Cattle Flashcards
(230 cards)
1
Q
A
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)
2
Q
Surgical excision of SCC of the eye in cattle
A
* 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
3
Q
Who is commonly affected? Prevention?
A
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)
4
Q
Treatment of Infectious Bovine Keratoconjunctivitis
A
* 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
5
Q
What are the 9 habits/ factors that might affect pregnancy rates in Australian Beef herds?
A
- 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
6
Q
What are features of a highly fertile beef herd?
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 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
7
Q
When do you preg test heifers? Cows?
A
Heifers 6-8 weeks after joining finishes
Cows at or just before weaning
8
Q
When is a good time for rectal pregnancy diagnosis in cows?
A
* At 16 weeks, cotyledons are 10 cent coin size– a good point for rectal pregnancy diagnosis
9
Q
What are important consideration in deciding to use a bull?
A
EBVs regarding calving ease, gestation length, and birth weight, scrotal size, 200-600 day weight, mature cow weight, milk
* genetic diseases- lurking recessive disorders
10
Q
How long does it take to note an insult that stop spermiogenesis?
A
4 years
11
Q
What can cause sperm abnormalities?
A
Transport, diet, temperature, lameness, disease, stress, toxins
12
Q
How many cows can/should a bull (beef and dairy) handle?
A
Can handle: - Beef - 50
- Dairy- 30
13
Q
Should you ever run bulls in groups bigger than 3?
A
Yes, but you have to get them used to each other and sort out a pecking order. Similar age and size.
14
Q
What vaccinations should bulls have?
A
* 5 in 1 (Clostridial diseases), Lepto, Pestivirus, Vibriosis, Campylobacter (if they are in an area that has it, not Tasi)
15
Q
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?
A
* 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
16
Q
What is the definition of a fertile bull? What is a sub-fertile bull?
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- 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
17
Q
What is bull reporter?
A
Provides standard certificates for Veterinary Bull Breeding Soundness Evaluations
18
Q
What are the 5 components of the VBBSE?
A
- Scrotum
- General Physical Examination
- Crush Side Semen Evaluation
- Serving Ability Testing
- Semen Morphology Testing
19
Q
What is a VBBSE?
A
* Measure of risk– “no risk factors for reduced fertility were identified for this part of the VBBSE examination”
20
Q
What does “Qualified” on a VBBSE mean?
A
* Not all attributes for this component were consistent with ACV standards but these abnormalities may not necessarily preclude the bulls use.
21
Q
What does a “cross” mean for a VBBSE?
A
* 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.
22
Q
What does the scrotal circumference reflect?
A
* Reflects daily sperm output
* Can indicate puberty (>27.5 cm)
* Highly heritable & repeatable
* Related to age at puberty in heifer calves
23
Q
What are the general scrotal sizes in bos taurus and bos indicus bulls at 12-15 months, 18 months, and 2 years and older?
A
25
Q
What are the three common diagnoses of testicles in bulls?
A
* Unilateral hypoplasia/degeneration (one is 20% smaller than the other)
* bilateral hypoplasia/degeneration
* Epididymitis (seminal vesiculitis, tumours, abscesses, spermatocoeles, spermatic granulomas)
26
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
27
When would you suspect orchitis?
One testicle is larger and hard as a rock
28
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
29
What is urolithiasis?
\* blockage of the penis with urine build up
30
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
31
Papillomas of the penis- common in 1-2 yos
\* can be spread sexually, unsuitable for mating until healed
32
Persistent frenulum
33
Penile haematoma, can occur in scrotum as well
34
\* 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)
35
36
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
42
How do you collect semen?
\* Rectal massage or electro- ejaculation
\* through a funnel into a test tube (cleaned, dry and free of spermatotoxic agents)
43
Why is condition score so important in cattle?
related to disease and fertility
44
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?
