Cattle Flashcards
SCC
* increased incidence in unpigmented skin surrounding the eyes e.g. eyelids
* Herefords over represented– selective breeding aiming to reduce incidence
* can invade underlying tissues and become ulcerated
** Treatment: immediate sale for slaughter if tumor is less than 2 cm, removal of tumor with a view to subsequent sale and slaughter, surgical eye ablation, euthanasia (illegal to put cattle with SCC larger than 2 cm in Victorian saleyards– up to 2 cm that are not bleeding or discharging may be put to the saleyard– if less than 3 cm then owner’s risk of non payment)
Surgical excision of SCC of the eye in cattle
* LA upper and lower eyelids and deep into the orbit tissues
* first incision around the upper eyelid– remove eyelid tissue avoiding ingrown eyelashes and complete removal of tumour tissue– but also leave enough skin for closure
* Second incision is around the lower eyelid
* Can suture the eyelids closed before commencing the first incision
* Dissection of the orbital tissues and musculature is next– optic nerve and eye removed
* Dead space left constitutes significant infection risk– antibiotic ointment (cloxacillin) liberally placed in the empty orbit before closure (some also use sterile packing material removed later via the medial canthus)
* Remove excess blood from the skin and applying anti-fly topical spray
Who is commonly affected? Prevention?
Infectious bovine keratoconjunctivitis in cattle
** +/- photophobia and blepharospasm
* Moraxella bovis (causative agent)- toxins produced by organism cause inflammation and ulceration of the cornea (and conjunctiva)
* Outbreaks can occur in hot, dusty conditions, particularly if animals have been yarded
* Flies aid in spread
** Commonly young cattle, 5-10% of a group affected (can be 80%), if not rapid or effective treatment animals left with corneal scarring (opacity) that can reduce sight…. short immunity to disease in recovering cattle
** Piliguard- vaccine that prevents the bacteria attaching to the surface of the eye by their pili (3 to 6 weeks before summer risk period & re-vaccinate annually)
(pink eye) (corneal opacity, corneal ulcer, vascularization of the cornea part of the inflamm/ immune response, severe: eyeball rupture)
Treatment of Infectious Bovine Keratoconjunctivitis
* Cloxacillin eye ointment
(1/4 to 1/2 of 3 g tube per eye)
*Repeat at 48 or 72 hours
* Treat both eyes
* Can also inject procaine penicillin into the bulbar conjunctiva
* Can also supplement topical treatment with parenteral oxytetracycline
What are the 9 habits/ factors that might affect pregnancy rates in Australian Beef herds?
- Calving pattern- short calving pattern 6-8 weeks!!! (need to start joining 3 months after the start of calving to calve at the same time next year): cows calve, post partum anoestrus 30-60 days, cows joined 50-70% conception rate, cows joined again 50-70% conception rate
- Heifer critical mating weights (later calved heifers will be 13-14 months at joining- nutrition is critical)
- heifer weaning (minimum age- 100 days from when last calf was born, maximum 6 months. If condition score drops to 2.5, immediately wean calves)
- heifer nutrition
- parasite control
- reproductive diseases
- selection of heifers for joining- retaining more heifers creates a younger herd- retain 30%; younger is better less cancer & grass tetany, BW peaks at 7-8 years, weaning weights of calves decline in older cows, cow value declines after 6-7 years
- Oestrus synchrony
- Pregnancy Diagnosis
What are features of a highly fertile beef herd?
* Calving pattern 8 weeks in cows and 6 weeks in heifers
* 70% of females calve in first cycle
* Calving rate > 95%
* Use highly fertile serving capacity bulls
* Heifers calve down as 2 years old (need to reach appropriate weight at 15 months of age)
* Heifer dystocia rate
* High heifer retention rate enabling cows to be sold at 8 years old having reared their 6th calf
When do you preg test heifers? Cows?
Heifers 6-8 weeks after joining finishes
Cows at or just before weaning
When is a good time for rectal pregnancy diagnosis in cows?
