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DVM 3 - 1 > Cattle 1 > Flashcards

Cattle 1 Flashcards

1
Q

What are the 8 main drives of profit on beef farms

A
  1. Stocking density
  2. Cattle genetics
  3. Fertiliser management, reducing bought in feeds
  4. Pasture growth and utilisation
  5. Marketing of end product
  6. Efficient labour usage
  7. Disease prevention and control
  8. Time of calving
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2
Q

features of highly fertile beef herd - calving pattern, female calve in first cycle, calving rate, age of heifers, heifer dystocia

A
  • Calving pattern 8 weeks in cows and 6 weeks in heifers
  • 70% of females calve in first cycle
  • calving rate > 95%
  • use highly fertile high serving capacity bulls
  • heifers calve down as 2 year old
  • heifer dystocia rate < 5%
  • high heifer retention rate enabling cows to be sold at 8 years old having reared their 6th calf
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3
Q

List the 7 habits for effective heifer and cow management

A
  1. Calving Pattern
  2. Heifer Critical Mating Weights
  3. Heifer Weaning
  4. Heifer Nutrition
  5. Parasite Control
  6. Reproductive Diseases
  7. Selection of Heifers for Joining
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4
Q

Calving pattern what do you want, how to achieve and important reproductive events

A
  • Most beef farms do seasonal calving
  • Management practices need to be implemented in order to get shorter calving periods
    Reproductive events
    1. Cow calves
    2. Post-partum anoestrus - 30-60 days
    3. Cow starts cycling
    4. Cows joined - 50-70% conception rate
    5. Cows joined again -> 50-70% conception rate
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5
Q

Calving pattern how long from start of calving to start of joining and how long to calve for and what if longer

A

How long from start of calving to the start of joining
- 12 months in the year, pregnant for 9 months so starting joining 3 months after start of calving
How long should we calve for?
- 6-8 weeks
- If longer, the calvers at the end of the calving are harder to get in calf quickly enough -> only 50% cycling instead of 91%
○ You will get more pregnant (better than empty cow) BUT
§ Average weight of progeny is lighter
§ Not worth as much at sale
§ Need more old cows because more heifers don’t meet critical mating weights
§ Hard to cut back the calving interval by simply having shorter joining periods
- A good strategy is to focus on the heifers

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6
Q

Heifer critical mating weight what is it and how old are heifers at joining

A
  • Puberty is related to body weight as well as age
  • CMW definition: 84% conceive in 6 weeks
  • Will vary with breed and herd
  • Most breeds start cycling at about 52% mature BW
  • Typical benchmark is 60-65% of average mature BW for the herd
  • Growth rate about 1kg per day
    How old are heifers at joining
  • Aim to calve at 2 years so oldest will be 15-16 months old, later clavers 13-14months
  • THEREFORE later calving heifers need to achieve CMW at an earlier age - WHY CALVING PATTERN IS SO IMPORTANT
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7
Q

Heifer weaning when to wean and how related to energy in the paddock and the mothers nutrition

A

When to wean
- Minimum Age = 100 days from when the last calf born
- Maximum Age = 6 months, depending on season and available feed
○ Why 6 months? At 6 months some bulls will be reproductively available
- If Cow condition drops to 2.5
Energy
- Certain amount of energy in the paddock
- Feed in paddock
○ 1. turn feed into calf OR 2. turn feed into milk THEN turn milk into calf
- At some point it is more efficient to turn the energy directly into the calf -> WANT TO WEAN AS SOON AS POSSIBLE
- Also FOR THE MOTHER
○ Dam eat feeds
§ Some feed used for maintenance
§ Some feed turn into milk
§ Excess feed stored as fat -> when wean move to this
○ Therefore in droughts “early weaning can be a good strategy”

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8
Q

Selection of heifers for joining how much retain of heifers, which age group better and 5 reasons why

A
  • Herds often retain 40-50% of heifers
  • This is equivalent to 20 -25% of herd size
  • Retaining more heifers will lead to a younger herd- BETTER
    1. Cow value declines after 6-7 years
    2. Bodyweight peaks at 7-8 years
    3. Weaning weights of calves declines in older cows
    4. Older cows are more likely to die
    ○ Grass Tetany
    ○ Cancers
    5. More flexibility to cull for genetic gain
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9
Q

Oestrus synchrony why important on beef farms and different with dairy cattle

A
  • Increasing in popularity on beef farms
    ○ Useful to decrease calving length
  • Need less bulls (??)
  • More inseminations in 6 weeks
  • Programs similar to dairy cattle - Some differences
    ○ Beef cattle respond differently to GnRH and P4
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10
Q

pregnancy diagnosis when occur for a short or long joining period

A
  • If using a short joining period:
    ○ PD heifers 6-8 weeks after joining finishes
    § If empty cull straight away
    ○ PD cows at or just before weaning
    § Calf at foot so wouldn’t cull before this point if empty
  • If using a longer joining period
    ○ 16 weeks is a good point for rectal pregnancy diagnosis –10c piece cotyledons - MOST IMPORTANT FOR PREGNANCY DIAGNOSIS
    ○ Join 16 weeks, pregtest 8 weeks later
    ○ Three groups:
    1. NPD = empty
    2. <16weeks = late
    □ Can sell these as increase costs of cow as in calf
    3. > 16 weeks = early
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11
Q

Bull selection what based on but what is the issue with this and example

A
  • EBVs are used to determine genetic value of the bull
  • “breedplan” allows you to decide which EBVs are most important for your farm as there are a lot
    Genetic diseases
  • High genetic merit bulls often have lurking recessive problems
  • Single gene recessive diseases are not uncommon
  • Eg. Angus:
    ○ Fawn Calf Syndrome
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12
Q