45
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
46
Common congenital conditions in cattle
\* Segmental aplasia of the paramesonephric (mullerian ducts): uterus unicornis, uterus didelphys, persistence of the hymen or Freemarints
47
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
48
How long after calving?
uterus 12 hours after calving
49
How long after calving?
\* 30 days after calving
50
How can you tell a bull has successfully achieved intromission?
Ejaculative thrust
51
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
52
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)
53
Discuss the pros and cons of performing serving ability testing as part of a pre-mating examination of bulls on a Victorian beef farm?
54
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
56
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
58
When the tail end is revisted, what do you look at?
\* Examine udder, teats, and milk
\* Vaginal exam
\* rectal exam
\* assess limbs and feet
61
What do ovaries feel like in anoestrus, CL, follicle, cyst, neoplasm?
62
What are the 3 types of ovarian cysts seen in cows?
1. Follicular cysts- nyphomaniac behaviour because they secrete oestrogen or androgenic steroids
2. Luteal cysts- thicker walled- secrete progesterone-- affected cows are anoestrus
3. Cystic corpus luteum- no change in oestrus cycle, incidental finding
65
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
66
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
67
Four most commone diseases of the uterus in cows?
1. RFM
2. Acute Septic Metritis (puerperal metritis)
3. Endometritis
4. Pyometra
68
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)
69
Main players in the bovine oestrus cycle
70
If the cow is ill with an RFM, what does she also probably have?
Acute Septic Metritis (puerperal metritis)
71
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
72
Describe two phases of the bovine oestrus cycle
74
Speak through the luteal phase
75
"Key to the bovine oestrus cycle"
76
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
77
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
78
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)
79
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
80
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)
81
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
84
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
85
GnRH actions on oestrus synchronization
86
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)
87
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
88
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
89
Main areas of assistance vets provide on a dairy farm
90
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
91
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
92
At 16 weeks, how big is the foetus?
10 cent piece size
93
When is the foetus 10 cent piece size? Fremitus? When can't you tell the pregnant from non-pregnant side?
94
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
96
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)
97
What is the submission rate? Conception rate? Pregnancy rate? 6 week in calf rate? 100 day in calf rate? Empty rate?
98
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
100
What ends the luteal phase?
\* PG from the uterus-- maternal recognition of pregnancy (trophoblast secretes interferon tau)
101
How can you tell the gestational stage?
103
Possible causes of bovine abortion
105
Cows recommencing cycling after calving depends on what?
\* NUTRIENT STATUS, sucking, season, presence of bulls
106
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)
107
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!!\*\*
108
What are the drugs used to control the bovine oestrus cycle?
\* PG, P4, Oestrogens, GnRH
110
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)
112
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
113
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
114
How do hCG and eCG work with synchronizing oestrus in cattle? When is it used?
\* eCG- mostly FSH activity: hastens follicle development, superovulation programs
\* hCG- mostly LH activity: forces ovulation, superoverulation programs
115
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
118
How can we increase Ovsynch fertility?
\* Changing the timing of the FTA
\* Maximize ovulations to the first GnRH-- start on day 5-9 of the cycle
\* Fertilizing the follicle (give eCG at the time of PG)-- increases growth of follicles, FSH prevents regression and keeps it young
\* Adding progesterone (esp. in non-cycling cows)
119
What are the 4 main programs for seasonal herds?
1. Ovsynch
2. Ovsynch + Pregnecol
3. Ovsynch + Progesterone (CIDR or CueMate)
4. Ovsynch + Pregnecol + Progesterone
120
What are the two basic types of synchrony?
\* PG synchrony
\* OvSynch
121
What are the four most common reasons for dystocia in cattle? Options for extraction?