* At 16 weeks, cotyledons are 10 cent coin size– a good point for rectal pregnancy diagnosis
What are important consideration in deciding to use a bull?
EBVs regarding calving ease, gestation length, and birth weight, scrotal size, 200-600 day weight, mature cow weight, milk
* genetic diseases- lurking recessive disorders
How long does it take to note an insult that stop spermiogenesis?
4 years
What can cause sperm abnormalities?
Transport, diet, temperature, lameness, disease, stress, toxins
How many cows can/should a bull (beef and dairy) handle?
Can handle: - Beef - 50
- Dairy- 30
Should you ever run bulls in groups bigger than 3?
Yes, but you have to get them used to each other and sort out a pecking order. Similar age and size.
What vaccinations should bulls have?
* 5 in 1 (Clostridial diseases), Lepto, Pestivirus, Vibriosis, Campylobacter (if they are in an area that has it, not Tasi)
You are called to a beef farm because a heifer is having trouble calving. This is the 8th heifer out of a group of 50 that has had trouble this year. What advice can you give to the farmer about the prevention of heifer dystocia in the future?
* Minimize calf size
* Maximize dam size
* Low birth weight bulls
* Make sure heifers grow properly- do not have parasites impeding growths
* Ensure calving pattern is right
What is the definition of a fertile bull? What is a sub-fertile bull?
* 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- 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
What is bull reporter?
Provides standard certificates for Veterinary Bull Breeding Soundness Evaluations
What are the 5 components of the VBBSE?
- Scrotum
- General Physical Examination
- Crush Side Semen Evaluation
- Serving Ability Testing
- Semen Morphology Testing
What is a VBBSE?
* Measure of risk– “no risk factors for reduced fertility were identified for this part of the VBBSE examination”
What does “Qualified” on a VBBSE mean?
* Not all attributes for this component were consistent with ACV standards but these abnormalities may not necessarily preclude the bulls use.
What does a “cross” mean for a VBBSE?
* 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.
What does the scrotal circumference reflect?
* Reflects daily sperm output
* Can indicate puberty (>27.5 cm)
* Highly heritable & repeatable
* Related to age at puberty in heifer calves
What are the general scrotal sizes in bos taurus and bos indicus bulls at 12-15 months, 18 months, and 2 years and older?
What are the three common diagnoses of testicles in bulls?
* Unilateral hypoplasia/degeneration (one is 20% smaller than the other)
* bilateral hypoplasia/degeneration
* Epididymitis (seminal vesiculitis, tumours, abscesses, spermatocoeles, spermatic granulomas)
What is a sperm granuloma?
* when one of the seminiferous tubules bursts–>noxious substance when it gets into the tissues, prevents passage of sperm out of the system
* usually painful
When would you suspect orchitis?
One testicle is larger and hard as a rock
What is a varicocoele?
One of the blood vessels becomes blocked or bursts in the pampiniform plexus
* if this occurs end up with toxic sperm because lack of thermoregulation
What is urolithiasis?
* blockage of the penis with urine build up
What is a preputial prolapse?
* Anatomical faults predisposing to prolapse (most Bos Indicus breeds)- long pendulous sheath, large preputial orifice, absence or poor develoopment of the retractor prepuce muscles
** prepuse injuries are one of the most important causes of infertility in bos indicus and bos indicus derived bulls in northern Australian herds
Papillomas of the penis- common in 1-2 yos
* can be spread sexually, unsuitable for mating until healed
Persistent frenulum
Penile haematoma, can occur in scrotum as well
* Balanitis- inflamm of the penis
* Posthitis- inflamm of the prepuce
* Balanoposthitis- inflamm of both
X high risk
(Bottom photos is ulcerative posthitis, caused by C. renale- occasionally seen in bulls and is often associated with high protein diets– increased urea content of urine)
What is prepuce stenosis (phimosis)?
* prepuce stenosis is common in all breeds of bulls– commonly follows injury and infection of the interal lamina of the prepuce at mating–X because high risk
How do you collect semen?