What are the 3 important management of bulls

A
  1. EBVs and genetics
  2. Bull Management
  3. Assessment of fertility
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13
Q

What is the 5 important things involved with bull management and how long sick bull performance affected

A
  1. Management of sick/lame bulls
  2. Management of the Bull Team
  3. Bull:Cow ratio
  4. Vaccinations
  5. Fertility Testing
    Management of sick/lame bulls
    - How long does it take to produce a sperm cells -> 70 days
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14
Q

Spermatogenesis overview what does it consist of and the cycle of the seminiferous epithelium, how long does it take

A

Consist of:
• Spermatocytogenesis ( = Phases one and two, or Proliferation and Meiosis)• Spermiogenesis (= Phase three, or Differentiation)
• Note cellular bridges allowing cells to develop as cohorts
Cycle of the Seminiferous Epithelium
- This is a useful analogy to help understand the cycle of the seminiferous epithelium
- Each 12 month cycle has two stages (semesters)
- It takes 4 cycles (years) to complete the process
○ Cell division
○ DNA packaging
○ Add a motor and energy cells
○ Switch it on

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15
Q

Toxic sperm how occur and type of defect formed

A
  • After fertilization, the DNA must be carefully unpacked
    ○ If the packing is done poorly, it will be unpacked poorly and the fertilized egg will die
  • Eggs can only be fertilized once
    ○ “Uncompensible defects”
    § Minor insults can be worse than major ones -> major cannot get to egg but minor can get to egg BUT NOT FERTILISE
    § Dead sperm can be compensated for by other sperm - compensible defect
    § Toxic Sperm waste eggs - cannot be changed with increasing sperm
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16
Q

List some things that can cause sperm abnormalities, how long do they last and how do we aviod toxic sperm

A 
What can cause sperm abnormalities 
- Transport, Diet
- Temperature, Lameness
- disease, stress, toxins
How long do they last 
- 30-40 days later it may then become apparent 
How do we avoid Toxic Sperm ?
- Know the history
- Own the bull for 70 days
- Don’t use a sick or injured bull for at least 70 days
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17
Q

Training of virgin bulls, bull:cow ratio and bull groups what is important

A

Training/management of virgin bulls
- School them - know what they want to do but not how to do it the best way
○ Virgin bulls watch other bulls
- Give them an extra 10 days
Bull:cow ratio - 1:50 animals
Bull groups
- Not a specific amount of bulls in the group
- Run bulls in groups for a couple of months before mating so they can sort out a pecking order
- Use bulls of similar age and size if possible

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18
Q

What are the 4 main things you should vaccinate bulls against

A
  1. 5 in 1 (Clostridialdiseases)
  2. Leptospirosis
  3. Vibriosis
  4. Pestivirus
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19
Q

What are the 6 important factors that prevent heifer dystocia

A
  1. Minimising calf size by choosing appropriate EBV values in bulls
  2. Maximising the dam size - right condition score
  3. Parasite control and vaccination
  4. Genetics - low birthweight EBV Bulls
  5. Calving pattern –older=bigger!
  6. Nutrition –pre-weaning nutrition is vital
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20
Q

Fertile bulls what percentage of normal heifers within 3-9 weeks and what makes a subfertile bulls

A
  • Can impregnate (pregnant at 42 days) by natural service at least 60% and 90% of 50 normal, cycling, disease free animals within 3 and 9 weeks respectively
    Sub‐Fertile Bulls
  • Can achieve pregnancies by natural service but not at the rate of fertile bulls
  • Can produce viable semen but cannot achieve pregnancies by natural service
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21
Q

What are the 3 main reasons for examination of the bull

A
  1. Infertile bulls – make a diagnosis, insurance
  2. Pre‐mating – make a prognosis (VBBSE or Bull check as it is called now)
  3. Bull management is different in Northern vs Southern beef herds
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22
Q

Veterinary bull breeding soundness evaluation (VBBSE) what is it, what does it do and the 5 components it reports

A
  • a protocol developed by the ACV to be a relatively quick and economic procedure for screening bulls prior to sale or use.
  • not a guarantee
  • Screen out “high risk” rather than screen out “Infertile”
  • Uniform accepted standards
    The 5 components are reported:
    1. Scrotum
    2. General Physical Examination
    3. Crush Side Semen Evaluation
    4. Serving Ability Testing
    5. Semen Morphology Testing
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23
Q

Veterinary bull breeding soundness evaluation what gives a tick, qualified and cross

A

Tick
- All attributes for this component measured were consistent with the ACV standards.
- No risk factors for reduced fertility were identified during for this part of the VBBSE examination
Qualified
- Not all attributes for this component were consistent with ACV standards but these abnormalities may not necessarily preclude the bulls use.
- seek veterinary advice
- Retesting may be recommended.
Cross
- Some attributes for this component measured were not consistent with ACV standards.
- This bull has a significant risk of reduced fertility in the short term at least - may come right eventually
○ In these cases should be retested
- seek veterinary advice

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24
Q

What is important first step for Veterinary bull breeding soundness evaluation (VBBSE)

A 
Identify the Bull
- Decide what you will record
- Always record
○ Age (even if only roughly)
○ Breed
○ Some primary ID
- Certificates:
○ “Identified by” vs “Identified to me as”
- Take Tail Hair if you might end up in court!
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25
Q

Scrotal circumference with Veterinary bull breeding soundness evaluation (VBBSE) why important and normal testes

A
  • Reflects daily sperm output
  • Can indicate puberty (>27.5 cm)
  • Highly heritable & repeatable
  • Related to age at puberty in heifer calves
    “Normal Testes”
  • Significant variation in shape can be normal
  • Symmetry – Left should equal Right (max 20% variation)
  • Firmness and Resilience = tone
  • Scored 1 – 5
  • No “abnormalities”
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26
Q