\* manipulaton, extraction, foetotomy, caesarean, euthanasia
123
Pregnancy Diagnosis in cattle
\* Rectal palpation from 6-8 weeks (size is not a definitive pregnancy test)
\* Ultrasound from 4-6 weeks
\* Sector scanning 5- 16 weeks
\* Blood or milk tests- does not age pregnancy
124
Rectal PD signs
Suggestive signs:
\* Change in size and location of the repro tract (uterine size)
\* Detection of fluid in the uterine lumen (fluctuance)
\* Middle uterine artery enlargement/ fremitus
\* A heavy cervix
Definitive signs:
\* Palpation of the chorioallantois using the foetal membrane slip technique
\* Palpation of the amniotic vesicle
\* Palpation of placentomes (make sure you count three)
\* Palpation of the foetus
127
With ultrasound, when can you see cotyledons? What can you see at 8 weeks?
\* 16 weeks (thorax 2.5-3 diameters)
\* 8 weeks: head and legs, size = 1 diameters
128
Why preg test on a cattle farm?
\* Culling empty cows,
planning drying off, feed budget, planning inductions, retrospective mating analysis
129
Information required for PD cows
\* Cow IDs
\* Calving dates
\* Mating dates (work off this instead of PD)
131
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
132
What is embryonic loss, abortion, specific definition of premature, and stillbirth?
\* Embryonic loss- loss of pregnancy between 12 and 45 days gestation (normally seen as return to oestrus)
\* Abortion- expulsion of a foetus (alive/dead) from day 45 of gestation onwards
\* Premature- birth of a live, viable foetus \> 260 days but before full term
\* Stillbirth - expulsion of a full term foetus which died during parturition
133
How is abortion investigation conducted?
\* Requires a methodological approach
- thorough history (cases and the herd)
- physical examination (cow, foetus and placenta)
- collection of samples (cow, foetus, placenta)
\* Interpretation of results
134
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.
1. All milk must have BMCC's less than 400,000 cells/mL
2. At least 90% of milk supply from Australian dairy farms must have BMCC's of less than 250,000 cells/mL
135
How are farmers paid based on their milk?
136
What are you looking for with the placenta?
\* Possible necrosis, haemorrhage, adventitial placentation (extra, small cotyledons), ridged cotyledons, intercotyledonary thickening
137
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
138
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
140
Examples of contagious pathogens of mastitis
141
Environmental pathogens of mastitis
142
What samples are you going to take to assess an abortion?
\* Vaginal secretion, faeces, milk
\* Cotyledons, intercotyledonary area
\* (BAKS SLLAP) Foetus: brain, aqueous humour, kidney, serum/ heart blood, spleen, lung, liver, abomasal contents, peritoneal fluid
143
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
145
What is Vibriosis?
\* Campylobacter fetus subsp venerealis (CFV)
\* gram negative rod
\* Sexually transmitted after single service transmission to susceptible cows 40-75%, lives in bulls- bulls are asymptomatic carriers, lives in penile crypts, persistent in older bulls
\* Obligate parasite of the reproductive tract
\* Affects cow fertility (infected after mating but no obvious signs), fertilization occurs but EEL/ Abortion (usually 50-70 days)
\* Permanent infertility and later abortions possible, are resistant for a short period, some are persistent carriers
146
Diagnosis of Vibriosis with herd fertility pattern? Diagnosis other ways?
\* poor conception rates, lots of late cows, usually cows cease cycling first few week as they should
\* Isolate bacteria- need special media
\* Cows- vaginal/ cervical mucus swab, Culture or PCR
\* Bulls (preferable)- preputial washes or scrapings
147
Prevention and Control of Vibriosis?
\* Older bulls permanently infected, some cows persistent carriers, some become immune 3-6 months after service
\* Vaccination is curative and protective SO vaccinate ALL bulls in advance of breeding season
\* Vaccinate heifers if there is a problem
\* Use AI, Use younger bulls because less problematic
149
Diagnosis of Leptospirosis? Prevention?