* Rectal massage or electro- ejaculation
* through a funnel into a test tube (cleaned, dry and free of spermatotoxic agents)
Why is condition score so important in cattle?
related to disease and fertility
How do you condition score a cow?
Look at tail, hip, pin bone
** Is the area between the pin bone and the tail deeply sunken, sunken, slightly sunken or filled in?
* If deeply sunken, look at the inside of the pins (between the tail and the pins), are they hollow?
* look at the back bone… is it bumpy or sharp ridge?
Semen Eval and ACV Crush Side Semen Standards?
Evaluating semen
* mass activity at 40 x (no cover slip)
* individual motility at high power (diluted semen, +/- cover slip)
** Concentration- density of 1 or more– 200 sperm per 100 x field under cover slip
* absence of blood or urine staining
* Absence of flocculant material and large numbers of pus cells
* Percent of progressively motile
- Tick- 60% +
- Pass- 30-59%
- Fail
Common congenital conditions in cattle
* Segmental aplasia of the paramesonephric (mullerian ducts): uterus unicornis, uterus didelphys, persistence of the hymen or Freemarints
What is a Freemartin? Diagnosis?
* Cervix is always missing
* Fusion of chorio-allantois of each twin, with common blood supply– antimullerian duct hormone and testosterone secreted by the male inhibit development of the female tract
* Mixed sex twins result in infertile female
* Calves- vaginal length– 5-8 cm compared with 10-15 cm…. thermometer case test
* Yearlings- pregnancy diagnosis, can’t find uterus… synchrony can’t insert CIDR
How long after calving?
uterus 12 hours after calving
How long after calving?
* 30 days after calving
How can you tell a bull has successfully achieved intromission?
Ejaculative thrust
What is serving capacity? Serving ability?
* 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 (e.g. corkscrew penis) 1. Erection, 2. Intromission 3. Ejaculation
How is sperm morphology conducted?
* Sent to a lab
* Should have 70% normal sperm for AI, 50-70% normal sperm acceptable for paddock mating (not more than 20 % uncompensable; not more than 30% of other individual abnormalities)
Discuss the pros and cons of performing serving ability testing as part of a pre-mating examination of bulls on a Victorian beef farm?
What are the first assessments made on the tail end of a cow?
* Collect urine, take temp, coccygeal pulse, check vulval mucous membranes, RR and nature, condition score, abdominal size and contour, assess skin and hair, check general conformation
What is endometritis? Differentiation from metritis? Clinical signs with endometritis? Diagnosis? Treatment?
* Inflammation of the endometrial lining of the uterus without systemic signs, associated with chronic postpartum infection of the uterus with pathogenic bacteria– pus is white (vs. pus is brown and smelly = metritis)
* Clinical signs: white purulent discharge in uterus (or vulva), failure to conceive, massive infiltration of neutrophils into uterus, rarely get sick
* Diagnosis: Visually (pus), metricheck, speculum, vaginoscopy (1-2 weeks before mating start date if you’re doing the whole herd)
* Treatment: Controversial because they get better with time– so delay treatment until 2 weeks before planned start of joining… “VVing”– Visual vaginals the herd OR just at risk cows; Treatment is not parenteral, it is not a systemic infection… administer INTRA- UTERINE; Cephalosporin– covers the bacteria causing endometritis BUT DOES NOT ACCESS THE UDDER
When the tail end is revisted, what do you look at?
* Examine udder, teats, and milk
* Vaginal exam
* rectal exam
* assess limbs and feet
What do ovaries feel like in anoestrus, CL, follicle, cyst, neoplasm?
What are the 3 types of ovarian cysts seen in cows?
- Follicular cysts- nyphomaniac behaviour because they secrete oestrogen or androgenic steroids
- Luteal cysts- thicker walled- secrete progesterone– affected cows are anoestrus
- Cystic corpus luteum- no change in oestrus cycle, incidental finding
What can cause contamination and therefore inflammation of the cow uterus?
* Parturition: yards, dystocia (farmer and vet), damage to tract, RFM, relaxed and stretched vulva, 3rd degree perineal laceration
Defence mechanisms to uterine inflammation?