List the 11 main abnormalities of the testes

A

1) unilateral hypoplasia/degeneration - one testis more than 20% smaller
2) bilateral hypoplasia/degeneration - small scortal circumference
3) epididymitis - Associated with seminal vesiculitis, tumours, abscesses, spermatocoeles, spermatic granulomas
4) small testicles
5) cryptorchid
6) biphallus - two penises
7) sperm granuloma - block movement of sperm
8) orchitis
9) haematoma
10) scortal (inguinal) hernia
11) varicocoele - pampiniform plexus burst

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27
Q

Small testicles who occurs and which process could be involved

A

○ Bilateral testicular hypoplasia/degeneration
○ Be careful of terminology –
§ “hypoplasia” means it has always been there and stud breeders don’t like that if you diagnose it on client farms!
□ Implies genetic issue
§ Degeneration means it was once normal and has shrunk
□ Infectious cause
§ Use both if not sure!

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28
Q

examining the penis and prepuce

A
  • Palpate the penis cranial to the scrotum
  • Observe during rectal palpation
  • Observe at electroejaculation
  • ACP or pudendal nerve blocks can assist
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29
Q

What are the 9 main abnormalities of the penis/prepuce

A

1) urolithiasis
2) preputial prolapse
3) prepuce stenosis (phimosis)
4) papillomas of the penis
5) penile haematoma
6) persistent frenulum - genetics - DO NOT BREED
7) balanitis, prosthitis and balanoposthitis
8) IBR = bovine herpes virus - vaccinate
9) hair strangulation of penis

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30
Q

Preputial prolapse predipsoing factors, cause and fertility

A

○ Mostly Bos indicus breeds
○ anatomical faults predisposing to prolapse:
§ long pendulous sheath,
§ large preputial orifice
§ absence or poor development of the retractor prepuce muscles.
○ These are inherited faults and selection against them has resulted in a reduced incidence of prepuce injuries.
○ Prepuce injuries are one of the most important causes of infertility in Bos indicus and Bos indicus derived bulls in northern Australian herds.
○ Bulls with extreme faults such as a long wide pendulous sheath should not be certified as low risk for breeding as they are prone to prepuce injury during mating.

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31
Q

Prepuce stenosis (phimosis) what group has high prevalence, common sequale to what and how reported on fertility exam

A
  • high prevalence in Bos indicus and polled Bos taurus bulls as well as 2-4 year old
  • It commonly follows injury and infection of the internal lamina of the prepuce at mating
  • should be reported as a X – High Risk on the Physical examination screen
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32
Q

Papillomas of the penis common in what age, where most commonly located, types and treatment with prognosis and fertility

A

○ common in bulls between 1 and 2 years of age
○ lesions often confined to the free part of the penis
○ may be pedunculated – often can snip off – but treated bulls should be monitored and closely examined prior to the next mating season or prior to sale as warts can re‐occur within 1‐2 months of treatment
○ may be diffuse ‐ usually encircles the glans penis resulting in analgesia of the penis and failure to achieve intromission detected by manual examination of the penis or during a serving assessment.
○ prognosis is good and many cases will recover spontaneously
○ As warts are a viral disease that can be spread sexually, bulls should be considered unsuitable for mating until they are healed.

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33
Q

Define balanitis, posthitis and balanoposthitis and how report on fertility exam

A

○ Balanitis ‐ inflammation of the penis
○ Posthitis ‐ inflammation of the prepuce
○ Balanoposthitis ‐ inflammation of both
○ A range of causes including IBR
○ Risk of adhesions is high
○ Report as X – High Risk (may still use on endemic farms)

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34
Q

Physical examination for Veterinary bull breeding soundness evaluation (VBBSE) what are the 8 things involved and what looking for

A
  1. Identify the bull
  2. Condition score
  3. Check the eyes - squamous cell carcinomas, vision impairment
  4. Sheath structure
  5. Examine the hooves - scissor claw, curled tow, worn claw, sand cracks
  6. Examine leg structure and conformation - posty leg, sickly hock, degenerative joint disease
  7. Examine gait
  8. Reproductive Organs
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35
Q

Crush side semen evaluation for Veterinary bull breeding soundness evaluation (VBBSE) what are the 3 ways semen is collected and what tested for

A
  • Semen is collected and examined at the Crush Side
    1. Rectal Massage -> massage seminiferous tubules
    2. Electro‐ejaculation -> place probe into rectum and increase charge with contractions until bull ejaculates
    3. (Artificial Vagina) - not done in the field
  • Need DRY equipment
  • Need WARM equipment
  • Collect a sample for morphology
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36
Q

Crush side semen evaluation for Veterinary bull breeding soundness evaluation (VBBSE) what are the standards for the semen to pass

A
  • Density of 1 or more
    ○ 200 sperm per 100x field under a cover slip
  • Absence of blood or urine staining
  • Absence of flocculant material and large numbers of pus cells
  • Percent progressively motile -> actively moving forward
    ○ Tick – 60% +
    ○ Pass – 30% ‐ 59%
    ○ Fail ‐ < 30%
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37
Q

Serving ability testing for Veterinary bull breeding soundness evaluation (VBBSE) how perform and where more common

A
  • Can be done individually or in groups
  • Can use restrained or unrestrained females
  • Females may or may not be in oestrus
  • If females not in oestrus, they need to be restrained in crates
    ○ Welfare issues ?
    ○ Disease spread ?
  • More common up north … as south can see bulls within the paddock
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38
Q

