. Correct position of the needle point can be determined by failure to strike bone during travel of the needle point and lack of resistance to injection of the cmobined lignocaine and xylazine solution. it is not possible to use the hanging drop technique. Combined extradural injection of xylazine and lignocaine at the first interococcygeal site provides effective analgesia permitting replacement of rectal cervical or uterine prolapse after 5 minutes with analgesia persisting for 36 hours. in practical terms 2 mls of 2 percent lignocaine and 0.25mls of 22 percent xylazine are mixed in the same syringe. Does not cause significant sedation in sheep (contrast to catlte).

569
Q

What happens if you inadvertently inject the combined xyxlazine and lignocaine solution into fascia and tissue surrounding the sacrococcygeal site?

A

this results in mld sedation of the sheep for two to three hours. in this event the sacrococygeal extradural injection should be attempted again but using only lignocaine. in some shee mild pelvic limb paresis may persist for up to 48 hours after extradural injection with periods spent in sternal recumbency but these ewes can stand unaided. The vaginal prolapse will frequently return to the normal position within five minutes once caudal analgesia has been effected and tenesmus caused.

570
Q

Describe how to do a modified buhner suture in replacing a ewe vaginal prolapse?

A

a moodified buhner suture of 5mm nylon tape is placed in the perivulvar subctuaneous tissue 2cm from the labia andd tightened to allow an opening of 2cm diameter. systemic penicillin at a dose of 20,000 should be injected once daily for three to five days. the ewe is Marked and shepherd instructed to observe her for signs of parturition. The suture can easily be untied to allow examination of the posterior reproductive tract for signs of first stage labour. oedema surrounding the vulva often results following placement of the buner suture but this rarely causes significant problems and no specific treatment is neccessary except monitoring that the ewe can urinate freely. Suturees which penetrate the vaginal mucosa such as single interruptd or mattress sutures must be avoided as urine scalding of vaginal mucosa around the suture material in conjunction with secondary bacterial infection forms a large diptheritic areas which causes considerable discomfort and tenesmus. Single interrupted and mattress sutures must be removed to permit digital examination of the posterior reproductive tract during periods of suspected first stage labour and cannot easily be retied.

571
Q

Describe what a uterine prolapse looks like in a ewe

A

Uterine prolapse usually occurs immediately after prolonged/assisted second stage labour culminating with the delivery of a large singleton lamb. partial uterine prolapse occurring after an interval of 12 to 48 hours generally results from tenesmus caused by pain arising from infection and swelling of the posterior reproductive tract which have developed consequent to excessive and unskilled interference by the shepherd during delivery of the lambs. the everted uterus is readily identifiable by its large size extending from the vulva to below the level of the hocks with prominent caruncles and adherent foetal mebranes.

572
Q

What is the treatment for a uterine prolapse?

A

Unless the uterus is replaced correctly and fully inverted to its normal position within the abdomen the ewe will continue to strain causing considerable distress and suffering and re prolapse. for welfare reasons a prolapse of several hours duration must only be replaced by a veterinary surgeon under extradural anaesthesia. The prolapsed tissues are cleaned and the foetal membranes removed if this can be achieved without significant haemorrhage. the prolapse is gently replaced using the palms of both hands starting with the body of the uterus progressing to the uterine tip. remember to correctly evert the uterine tip restoring the normal comma shaped uterine tip. antibiotics, either procaine penicillin or oxytetracycline should be administered intramuscularly daily for three to five consecutive days after replacement of the uterine prolapse to limit bacterial infection of the traumatised tissues. While it may prove difficult to prevent sporadic uterine prolapse following the delivery of a large singleton lamb, uterine prolapse after a protracted unskilled interference can be avoided by timely correction of the dystocia by a veterinary surgeon.

573
Q

Describe an Embryotomy procedure in cattle

A

Neither necessary nor recommended except when the calf is in anterior presentation where the hips are firmly lodged at the entrance to the maternal pelvis (hip lock). If the calf is alive, it is euthanased. The cow is given a sacrococcygeal extradural injection of flunixin or ketoprofen injected intravenously. the dead calfs head and thorax are removed as close to the cows vulval lips as possible using a knife and embryotomy wire. the calf is then repelled into the uterus to allow the embryotomy wire to be passed between the calfs hindlegs held in the jaws of a pair of haemostats. The calfs pelvis is split using the embryotomy wire. there is no requirement for an embryotome, plastic tubing can be used to protect the vagina from the embryotomy wire where necessary. obturator nerve paralysis is common in affected cows, be aware of the need for supportive care.