* Physical barriers: vulva, vestibular seal, cervix
* Oestrogen at oestrus- enhances: uterine contractions, flow of mucous, action of cilia
* Uterine contractions
* Chemotaxis- attracts leucocytes
Four most commone diseases of the uterus in cows?
- RFM
- Acute Septic Metritis (puerperal metritis)
- Endometritis
- Pyometra
What classifies RFM in a cow? Treatment? Risk factors?
* not expelled within 24 (10-15% on some farms)
* Treatment: no treatment if cow is not showing systemic signs for at least 3-4 days (most are not sick)
* Risk factors: slow calvings, dystocia (slows exanguination of the foetal side of the placenta); low energy (causes slow calvings); low Calcium (smooth muscle contraction to push out the placenta); infection (slows maturation of the placenta)
Main players in the bovine oestrus cycle
If the cow is ill with an RFM, what does she also probably have?
Acute Septic Metritis (puerperal metritis)
All cows are infected with metritis after calving, however when does it become abnormal? How long is lochia discharged postpartum? What are potential consequences of metritis? Signs and symptoms? Treatment?
* Uterine fluid should be negligible 2-3 weeks after calving
* Lochia (uterine fluid, placental fragments, caruncles) discharged for 2 weeks postpartum
* Fluid from the uterus may ascend into oviducts causing salpingitis and severe adhesions, preventing ascent of sperm and descent of the ovum to the site of fertilization; endometritis
** Signs and symptoms: high temp, depressed, foul smelling reddish coloured uterine fluids +/- membranes
* Treatment: Oxytetracycline hydrochloride + parenteral antibiotics if pyrexic
Describe two phases of the bovine oestrus cycle
Speak through the luteal phase
“Key to the bovine oestrus cycle”
Who are at risk cows for endometritis?
* RFMs or metritis
* stillbirth or calf dies within 24 hours
* twins
* dystocia
* milk fever
* vulval discharge
* calving induction
How can you control endometritis on a herd level?
* Nutritional problem (adequate feeding esp. postpartum)
* Reduce dystocia by selective breeding
* Ensure clean calving environment
* Reduce RFM
How is pyometra often diagnosed? Pathogenesis? Treatment?
* An incidental finding at preg testing (enlarged uterus with a doughy feel)
* Pathogenesis: chronic uterine infection–> damage to uterine wall–> does not produce PG–> CL with indefinite life span–> no oestrus activity to remove infection
* Treatment: PG- get them cycling, +/- intrauterine antibiotics (often found after joining has finished so treatment is often not undertaken)
How does PG work? What does it do?
* Acts on mature CL
* CL regression in 24 hours “If given after the first 5-7 days of the cycle, induces oestrus within 7 days in most cycling cows”
* Given by injection
(* Wear gloves)
** Can also be used to induce abortion up to about day 120
In a per-rectal examination of a cow, what you can you palpate?
*rectal wall and caudal sacs of the rumen
* bladder and left kidney
* Cervix, uterus, oviducts and ovaries
* deep inguinal lymph nodes and bony rim of the pelvis and sacrum
(cannot palpate intestines)
How does progesterone work to synchronize oestrus?
* Controls pituitary response to progesterone
* Exogenous supply prevents ovulation
* Need long term treatment (rather than a bolus)– need to synchronize drop in progesterone
* CIDR, Cue-mates and DIBS
What is OvSynch?
* GnRH on day 1– causes ovulation and new follicular wave, or there is a new follicular wave anyway
* PG 7 days later- luteolysis: CL’s should have had time to form
* GnRH 48 hours later: cause ovulation “sooner”
* AI cows 12- 24 hours later
GnRH actions on oestrus synchronization
Outcome of follicular cysts? Treatment of ovarian cysts:
Persist for up to 70 days, regress replaced by normal follicle (10-50%), undergo atresia and replaced by new cyst
* Treatment: manual rupture (risk of haemorrhage and adhesions), GnRH IM causing release of LH and luteinisation of the cysts (not ovulation), Progesterone (P4 to deprive the cyst of LH), Ovsynch program + P4 device (treats luteal and follicular cysts)
Bovine oestrous cycle– when does it start and end? Pause? Length? How long is oestrus?