Define serving capacity and serving ability

A

Serving Capacity
- counting the number of successful services in a 20 minute test
- Used for genetic evaluation
Serving ability
- can the bull serve a cow. Only one instance needs to be observed
- Used to diagnose ability and disease (eg corkscrew penis)

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39
Q

What are the 3 components of the serving ability test for VBBSE and what hampers the bull being able to do these

A 
1. Erection 
○ Hampered by:  haematomas, persistent frenulum, preputial trauma 
2. Intromission
○ Hampered by 
○ Corkscrew Penis
§ Premature Spiral Deviation
§ 2.5 – 5 years old
§ Progressive
○ Dorsal analgesia of the Penis - common 
§ Nerve damage from injury
§ Cannot “seek” -> doesn't know where penis is so cannot penetrate 
○ Painful Penises
3. Ejaculation 
○ Pain causes unwillingness to ejaculate
§ Back Pain
§ Penis Pain
○ Problems with neural coordination
§ Sensory nerves of penis
§ Lumbar spondylosis
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40
Q

Sperm morphology testing for Veterinary bull breeding soundness evaluation (VBBSE) how occurs, what identify and what need for AI and natural mating

A
  • 8 drops of semen into a vial of buffered formol saline and send to lab
  • Easy
  • Identifies some permanent conditions
  • Identifies some transient conditions
  • Compensable vs non‐compensable defects
  • Should have 70% normal sperm for AI
  • 50%‐70% normal sperm ok for paddock mating
  • Provided that
    ○ Not more than 20% uncompensable
    ○ Nor more than 30% of other individual abnormalities
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41
Q

Causes of mastitis and significance

A
  • Almost always infectious
  • Non-infectious causes include -> trauma, chemical, injury
    Significance
  • Major cause of disease in cattle
  • Most economically important disease to dairy industry
  • Veterinarians have major role in diagnosis and treatment and provide advice on control
  • Involved at cow, herd and industry level
    Involves prevention and improvement at the herd/industry level
42
Q

What are the 8 main losses for mastitis and a cost of each clinical case

A
  1. Reduced milk production
  2. Loss of body condition (poorer fertility, disease susceptibility)
  3. Inferior milk quality - reduced payment
  4. Cost of treatment (antibiotics, discarded milk, time)
  5. Loss of cattle due to disease
  6. Culling of chronically infected cattle
  7. Cost of preventative measures (teat disinfectants)
  8. Possible antibiotic contamination of milk/meat
    Costs
    - Each case of clinical mastitis is estimated to cost over $175
43
Q

Coutdown downunder (2020) what is it, goals and involves

A
  • Funded by Dairy Australia and Industry
  • Aim to increase milk quality and decrease mastitis levels in Australian dairy herds
  • Therefore increase farm profitability
  • Goals
    ○ All milk supply to have BMCC <400,000 cells/mL
    ○ 90% milk supply to have BMCC<250,000 cells/mL
    Involves
  • Farmer education
  • Farmer short courses (cups on/cups off courses)
  • Advisor courses
  • Technotes - every practitioner in dairy practice should have access to technotes
  • Mastitis focus report
44
Q

How does milk quality affect farm economics and changes in milk composition due to mastitis

A

Farmers are paid for their milk based on composition (Protein % and Fat %) - milk solids
- Penalised financially if milk of poor quality as reflected by BMCC, TPC (total platelet count), thermoduric (how many bacteria are heat resistant (milk is pasteurised so important)), antimicrobials
Changes in milk composition due to mastitis
- ↓Lactose - ↑sodium and chloride
- ↓Casein - milk protein for starting cheese and yoghurt
- ↑Plasmin - degrades casein levels
- ↑Lipase - degrades fats into fatty acids giving rancid flavour, inhibits starter cultures

45
Q

What is normal teat anatomy and what and how provides barrier to infection

A
  • Four separate mammary glands, own teat
  • Branching duct system, alveoli to ducts to sinuses
  • Myoepithelial contraction of cells surrounding the alveoli due to milk let down reflex
  • Teat canal provides physical barrier to infection
    ○ Keratinised epidermis
    ○ Teat sphincter muscle contracts sealing teat
    ○ Desquamation of epithelium produces fatty material with bactericidal effect
    ○ Waxy material and bacteria removed during milking - high risk time just after milking before formation of new seal
    ○ Rosette of Furstenburg contains lymphocytes and plasma cells
46
Q

What are the main cause of infectious masttis and the 2 types of pathogens

A
  • Bacteria - most important
  • Fungi -> aspergillus, Trichosporon, candida
  • Viruses
  • Mycoplasmas
  • Yeasts
  • Algae - prototheca
    Two types of pathogens
    1. Contagious -> or cow associated pathogen
    2. Environmental -> non cow associated pathogens
47
Q

Contagious mastitis pathogens when spread and list 4 main ones, do they respond to treatment

A
  • Spread at milking time
    1. Staph aureus
    § Responds well to treatment
    2. Strep agalactiae
    strep doesn’t respond as well to treatment
    3. Strep dysgalactiae
    4. Mycoplasma
    § Not as common but if have an outbreak highly contagious throughout the herds and highly problematic
48
Q

Environmental mastitis pathogens how spread and list 5 important ones

A
  • Spread via environment
    ○ Paddocks, mud, faeces, calving pads, bedding, tracks
    1. Strep uberis
    2. E. coli
    § Generally highly clinical, gangrenous, toxic - depending on virulence factors
    3. Strep Dysgalactiae
    4. Pesudomonas
    § Very nasty cause again - highly toxic clinical signs
    5. A. pyogenes, Nocardia
49
Q

What is the overlap between contagious and environmental mastitis pathogens

A
  • There is variation within any bacterial species - depends on the strain
    ○ Strep. Uberis and E. coli can act as contagious pathogens
    ○ Staph aureus has been found to spread by environmental means
50
Q