574
Q

Describe the analgesia needed for a C section operation in bovine animals.

A

After infiltration of the left flank incision site with approximately 3-5mg/kg of 2 percent lignocaine. A distal paravertebral anaesthesia is much more effective. Injections of local anaesthetic can be performed with the cow restrained in cattle stocks then haltered and released into a pen for surgery.

575
Q

What sedation should be used for C section operation in cattle

A

Xyalzine has an ecbolic effect and may render the uterus more friable and less manoeuvrable. for standing surgery, xylazine affords no analgesia, apparently sedated cattle can still kick.. many surgeons use IV ACP for mild sedation. some surgeons use intravenous romifidine for mild sedation which if off label. romifidine is much more predictable than xylazine. Xylazine at a dose rate of 0.07mg/kg injected into the extradural space at the Sacrococcygeal site produces only sedation in cattle and not analgesia of the flank.

576
Q

Why would clenbuterol be injected prior to C section in cattle?

A

Clenbuterol injected prior to surgery is used by some surgeoons to aid manipulation of the gravid uterus and slow the rate of uterine contraction after removal of the calf. it is reversed by injection of oxytocin after completion of the operation. Most surgeons give a sacrococcygeal extradural injection of 2percent lignoocaine to prevent tenesmus during surgery.

577
Q

Describe the procedure of a C section in cattle

A

Surgery is performed through a large left flank incision midway between the last rib and the wing of the ilium commencing 15cm below the level of the transverse processes of the lumbar vertebrae. a 25cm incision is made through the skin, external abdominal oblique muscle, internal abdominal oblique muscle using a scalpel blade. the transversus muscle and closely adherent peritoneum near the top of the incision are grasped with forceps and raised before a small nick is made and extended. Uterine incision is made starting on the greater curvature 10-15 cm from t he tip of the uterine horn at the level of the calfs fetlock joints in those calves in anterior presentation and extended towards the cervix as necessary using scissors. The uterne incision is normally extened to just over the calfs tailhea. while the incision may be started with the uterine tip exteriorised it is usually necessary to enter the abdomen whilst extending the incision. Always make sure the uterine incision is long enough. Two suture lines are not often necessary to close the uterus.

578
Q

Describe what happens to a cow after calving in terms of reproduction events

A

After calving there is time where the cow needs to recover, the uterus invoutes, expels any infection and ovarian cyclicity returns. Even if the cow does express signs of oestrus, the cows will not be served as the likely success rate will be poor. This period when the farmer decides not to inseminate is the Voluntary Waiting period time - should last for 42-50 days after calving. Once the cow has reached the end of VMP she will need to be observed in oestrus then inseminated. Average cow will be inseminated for the first time, if observed again in oestrus 21 days later will be re inseminated and if insemination was not successful then she will be served for the third time after oestrus 21 days later. If this third service is successful the cow will become pregnant. Pregnancy is confirmed by either Transrectal ultrasound scanning from 30 days P insemination or manual rectal palpation from 6-8 weeks post insemination. On average dairy cows are pregnant for 282 days and so she will calve again at this period following the third insemination. This is therefore used to predict future calving dates.

579
Q

What are the four key requirements to good reproductive efficiency in dairy cows?

A

Rapid resumption of ovarian cyclicity after calving - this requires that the uterus is fully involuted ie no endometritis and that ovarian function is not compromised by conditions such as cystic ovarian disease or extended post partum nutritional anoestrus. Get cows served in good time after calving - affected by Voluntary waiting period and how soon after calving farmers are prepared too serve cows without compromising conception rates. Get cows submitted for service - determined by heat detection and the ability to get cows inseminated. get cows to conceive to service - this is assessed via conception rates i.e how many successful inseminations are performed.

580
Q

What is the calving interval/index?

A

The most common traditional measure of herd fertility. It measures the average interval in the herd from one calving to the subsequent calving. It is comprised of the calving to first service interval, interval between the first and subsequent services, conception rate and pregnancy length. in A good herd - calving interval 365 days. Skewed by variations in gestation length (abortions), also requires cows to conceive and calve before it can be measured, so does not include any cows that have not got back into calf. Very retrospective due to long pregnancy length.

581
Q

what is the predicted calving interval?