* Polyoestrus- puberty until death
* Pauses during pregnancy and post partum anoestrus
* Cycle length 18-24 days
* Oestrus lasts 2 hours and 2 days
Where does a CL come from? What does it do? Where does it go?
* CL arises from recently ovulated follicle
* Produces progesterone (P4) until PG then luteolysis
* After prostaglandin- it regresses- becomes a corpus albicans and shrinks to nothing
Main areas of assistance vets provide on a dairy farm
Where does a follicle come from? What does it do? Where does it go?
* Follicular waves… recruitment, selection, dominant follicle
* Grows in response to FSH/LH, produces oestrogen
* LH surge makes it ovulate, “Graafian Follicle,” Morphs into CL
Brains contribution to the oestrus cycle in a cow
* Hypothalamus- responds to oestrogen–> releases GnRH
* Key to the oestrus cycle:
- hypothalamus response to oestrogen
- Negative feedback if P4 present
- Positive feedback if P4 is absent
* Anterior Pituitary- responds to GnRH–> produces FSH and LH
At 16 weeks, how big is the foetus?
10 cent piece size
When is the foetus 10 cent piece size? Fremitus? When can’t you tell the pregnant from non-pregnant side?
What hormones does the uterus produce (relevant to the oestrus cycle)? When? What about during pregnancy?
* Prostaglandin at about d17 if not pregnant
* Progesterone during pregnancy
What is the difference between immature CL and mature CL? During what phase is the CL mature?
Immature CL not producing as much P4 and do not respond to PG
** Dioestrus (d 6-7- CL mature)
What is the submission rate? Conception rate? Pregnancy rate? 6 week in calf rate? 100 day in calf rate? Empty rate?
What is happening to the follicles during the luteal phase?
Follicular waves–> oestrogen–> suppresses FSH (because P4 is around)–> follicles need FSH–> after 8 days follicle regresses and new cycle starts
What ends the luteal phase?
* PG from the uterus– maternal recognition of pregnancy (trophoblast secretes interferon tau)
How can you tell the gestational stage?
Possible causes of bovine abortion
Cows recommencing cycling after calving depends on what?
* NUTRIENT STATUS, sucking, season, presence of bulls
Why do we want to control the oestrus cycle?
* To get cows cycling (anoestrus or NVO- non-visible oestrus)– usually apply some progesterone and then remove it
* Synchronize cows (batch treatment of cows, repo and management benefits)
* Increase fertility
* Embryo transfer (superovulate animals)
What is Leptospirosis? What are the cow adapted? Pig adapted?
* Gram negative, likes moist environments, zoonotic, notifiable, affects many species
Maintenance hosts: “host adapted species,” chronic disease but not usually severe, persists in kidney and genital tract, low antibody response, effective transmission
Incidental hosts: all other species, acute disease, sporadic transmission with incidental host species, significant antibody response, lots of bacteria in tissues
* L. hardjobovis- cattle adapted, chronic disease (cows are asymptomatic), sporadic abortion, mastitis
* L. pomona- pig adapted, acute febrile disease- sick cows, haemaglobinuira, icterus, abortion, mastitis, death in calves
** HUMANS are not host adapted to either!!**
What are the drugs used to control the bovine oestrus cycle?
* PG, P4, Oestrogens, GnRH
2 Prostaglandin protocols in cows
* Cycling cows only - no effect if in post partum oestrus
* “Modified Why Wait” : 5-7 days of AI then PG (saves a week, can treat NVOs at day 14)
* “Double PG Programme” : 2 shots of PG 14 days apart (inseminate the whole herd in a week, use tail paint to ID where cows are in the mgt cycle)
How does oestrogen work in synchronizing the oestrus cycle? When can you NOT use it?