Name the 5 cow risk factors for mastitis

A
  1. Age - prevalence increases with age
  2. Stage of lactation - first month/dry period
  3. Teat conformation - wide teat canal
  4. Teat condition - lesions
  5. Production - high production
51
Q

Name 4 management risk and pathogen risk factors for mastitis

A

management
1. Environment - mud and faecal contamination
2. Seasonal conditions - heat, humidity, wet and muddy conditions
3. Milking practices - hygiene, stress, machine issues - IMPORTANT - EXAM
4. Existing prevalence in herd
Pathogen
1. Viability in environment
2. Virulence factors - colonisation of duct, adhere to mammary gland
3. Toxins - E. coli and Staph aureus
4. Antibiotic resistance - large problem with herd level conditions especially with staph - why may need to cull cow

52
Q

Pathogenesis for mastitis and what would vet do on mastitis call

A
  • Infection almost always via teat canal
    ○ Colonise canal or forced through canal during milking - cups on cups off training important
  • Once reach cistern either produce toxins or induce inflammation (defence mechanisms)
    Vet
  • Treating presumptively with antibiotics -> look at clinical signs and make educated guess of the microbe causing the issue
  • Take a sample -> if not responding to above treatment than culture
    ○ Can culture straight away but most farmers won’t want you to straight away
53
Q

List some udder, milk and systemic clinical signs of mastitis

A 
- udder 
○ Heat, oedema, swelling
○ Gangrene
○ Abscess
○ Pain (lameness) 
- Milk
○ Clots, wateriness
○ Blood, serum 
○ Gas, odour 
- Systemic reactions 
○ Pyrexia 
○ Anorexia 
○ Tachycardia 
○ Absence of GIT sounds -> not eating 
○ Depression 
○ Recumbent -> not just milk fever -> NEED TO LOOK AT UDDER IN DOWNER COW (may need to move on the side) 
○ Shock
54
Q

What are the 3 classifications of clinical mastitis and how classified

A 
1. Peracute 
○ Severe inflammation 
○ Marked heat and swelling, changes in milk 
○ Systemic reaction - may be fatal 
2. Acute 
○ Inflamed quarter, changes in milk 
○ Systemic reaction; less severe 
3. Subacute 
Mild inflammation of mammary gland
55
Q

Examination of udder for mastitis evaluation what do

A
  1. Visualise - asymmetrical udder can be normal as well as extra teats
    ○ Gangrenous teat -> may lose the teat (become 3 teater), or may have loss in milk production for awhile depending on systemic effects
  2. Palpate
  3. Strip milk samples
    ○ Compare quarters
    ○ Use black background
    ○ Cannot usually make aetiologic diagnosis
56
Q

What are the 3 situations of mastitis incidence that required vet

A
  • More than 5 cases per 100 cows in first month of lactation
  • More than 3 cases in last 50 cows calved or
  • More than 2 cases per 100 cows in each subsequent month
57
Q

Sub-clinical mastitis what is the main issue, diagnosis

A
  • Mainly economic issues
  • Diagnosis by ICCC data
    ○ Get ICCC via herd testing
  • Reduced milk yield - not always
  • May have changes in milk - watery - well isn’t that clinical???
  • May palpate changes in udder - fibrosis
  • Bacterial culture
58
Q

Clinical pathology for evaluation of mastitis list 6

A
  1. Milk culture
  2. ICCC
  3. BMCC
  4. RMT (rapid mastitis test)
  5. Conductivity (built into milking set-up)
  6. NAGase (similar to rapid mastitis test but have different reagents)
59
Q

Milk culture when use, why and technique

A
  • Clinical cases
  • Sub-clinical - based on ICCC and other tests such as RMT (rapid mastitis test)
  • Antimicrobial sensitivity
    Technique
  • Wear gloves
    1. Clean teat - 70% alcohol, front teat clean first
    2. Collect front teats firsts
    ○ Sub-clinical: 4 quarter teat collection all in the same bottle
    ○ Clinical: just collect from clinically affected teat
    3. Milk a few squirts onto ground first
    4. Hold bottle at 45 degree angle
    5. Even amount of milk from each quarter
    6. Replace cap and wash hands -> with cap hold upside down to prevent contamination
60
Q

Milk culture which cows to culture, what need to do with samples after collection what does this affect and why no growth for some

A
  • If high number of high ICCC cows, collect samples from these
  • If high number of clinicals, collect theses
    Freezing of samples
  • All pathogens survive freezing (except nocardia)
  • Freezing increases detection of staph aureus
    No growth
  • 10 to 40% of cultures may not detect bacteria
    ○ Eliminated from udder
    ○ Concentration too low
    ○ Antibiotics
    ○ Unusual pathogen (anaerobe, mycoplasma, fungi) - need specialised cultures
    ○ Non-bacterial cause
61
Q

ICCC what cells normally present, normal count, when increase

A
  • Somatic cells are present in normal milk
  • Epithelial cells and mononuclear leukocytes
  • Usually in the order of 100,000 cells per mL
    INCREASE
  • after calving (fall below 300,000 within 5 days)
  • end of lactation
  • Infection - On average 3.8 times higher than non-infected cow - Over 250,000 cells per mL for a 4 quarter sample suggests infection in at least one quarter - Cow with one count over 250,000 cells/ml, consider infected for entire lactation
62
Q

ICCC when done on farm, uses and if high incidence in heifers and older cows what suggests