A

It is derived from the average calving to conception interval plus 282 days.

582
Q

list the target calving intervals for different types of units

A

Block calving herds - 365 days
Up to 7000 litre lactation average - 265 days
7000-8000 litre lactation average - 375 days
8000-9000 litre lactation average - 385 days
Over 10,000 litre lactation average - 400 days.

583
Q

What is the conception rate?

A

this is defined as the number of successful services divided by the total number of services, expressed as a percentage. it is sometimes also expressed as the number of services per conception: 3 services per conception = 33% conception rate. The critical issue is defining what is a service success - if PD results are unknown then the conception is assumed from non return to service after 40-60 days following service which is over optimistic.

584
Q

What is the 100 day in calf rate?

A

Percentage of cows that are pregnant by 100 days in milk and is a similar measure to the calving to conception interval. If the average calving to conception interval is 100 days then the 100 day in calf rate will be 50%.

585
Q

What is the 200 day not in calf rate?

A

This is the percentage of cows that are not pregnant by 200 days in milk and is a similar measure to the culling rate for failure to conceive as cows that are not back in calf by 200 days in milk are unlikely to be retained in the herd. target is less than 10%.

586
Q

What is the pregnancy rate?

A

More formally called the 21 day pregnancy risk. It is defined as the percentage of cows eligible to become pregnant in a given time frame that do actually become pregnant. the timeframe usually used is 21 days. It measures the rate at which cows become pregnant in 3 weeks blocks, and it is current up to date figure that can be used to pick up problems rapidly.

587
Q

What is the herd pregnancy/insemination inventory?

A

This very basic figures assesses the number of cows that are inseminated and become pregnant within a given time frame usually every 3 or 4 weks. it is of value in large herds calving all year round, where targets can be set for the number of pregnancies required each month to maintain the calving profile.

588
Q

What is the veterinary PD rate?

A

This is a simple calculation of the number of cows pregnant at the routine visit, divided by the total number of cows presented for PD. as well as assessing conception rates it also gives a guide to heat detection as most of the non pregnant cows should have been identified by return to service and not presented for PD. 90% of cows should be in calf at manual PD 6-8 weeks and 75% in calf at ultrasound scanning from 30 days post insemination.

589
Q

Why does poor dairy herd reproductive efficiency cost the farmer?

A

Obvious costs associated with poor fertility in a dairy herd such as extra services or vet treatments, but the largest costs associated with poor dairy herd reproductive efficiency are reduced milk prouction. Cows take longed to get back in calf again and have extended lactations so spend less time in early lactation when they produce more milk and more time in late lactation. feed conversion efficiency in early lactation is higher and so the feed costs will be spread over a greater number of litres of milk. The improved herd fertility will enable more replacement heifers to be produced so maintaining overall herd size or even allowing for expansion.

590
Q

Describe what should be done on a routine herd health fertility visit?

A

Post natal check - in some herds with high levels of endometritis or block calving herds all cows are examined routinely at 21 days post calving. this will involve additional time and cost and is unnecessary in most herds. the alternative is to examine at risk cows eg after abortion, premature calving, stillbirth, RFM, prolapse, discharge, difficult calving. Oestrus not observed or not seen bulling - this examination would include cows that have had no observed oestrus event by 42 days calved and no first service by 65 days calved. it would also include cows that have had no oestrus activity by 14 days following a PD negative diagnosis or fertility teratment.

591
Q

How is pregnancy diagnosis made?

A

Usually performed using transrectal ultrasound from 30 days post service or by manual palpation per rectum from 42-60 days post service. The aim is for accurate and early diagnosis of PD negative cows so that they can be presented for re insemination as soon as possible. estimated that 5-10% of cows will lose their pregnancy between 30-60 days post service and therefore recommendations are to repeat the PD at 60 days post service to pick up any cows with non viable foetuses or early embryonic death. Pregnancy associated glycoproteins in the milk test - cannot be used in first 60 days after calving as there will be PAGs still present in the milk from the previous pregnancy.

592
Q

What are repeat breeder cows?

A

This is defined as cows that are not pregnant after three or more services. unless detectable abnormalities are present, treatments are usually based on either double services or giving GnRH analogues on the day of service or day 11 post service.

593
Q

Which measures suggest that oestrus detection is an issue on the farm?