* Banned for use in milking cows
* effect depends on progesterone levels
* If P4 present, starves follicle of FSH– starts new follicular wave
* After P4 drops, adds fuel to positive feedback loop of FSH and oestrogen causing ovulation
What is BVDV (Pestivirus)?
* Persistently infected calves from when dam is actuely infected in 1st trimester (40-125 days) OR when dam is a persistently infected carrier
* Most PIs die are are culled within 18 months- 2 years
* PIs are the main source of BVDV spread and maintenance– 1 hour of direct contact transmits
Neosporosis in cattle
* Neospora caninum, intestinal disease of dogs worldwide, oocysts found in dog faeces, cattle intermediate hosts, abortion in cattle, vertical transfer in cattle (transplacental)
* Abortion- 3 months to full term (most 5-6 months), sporadic or storms… fetuses die in utero: resorbed, mummified, autolysed
* Live calves: normal BUT PI! Neurological signs
What are the four most common reasons for dystocia in cattle? Options for extraction?
* manipulaton, extraction, foetotomy, caesarean, euthanasia
Tentative diagnosis? Treatment options?
* Macerated calf, Schistosomus reflexus (inside out calf)– can be born alive (shoot it or captive bolt)
** check for a twin, check cow for possible trauma
What is the Countdown Downunder (CDDU) program?
Funded by Dairy Australia- the aim of the program is to increase farm profitability and improve milk quality by reducing mastitis level in Australian dairy farms.
- All milk must have BMCC’s less than 400,000 cells/mL
- At least 90% of milk supply from Australian dairy farms must have BMCC’s of less than 250,000 cells/mL
How are farmers paid based on their milk?
Normal bovine udder
* 4 quarters each with their own teat
* Branching duct system of secretory epithelium producing lactiferous ducts which converge to form the lactiferous sinus– is continuous with the teat sinus– myoepithelial cells surround the alveoli which contract when the stimulus of milk let down occurs, forcing milk into the duct system
Protective mechanisms of teat
* Teach sphincter contracts sealing teat
* Desquamation of epithelium in canal produces fatty material with bactericidal effect
* Rosette of Furstenburg contains lymphocytes and plasma cells
Examples of contagious pathogens of mastitis
Environmental pathogens of mastitis
Clinical signs of mastitis
* Udder changes: heat, oedema, swelling, gangrene, abscess, pain (lameness)
* If systemic, signs: pyrexia, anorexia, tachycardia, absence of GIT sounds, depression, recumbent, shock
When would a dairy farm call in a vet for a mastitis problem?
Tests for mastitis?
* Rapid mastitis test (RMT)- reagent mixed with sample of milk– forms a gel if mastitic milk, changes color if pH is increased (valuable for deciding which quarters to culture from high ICCC cows)
* Conductivity- increase in sodium and chloride ions in mastitic milk therefore an increase in electrical conductivity (50% accuracy of detection of subclinical mastitis)
* NAGASE test- measures level of cell associated enzyme N-acetyl-beta-D-glucosaminidase in milk. A high level of this enzyme = a high cell count (automated, same day)
* ELISA- a direct capture ELISA of polymorphonuclear granulocyte antigen provides an estimate of cell count as low as 100,000 cells/mL
Milk culture technique
Treatment for Mastitis
* Frequent stripping- keep the teat canal viable, if you want to save it
* Antibiotics- parenteral (Mamasin- Penethamate hydriodide– stored as a powder, made up into a liquid before use) + 2mm intramammary (S. aureus- poor response during lactation, S. agalactiae very good response, S. uberis variable- can be difficult to cure)
* NSAIDs
* IV fluid
* Oral fluid
* Remove teat from gangrenous quarter
How do milking machines contribute to mastitis?