A
  • Many farms HERD test cows monthly or bimonthly for production and milk composition (about 40% of Australian farms)
    USES
    ○ Can be used to manipulate BMCC’s
    ○ Can be used to identify sub-clinical cows
    ○ Can be used to identity clinical cows
    ○ Using to treat cows
  • Unrewarding unless strep. Agalactiae
  • Heifers have high incidence of mastitis if over 20% have ICCC’S over 250000 during lactation
  • High incidence in heifers suggest spread of mastitis
  • High incidence in old cows but heifers infection free then infection not spread
63
Q

BMCC how used when should seek advice and production relation

A

Somatic cell count taken from bulk tank
- Used to form payment scales by milk factories
- Premium paid if milk produced under 200,000 or 250,000 cells/mL (depending on factory)
- Severe penalties if milk produced over 600,000 or 750,000 cells/mL depending on factor but considered poor if >400,000
- Should seek advice if:
○ Over 250,000 for 6 months
○ Receive penalty payment
Production
○ If BMCC increasing, production will be decreasing
○ 2.5% for every 100,000 above 200,000 cells/mL

64
Q

List 6 treatment options for mastitis

A
  1. Frequent stripping -> don’t stop milking
  2. Antibiotics
  3. NSAIDS’s
  4. IV fluid
  5. Oral fluid
  6. Remove teat from gangrenous quarter
65
Q

Intramammary and systemic antibiotics when used for mastitis

A 
Intramammary antibiotics 
- Effective in most cases of mastitis 
- Aseptic technique 
- Insert 2mm
- Identify cow 
Systemic antibiotics 
- Need to cross blood-milk barrier 
- Penethamate hydroiodide is hydrolysed to benzyl penicillin in the alveoli
66
Q

Antimicrobials for mastitis, what gets higher cure rate, which pathogens respond to treatment when and if no response what can you do

A
  • Combination of parenteral and intramammary may result in higher cure rate
  • Cure rates are dependent on pathogen
    ○ Staph aureus poor during lactation
    ○ Strep agalactiae very good
    ○ Strep uberis variable - can be difficult to cure
    If no response to treatment
  • Treat for longer
  • Try different antibiotic regime - culture
  • Dry off quarter
  • Chemically dry off quarter - infusing copper sulphate
  • Dry off cow - DCT
  • Cull
67
Q

Gangrenous mastits treatment options

A
  • If lost sensation in that teat -> just remove the teat
  • Systemic infection so need to treat systemically
    ○ IV - antibiotic and anti-inflammatory and possible IV fluids
    Another infected quarter -> give oxytocin -> promotes cow to let down milk
68
Q

List 3 ways the milk machine can lead to mastitis

A
  1. Failure of pulsation - can lead to damage to teat orifice
  2. Fluctuations in vacuum - contamination of teats with milk from other teats allowing transmission of bacteria
  3. Poorly maintained milking plant - can harbour bacteria
69
Q

Pulsation of milk machine what are the phases and liners what is important for mastitis

A

Pulsation
- Maintains circulation in teat
○ If issue then possibly getting milk pushed back to the teat causing damage
- Milking phase -> liner open - pulsation chamber at vacuum pressure - teat at this pressure
- Massage phase -> liner collapses (pulsation chamber at atmospheric pressure)
Liners
- Massage of teat
- Need to be replaced every 2000 -2500 milkings
- Matched to shell
- Worn liners carry bacteria and may not provide adequate teat massage -> due to cracks

70
Q

List and briefly describe 5 ways milking machine contributes to mastitis

A

1) act as fomite - staph aureus passed to next 6-8 cows
2) impaired teat condition - damage to liners, pulsation, high vacuum
3) increased colonisation of teat canal - lipid layer removed during milking, liners, pulsation failure
4) impact forces - Liner slippage can cause air to enter the claw at speeds up to 60km/h
○ This air can carry particles into open teat canals - responsible for 10-15% of new mastitis infections
§ Actually moves the air particles into the other teat not the teat that has slipped
- caused by: Worn liner, wet teats (farmers cleaning the dirty teat before milking)
5) leaving residual milk - undermilking due to poor liners

71
Q

What is important about milking technique for mastitis and how to reduce incidents

A
  • Spread of contagious mastitis occurs at milking
  • Entry of environmental bacteria into the teat canal often occurs at milking
    Milking Technique
  • Cows should enter shed willingly -> stress
  • Strip 3 to 4 squirts of milk to detect mastitis
  • Place cups onto clean (sometimes better to leave if cannot dry) dry plump (ready to be milked) teats
  • Avoid excessive air admission putting on cups
  • Avoid over milking and machine stripping (yanking the cups of the cow)
  • Allow cluster to “fall off” after vacuum broken
  • Milk mastitis cows last
72
Q

What is the aim of teat disinfection the two techniques and which is better and what is a good indicator of poor teat disinfection and what added for teat condition

A
  • Contagious pathogens found on teat liners 6 to 8 milkings after infected cow has been milked
  • Teat disinfection aimed at killing pathogens and improving teat condition
    Technique
    1. dipping - better result more time consuming
    2. spraying - easier but poorer results
  • Corynebacterium bovis in milk samples a good indicator of poor teat disinfection
  • Emollients added to disinfectants to keep teats soft and supple
73
Q

Teat condition how important for mastitis, how assess and what can influence

A
  • Very important part of mastitis control
  • Condition should be assess each milking
  • If mastitis a problem, score 20% of herd to determine whether teat condition a problem
  • Vacuum levels, liners, pulsation etc can all influence teat condition
74
Q

Dry cow management how long, why done and the 2 types

A
  • Minimum of 6 weeks required to allow udder tissue to regenerate
  • With no dry period milk production will be reduced in following lactation (seeing contray evidence to this fact)
  • A keratin teat plug seals teat canal at the start of dry period -> sturdier than other seal throughout lactating
    ○ Formation of keratin plug aided by DCT (dry cow therapy)
    1) antibiotic
    2) teat sealant
75
Q