A

If non service oestrus events are recorded a long calving to 1st oestrus interval, long calving to first service intercal, pooor pregnancy rates of cows presented for Vet PD, lower PD rates indicate that returns to service have been missed, poor heat detection or submission rates, heat detection analysis or interservice intervals which measure the intervals that cows return to service following a previous oestrus or service.

594
Q

What measures would suggest that oestrus identification (serving cows when not in oestrus) is an issue?

A

High numbers of services occurring 0-17 days after previous oestrus or service, disappointing conception rates, can be definitively diagnosed by milk progesterone analysis on the day of service (should be low)

595
Q

How can signs of oestrus expression be maximise in cows?

A

Have an adequate loafing area for cows to display signs of oestrus. avoid over crowding, provide non slippery floor surfaces, groove concrete flooring if necessary, avoid heat stress in the summer by improving ventilation and reducing relative humidity, minimise NEB or condition loss in early lactation, reduce social stress by minimising group changes, having adequate trough space, enough cubicles etc. lame cows are less active when in oestrus, treat lame cows. reduce diseases such as retained cleansings, endometritis and cystic ovarian disease.

596
Q

What methods can be used to improve oestrus detection?

A

Tail paint/chalk - rubbed off when the cow is mounted. needs to be applied regularly. Oestrus mount detectors - includes kamars, bovine beacon etc, applied to the spine above the pelvis of a cow with a change in colour when activated by pressure or rubbing when the cow is mounted. relatively cheap, good visual signs of mounting aciviyt, can be activated by cubicles if too far back. Activity meters - electronic devices attached to the cow via neck collar or leg, When a cow is in oestrus, activity will increase by 400% which is then flagged up by the computer system. costs vary according to system but for a 100 cow herd are in the region of £100 per cow. Milk progesterone testing - accurate identification of cows in oestrus which will have low milk progesterone levels. best use is for rapid detection of returns to service ro cows not sure of bulling. Use of teaser bulls - will attract cows in oestrus. Bull will stimulate oestrus activity in cows, natural method of oestrus detection, watch for lame bulls. Reproductive management systems - contracting out oestrus detection and inseminations to an external AI technition. Oestrus synchronisation protocols - use of various hormone treatment regimes with fixed time AI either ovsynch or PRID/CIDrs.

597
Q

Describe which aspects must be taken into consideration during semen collection and how this process is done

A

Prior to collection: license application, isolation of the bull, health tests for TB, brucella, trichomonas foetus, IBR, campylobacter fetus, EBL, BVD, some studs will do johnes, leptospira and Q fever additionally, nutrition, management. Collection utilises a tear animal or dummy. the bulls identity must be checked and verified and a DNA profile taken. an artificial vagina is used. adequate teasing is important. water, chemicals cold shock and bright sunlight must be avoided. Semen evaluated by raw semen motility and stained slight. Processing - extend semen diluents, add cryoprotectant, process in 4 degrees C environment, print straws, load and seal straws, freeze straws, quarantine.

598
Q

Describe good practices for semen handling/thawing

A

Avoid inadvertent thawing, ensure storage flask temperature is maintained, thaw i 35C water for a 1/4ml straw - 7 secs, for a 1/2 ml straw - 15 secs. Dry straw. load and avoid wind chill. catch animals for insemination before thawing the semen.

599
Q

What are the advantages of using AI? especially synchronised AI?

A

Choice of genetics, cost - £15 for a straw of semen versus cost of bull, biosecurity, flexibility, safety. Using synchronised AI - manage heifer introduction into the herd, optimise calving pattern in grass systems for dairy cows, optimise tight calving pattern for beef. Fixed time AI - no heat detection needed. Ideally want to manipulate oestrus cycle to allow tight synchrony whilst ensuring that the dominant follicle which is developing is within a time frame which will ensure good conception rates i.e its duration of dominance is less than 9 days.

600
Q

What are the different methods of oestrus synchronisation?

A

Double prostaglandin, progesterone device only, PRogesterone + PG, progesterone + PG, plus GnRH at progesterone device insertion, ovsynch GnRH, PG GnRH before AI, presynch ovsynch (double PG before ovsynch)

601
Q

What is embryo transfer?

A

Embryo transfer involves superovulating the donor cow, inseminating her to fertilise the multiple ova shed and non surgically recovering the resultant embryos seven days later. these can be examined, graded and transferred fresh not synchronised recipients which are also at day 7 of their oestrus cycle or frozen and stored for future use. The donor must display normal oestrous cycles prior to commencing Superovulation programme.