* Act as a fomite - S. aureus may be passed on to the next 6 to 8 hours
- worse if liners worn or ineffective claw vacuum/blocked air admission causes flooding
* Impaired teat condition- damaged or poor fitting liners, high vacuum, pulsation failures
* Increased colonisation of teat canal- lipid layer and keratinocytes must be removed during milking, pulsation failure may cause build up of bacteria in canal, pulsation, failure may be due to pulsators, liners, claw pieces, tubing
* Impact forces- liner slippage can cause air to enter the claw at high speed which can carry particles into open teat canals- responsible for 10 to 15% of new mastitis infections.. liner slippages are caused by worn liners, wet teats, low vacuum, heavy clusters, vacuum fluctuations
* Leaving residual milk- undermilking- reduces flushing of canal
* Failure of pulsation- can lead to damage to teat orifice
* Fluctuations in vacuum- contamination of teats with milk from other teats allowing tranmission of bacteria
* Poorly maintained milking plant- can harbour bacteria
What are liners in a milking machine?
* Responsible for massage of teat
* need to replace every 2000-2500 milkings
*Worn liners carry bacteria and may not provide adequate teat massage
Proper milking technique
* Cows should enter shed willingly
* Strip 3 to 4 squirts of milk to detect mastitis
* Place cups onto clean dry plump teats
* Avoid excessive air admission putting on cups
* Avoid over milking and machine stripping (slow milker– stick a rock on to add extra weight and will strip cups off a bit earlier)
* Allow cluster to fall off after vacuum broken
* Milk mastitic cows last
What are the disinfectants used on teats? How should you disinfect the teats? How can you test to ensure the disinfection is sufficient?
* Disinfect by dipping– use 20 mL/cow/milking if spraying… dipping use 10 mL/cow/milking if dipping
* C. bovis in milk samples a good indicator of poor teat disinfection
Blanket vs. Selective DCT
Selective DCT- if answer no to any questions.. treat cows that had clinical mastitis, cows with one or more ICCC over 250,000 cells/mL, older cows
What are the antibiotics used with DCT? What must you always consider with treating production animals?
Strep dysgalactiae as a cause of mastitis?
Mycoplasma as a cause of mastitis?
Pseudomonas aeruginosa as a cause of mastitis
Arcanobacterium pyogenes as a cause of mastitis
General treatment of mastitis, clinical case
Most likely ddx? Problems? Cause? Treatment?
* Udder oedema (or can be under her belly)- normally physiological event at calving
* Difficult for calves to suckle and machines may not attach properly
* Cause: interference with venous drainage from udder: pressure of foetus on pelvic cavity, large increase in blood supply to udder in heifers outstrips venous return
- high sodium/ potassium intakes
- hereditary
* milk let down problems + susceptible to mastitis
* Treatment: usually unnecessary, can use diurectics/ corticosteroids, Naquazone Bolus (diuretic with corticosteroid)… use diuretci after calving, induction to reduce severity (heifers), diet and control exercise for prevention
Ddx? Problem? What do you do?
Rupture of the suspensory apparatus
* Medial suspensory ligament divides udder in two halves
* Attaches udder to pelvic floor
* Can rupture either actuely or over a period of several lactations
* Rupture causes teats to splay outwards
** Problem: splayed teats difficult to milk (machines do not attach to teats properly), splayed teats more prone to environmental mastitis infections, splayed teats more prone to damage
** CULL
Photosensitisation due to high energy molecules from plant such as St. John’s Wort or buckwheat which releases free radicals in response to UV light
* Treatment: provide shaded environment, covering teats in zinc cream or black ointment, antihistamines and NSAIDs, antibiotics if infection
Teat blockage causes
Problems and causes of haemolactia?
Ddx? Problems? Spread? Diagnosis? Treatment?
Bovine herpest mammalitis- outbreaks uncommon in AUS
* Painful to be milked
* Insects can cause spread between herds
* Teat lesions site of entry to virus
* Diagnosis: virus isolation
* Treat by applying antibiotic lotion prior to milking then apply astringent following milking (iodophor teat disinfectants to minmise spread)
What is this? Who else can be infected? Spread? Treatment?
Pseudocowpox
* Paramyxovirus
* Zoonosis (milker’s nodule)
* Papular stomatitis- disease of calves
* Spreads slower than mammillitis- immunity short lived
* Need break in skin to cause disease
* Spread by milker’s hands, contaminated teat cups, biting insects
* No specific treatment- iodophor teat spray
Cowpox- exotic to Australia and rare in rest of world– spread by direct and indirect contact, erythma–> vesicle–> scabs
Condition? Cause? Problems? Treatment?