Antibiotic dry cow therapy what is the aim, better with what bacterial cause and what need to consider

A
  • treating infections either not cured or not detected during lactation
  • reducing number of infections over dry period
    § Effect of antimicrobial
    § Formation of keratin plug
    ○ DCT gives high cure rates because a high dose of sustained release antibiotic is delivered to each quarter
    § Better with staph aureus HOWEVER need to consider WITHHOLDING PERIOD
76
Q

Teat sealant dry cow therapy what does it provide and not do, cost and what is important

A

PROVIDES
- physical barrier to prevent infections over dry period (100days)
- Prevention of mastitis in heifers (haven’t been in milking shed yet) - given one month before calving (one syringe/teat)
DO NOT CURE INFECTIONS
- Hygiene is really important -> don’t want to introduce bacteria and then seal it in

77
Q

Management of dry cows which cows should be dries off, where place and when don’t bring back into milking shed

A
  • Cows producing <5L/day should be dried off
  • Cows producing > 12L/day should be managed so that production drops below 12L before drying off
  • Dry off and place cows in a clean and dry paddock and monitor daily for a week
  • Do not bring them back into milking shed for at least two weeks - automatic let down will kick in BAD
78
Q

List the 7 ways to manage mastitis

A

1) monitoring for mastitis via milk cultures, ICCC, BMCC, rapid mastitis test, NAGase test
2) treating clinical and subclinical infection
3) Looking at milking machine for faults
4) looking at milking technique for faults
5) scoring teat condition to see if that an issue
6) dry cow therapy - how conducted does it need to change
7) CULL COWS - with 3 or more clinical cases in lactation - not a long term fix

79
Q

Staph aureus causing mastitis reservoir, spread, presentation, treatment how easy and when

A
  • Reservoir - infected udders and skin of teats (Teat end damage)
  • Spread at milking by contaminated milk - all milking cows susceptible (esp. with teat sores/teat end damage)
  • Found on liners 6 to 8 cows after an infected cow is milked
    Presentation
  • Persistent sub-clinical infection generally but anything from that to sub-acute gangrenous
    Treatment
  • Very difficult to cure with antimicrobials
  • Very difficult to cure during lactation - dry cow therapy important - gives higher cure rates
  • Resistant to many antibiotics
  • Best results with young newly infected cattle
80
Q

Staph aureus control list the 7 steps/options

A
  1. Culture 20 cows if possible
  2. Identify chronically infected cows by use of cell counts
  3. Correct machine and milking problems
  4. Teat disinfection
  5. Separate high cell count cows
  6. Blanket DCT
  7. Cull chronically infected cows
81
Q

Strep agalactiae causing mastitis characteristics, presentation and treatment

A
  • Obligate parasite, however can survive on milking machines, milker’s hands and clothes
  • VERY RAPID SPREAD
  • Infected cows shed very large numbers of bacteria
    Presentation
  • Causes very high rate of clinical mastitis
  • Causes sub-clinical infections as well
  • Can cause plate count failure
    Treatment
  • usually very effective during lactation - Penicillin sensitive
  • DCT will cure up to 100% of infections
82
Q

Strep agalactiae control program list the 6 steps/options

A
  1. Identify bacteria with up to 20 milk cultures
  2. Farmer must be prepared to make changes with machines/milking techniques
  3. Thoroughly investigate
    ○ Milking technique
    ○ Milking machines
    ○ Teat disinfection
  4. Separate cows based on ICCC and clinical mastitis status - It may be economical to treat all or part of herd during lactation - Blitz therapy
  5. Use DCT on entire herd
  6. If cows carried through, treat them while others are dry
83
Q

Strep dysgalactiae characteristic, where found and control program

A
  • Considered to be environmental as well as contagious
  • Found on teat skin, especially on sores or cracks
  • Control program as for other contagious bacteria
84
Q

Mycoplasma spread and main issues

A
  • Spreads very rapidly from cow to cow
  • Hard to culture -> need specialised culture
  • Milking hygiene problems are risk factors
  • Response to treatment very poor
  • Often destroys milk production in cows
    ○ Often need to cull up to 75% of cows infected
85
Q

What are the 2 minor pathogens for contagious mastitis and what associated with

A
  1. Corynebacterium bovis
    ○ Indicator of teat disinfection problem
    ○ Not associated with clinical mastitis but can cause sub-clinical infections of teat canal
  2. Coagulase negative staphs
    ○ Occasionally cultured in milk of high ICCC cows
    ○ Not usually associated with clinical mastitis
86
Q

Strep uberis causing mastitis where found, factors that increase infection and presentation

A
  • The leading cause of clinical and subclinical mastitis in Australia
  • Found in all areas of the cow’s environment including muddy and faecal contaminated areas
  • Shed in the faeces of infected cows (can survive up to 2 weeks in manure/mud)
  • Putting machines on WET and/or DIRTY/MUDDY teat will increase incidence
    Presentation
  • Usually causes CLINICAL mastitis and can have very high incidence rates on farms
  • May cause BMCC penalties in early lactation
  • ## Some infection become chronic
87
Q

Treatment options for strep uberis mastitis

A
  • Treat early
    ○ Refractor cases are very difficult to treat
    ○ Some strains more resistant to treatment -> do sensitivity testing
  • Treat cases aggressively based on sensitivity
  • Combination of intramammary and parenteral antibiotics needed
88
Q