602
Q

How is superovulation induced?

A

Superovulation utilises commercially prepared follicle stimulating hormone to encourage a group of developing follicles to overcome the dominant follicle suppression and continue developing to ovulation with concomitant maturation of the oocytes. The FSH is commonly administered as a twice daily injection regime over four days commencing mid cycle. incorporated in this regime is a prostaglandin F2a injection usually given alongside the fifth FSH injection to return the donor cow to oestrus. it is usual to inseminate the donor cow soon after the onset of oestrus e.g the afternoon of the day of oetrus, with a second insemination the following morning.

603
Q

How is embryo collection performed?

A

On day 7 of the oestrus cycle. Embryos enter the uterine lumen from the oviduct at approx day 4 of cycle and although embryos can be collected successfully from the uterus between days five to nine, a day 7 collection allows recovery of the most flexible stages of embryo for both freezing and fresh transfer. collection is a non surgical procedure requiring catheterisation of the uterine horns.

604
Q

Describe the two types of embryo collection catheter which can be used

A

2- way which has two tubes within it. one allows inflation of a latex cuff near the tip of the catheter, whilst the other enables the flushing media to enter and leave the uterine horn. greater volumes of media are required as a larger segment of the uterine horn is flushed. 3 way - which consists of three tubes. one allows inflation of the cuff situated 10cm behind the tip. another tube allows media to enter the uterine lumen from the tip of the catheter and a one way flow is created by the media returning down the third tube via its entry hole at the level of the cuff.

605
Q

What flushing media is used for embryo collection?

A

Dulbeccos phosphate buffered saline is infused into the uterine lumen to allow slight distension before drainage by gravity flow along with the embryos and ova into a collection filter. the filter contains a metal micromesh with a pore diameter approximately half that of an embryo allowing excess media to run through whilst retaining the embryos.

606
Q

What is embryo searching?

A

it is performed once both uterine horns have been flushed. the contents of the filter are emptied into a Petri dish and examined under a steroscopic microscope at between x6-x10 magnification. recovered embryos are placed in an embryo holding solution, classified and graded.

607
Q

Describe how embryo freezing is done

A

embryo freezing involves first partial dehydration of the embryo in a crypprotectant to prevent freezing damage. the most commonly used cryoprotectants commercially are 10% glycerol and 1.5M ethylene glycol. step wise addition or removal is required for 10% glycerol in increasing or decreasing gradents of concentration respectively whereas one step thawing of embryos frozen in ethylene glycol can be performed as it crosses cell membranes more rapidly. embryos are frozen in 1/4ml plastic straws which must be identified with the donor name, sire name, collection team code, breed code and date code. The cooling curve used is pre programmed into the freezing machine and the straws are frozen at a controlled rate of freezing as this progresses to ensure optimal survival of the embryo. Freezer chamber temperature is at -6C this nucleated the freezing medium with an ice crystal when 1 or 2 degrees below its freezing point preventing supercooling and excessive temperature rise from the release of latent heat in the cooling process. At the end of the freezing programme the straws are plunged directly into liquid nitrogen before being placed in plastic goblets and stored under liquid nitrogen in cryogenic flasks.

608
Q

Describe thawing of straws for ET

A

reversal of the previous procedures. the straws are thawed in a flask of warm wated and if frozen in 1.5M ethylene glycol are then ready for immediate transfer. those frozen in 10% glycerol must first have this extracted from the embryo. The embryos are removed from the straws they are frozen in and passaged through decreasing concentrations of glycerol and sucrose solutions untill finally they are placed in embryo holding solution, re examined, graes checked and loaded into straws for transfer.

609
Q

How is the embryo transfer procedure done?

A

The ET procedure for the recipient is the same for fresh or frozen embryos. recipients need to have been synchronised to display oestrus on the same day as the donor cow or within a 24 hour period either side of that day. before transfer of the embryo the recipients ovaries are examined by manual rectal palpation or Ultrasound scanner for the presence of a CL. note is also made of which ovary has the CL. recipients receive an epidural anaesthetic and after cleaning the perineum the transfer gun is passed through the cervix and guided along the uterine horn ipsilateral to the corpus luteum before depositing the embryo.

610
Q

What sort of results can be expected with Embryo transfer?

A

On average 5-6 viable embryos can be recovered per collection. grade 1 embryos can be expected to give pregnancy rates of 60% fresh or 55% pregnant.