Black Spot
* Ulcerated, infected lesions of teat end– any damage to teat orifice causing eversion/ prolapse of teat canal
* Usually infected with Fusobacterium necrophorum, staph can also infect lesion
* If more than a few cases in any herd machine function should be investigated
* Scabs picked off before milking
* Painful
* Antibiotic ointment
What should you do if teat laceration?
* Assess viability of tissue- debride and disinfect area as appropriate
* Seal mucosa as healing impaired if milk seeps into subcutaneous tissues
* Intramammary antibiotics for 3 days + parenteral to prevent infection
* Hand milk for 7 days
* Suture mucosa separately with fine absorbable material 4/0
* Xylazine and local anaesthetic
Case study
Key problems from this list???
- herd composition 160 2 yo heifers, 5 lots of cattle purchased in last 2.5 years
- good computer based records and herd test every second month
- all cows blanket treated all quarters at drying off with range of DCT products for last 2 seasons
- previous season 40 cows culled for mastitis due to being unable to clear up
- used a variety of treatments– intramammaries and injectables
- changed liners every 6 months
- uses uddergard teat spray mixed daily
- milking the herd three times per day from mid-Sept to mid- Nov
- liners may not be changed often enough due to milking 3 x per day
What will you recommend with the following information?
Culture results: Strep uberis, last year Staph aureus, a few Strep agalactiae… build a new pad for calving but still have cases…. began weekly whole herd stripping and running separate mastitis herd…. how are they deciding how to differentiate? Stripping— now treating any sign of mastitis… Now Machine test done… Total : 559 cases since the start of calving
* check teat solution
* Under milking
* remember keratin plug comes out in the first strip– so you will see some solid bits– does not mean it is mastitis
** tie up the dog (stress)- won’t let down properly
* hygiene since strep uberis is the main problem…
* Also use teat sealant as strep uberis responds well
* keep count of clinical cases– saying he has had way more than he has had– so we can decide whether we do blanket or selective treatment
* Conductivity meters- but 50% accuracy
* Worm out liners, vacuum level slightly high
*minimize muddy areas
* almost changing liners a couple times a week because every 2,500 milkings and he is milking his 600 cow herd 3 times per day certain times of year
** 32 were heifers– what does that tell us about this farm?? Even with all of this management put in place, all these positive results and changes– heifers affected– it is in the environment– he has strep uberis on this farm (ENDEMIC PROBLEM– so you have to work with what you’re given)
Australian cattle mange
Two common causes of mange exotic to Australia
Secondary?
* FACIAL ECZEMA
* Pithomyces chartarum grows on pastures- dead leaf litter in warm, humid weather; sporulation after 4 days of >12 C with moisture
* Fungal spores contain Sporidesmin
* Sporidesmin> necrosis of bile ducts
* Typical photosensitisation signs: signs occur 10-14 days after exposure, severity varies but can cause acute death, subclinical cases can have significant liver damage
* Diagnosis: clinical signs and epidemiology; serum GGT (> 70 IU/L mild, > 300 moderate, > 700 severe)
* Treatment: Protect from sunlight, anti-inflammatories (and antibiotics) as support, zinc is not effective after exposure or once clinical signs become apparent
* Control: monitor paddocks by spore counts: > 100,000/g is dangerous…. provide zinc early (prior to exposure) e.g. zinc sulphate in water using automated dispensers, zinc oxide as an oral drench, BUT zinc toxicity is a signficant danger (small therapeutic margin, gastroenteritis; anorexia, decreased milk production)
** pasture fungicides available in NZ
Angiomatosis- non-neoplastic condition presenting with little knots of capillaries in various organs. It consists of many angiomas (benign tumours derived from cells of the vascular or lymphatic vessel walls (endothelium)). Rare genetic multi system disorder.
Skin diseases of calves