Control for strep uberis mastitis what are the 5 main options

A
  1. Reduce contamination
    ○ Calving pads/paddocks
    ○ Laneways
    ○ Water in dairy
  2. Put cups on clean dry teats
  3. Reduce lead feed energy intake if dry cows are running milk
  4. Teat spray cows prior to calving
  5. Milk cows as soon as possible after calving
    ○ Strip milk from all quarters every milking for one week
    ○ Consider predipping
    ○ Milking machine
    ○ Vat disinfection post milking
    ○ Dry cow therapy -> long acting product plus teat sealant to provide immediate seal
89
Q

Coliform mastitis which organism is most common, how infection occur, which cows most at risk and how disease occurs

A
  • E.coli most common
  • Teat skin is contaminated in the environment
  • Infection may occur any time including milking
    High risk
  • around time of calving
  • Induced cows, or those suffering milk fever
    How occurs
  • Most infections localised in teat sinus, disease is caused by toxins
  • Toxins can cause serious systemic disease
90
Q

Treatment and control of coliform mastitis

A
  • Mild cases may be treated by frequent stripping of quarter with the air of oxytocin
  • More severe cases systemic antibiotic, anti-inflammatory and fluid therapy - aggressive
    Control similar to strep uberis - hygiene
91
Q

Pseudomonas aerguinosa mastitis where found, presentation and treatment

A
  • Isolate from water supplies, including rubber hoses
  • Contamination usually in the dairy
    ○ Too much water on teats
    ○ Water contamination of intramammary preparations and DCT
  • Very sick cows - often die
    ○ No antibiotics registered for use in cattle have efficacy against this bacteria
92
Q

Arcanobacterium pyogenes where found, how spread, treatment and control

A
  • Part of summer mastitis complex seen in Europe during dry period
  • May be spread by flies
  • Not responsive to treatment
  • Many cases do not cause systemic signs
  • Blanket dry cow therapy or Cull
93
Q

Condition score dairy cattle, what is the numbering, important numbers and how to score

A 
- Dairy Cattle score 1-8 in Australia
○ But very few 1,2,7,8 so in practical terms scores are between 3 and 6 - thin 3 fat 5 
- 2-step “hands-off” scoring method only takes seconds
1. Look closely at area between tail and pins
a. deeply sunken 
-> 2. are pins hollow 
-> yes - 3, no - 2.5
b. suken
-> 2. backbone 
-> bumpy 4, flat 4.5
c. slightly sunken
-> 2. depression between hip and pin
-> Up-shape - 5, shallow - 5.5, flat - 6
d. filled in (same as slightly sunken)
94
Q

Vaginal exam of dairy cow what looking for, what can use

A
  • Colour of mucous membranes
  • Speculum or “metricheck” later on
  • Freemartins/vaginal disease
  • Uterine disease post – calving
95
Q

What are the 3 main congenital conditions of the dairy cow reproductive tract

A

1) segmental aplasia of paramesonephric (mullerian) ducts - ○ Uterus unicornis - just one uterus
○ Uterus didelphys - two cervixes
○ Persistence of the hymen
2) freemartins
3) cysts of gartners ducts - look abnormal but doesn’t affect fertility

96
Q

Freemartins how common, what is it, how occurs and what is always missing in teh female calf

A

○ Most commonly recognised non-inflammmatory condition of tubular tract
○ Mixed sex twins result in an infertile female
○ 95% incidence
○ Fusion of chorio-allantois of each twin, with common blood supply
§ antimüllerian duct hormone and testosterone secreted by the male inhibit development of the female tract
§ It’s normal to be Female
§ Hormones prevent female development in Males
○ Cervix always missing

97
Q

How to diagnose a freemartin female as a calf and yearling

A 
§ Calves – Vaginal length
□ 5-8cm compared with 10-15cm
□ “Thermometer case test”
§ Yearlings
□ Pregnancy diagnosis – can’t find uterus
□ Synchrony – can’t insert CIDR
98
Q

What are the 4 main defence mechanisms of the uterus and how can inflammation occur

A 
Defence mechanisms
○ Physical barriers – vulva, vestibular seal, cervix
○ Oestrogen at oestrus, enhances removal mechanisms:
§ uterine contractions,
§ flow of mucus,
§ action of cilia,
○ uterine contractions (less effective with age)
○ chemotaxis – attracts leucocytes
- Parturition – contamination from:
○ Yards
○ Dystocia (Farmers and Vets!)
○ Damage to tract
○ Retained foetal membranes
○ Relaxed and stretched vulva
○ 3rd degree perineal laceration
99
Q

What are the 4 main diseases of the uterus

A
  1. Retained Foetal Membranes (RFM)
  2. Acute Septic Metritis (puerperal metritis)
  3. Endometritis
  4. Pyometra
100
Q

Retained foetal membranes how common, defined as what are the 3 main steps involved with expulsion of membranes and therefore risk factors for this to occur

A
  • Common condition of cattle -10-15% of calvings on some farms
  • “retained” = not expelled within 24 hours
  • 3 main steps involved in expulsion of the membranes:
    1. Maturation of the placenta
    2. Exanguination of the foetal side of the placenta after the blood supply is cut off (which causes physical shrinkage)
    3. Uterine contractions (causing distortion)
  • Risk Factors
    ○ Slow calvings, dystocia (slows exanguination)
    ○ Low energy (causes slow calvings!)
    ○ Low Calcium (smooth muscle contraction)
    ○ Infection (slows maturation)
101
Q

Retained foetal membranes are they normally sick, when to treat and how

A

Most cows with RFM are not sick, If so probably has concurrent metritis
Treatment
- If placental separation has not occurred, removing them can cause bleeding and scarring
- Therefore, if the cow is not systemically ill, wait 5-7 days
○ Manual removal by pulling gently through cervix controversial
○ Wait until placental separation has occurred before removal

DVM 3 - 1 (33 decks)

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