\* Diagnosis: Dark field microscopy of fresh urine, paired serology, clinical signs
\* Prevention: Diagnosis is the most effective means-- they are not curative, Ultravac reduces urine shedding, Wear gloves and PPE
\* Treatment: Streptomycin: effective but banned! Oxytetracycline/ Ampicillin
150
Salmonella in Cattle
\* Notifiable, zoonotic
\* Salmonella dublin
\* Abortions sporadic
151
When would a dairy farm call in a vet for a mastitis problem?
152
Listeria in Cattle
\* Listeria monocytogenes
\* Zoonosis and notifiable
\* Spoiled silage main source of infection
\* CNS disease
\* Sporadic abortions
\* Survives cold and pH
153
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
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Milk culture technique
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Brucellosis in cattle
\* Brucella abortus- contagious abortion, not venereal-- ingested bacteria of aborted fetus, placenta, uterine discharge
\* Notifiable, exotic, zoonotic (Australia free since 89)
\* Clinical signs: abortion storms in second half of gestation, cows not sick, calves born week, RFM common (may lead to delayed involution and metritis), colonizes udder, supermammary LNs, proliferates in uterus= placentitis, endometritis, fetal infection
\* Bulls: orchitis, epididymitis, seminal vesiculitis
\* Cows become a carrier but may not abort again
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Diagnosis and prevention of Brucellosis?
\* Diagnosis: call DPI, ID bacteria- stained smears from aborted foetuses, serology mainly CFT (complement fixation test), ELISA (to discriminate between infected and vaccinated animals)
\* Control: Now eradicated, calf vaccination- strain 19 vaccine
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Diagnosis and management of BVDV?
\* Diagnosis: AGID (detects antibody), ELISA (detects virus)= PI from blood, tissue (ear notch, hair), vat milk
\* Management: Infected herd-- eradication and vaccination
Naive herd: biosecurity, screen incoming stock, isolation, vaccination
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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
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Diagnosis and Control of Neosporosis?
\* Diagnosis: histology- foetus brain definitive, focal encephalitis, brain contains cysts with tachyzoites and bradyzoites, placenta..... Serology of Dam: ELISA, IFAT
\* Control: No measures very effective, reduce fox population, dog control-- don't let dogs eat palcentas/ foetuses, vaccination of questional efficacy
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Benign Theileriosis in cattle? Clinical signs?
\* Tick-borne disease
\* Theileria orientalis
\* Multiple variants
\* Tick vector= Haemaphysalis longicornis "the bush tick"
\* Clinical disease rare in endemically affected areas but common and severe in non-endemic areas due to immunity levels
\* Often associated with introduction of cattle from endemic areas interstate
\* Clinical signs: fever, anaemia, tachypnoea, exercise intolerance, depression, lethargy, jaundice, death, abortion and still birth
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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
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Diagnosis and treatment of Benign Theileriosis in cattle?
\* Diagnosis: PCV below 15%, regenerative anaemia, demonstration of parasites within RBCs, PCR to distinguish between variants
\* Treatment: Oxytetracyclin and/or imidocarb, blood transfusion, minimize stress and movement
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Cause of late abortion in cattle
\* Cypress wind breaks toxic if cattle eat in late pregnancy
\* Isocupressic acid (in pine needles)
\* Lowered uterine blood flow, undilated cervix, weak uterine contraction
\*\* Also: Nitrate poisoning (certain plants, water), Mycotic abortion (leathery intercotyledonary placenta, mycotic plaques)
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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
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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
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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
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What are water belly calves? What do you have to do at parturition?
Abnormal fluid build up in the peritoneal cavity
\*\* can sometimes be caused by atresia ani OR failure to develop a little section of bowel-- sometimes born alive
\* Relieve the pot belly and the calf will come out (calves are not viable)
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What is Hydrallantois?
\* Abnormal accumulation of fluid in the allantois
\* Placentomes and calf not palpable
\* Refills quickly if drained
\* Abortion or maternal death
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What is hydramnios? Treatment?
\* Uncommon, pear shaped and soft
\* Slow onset
\* Placentomes and calf palpable
\* Calf often malformed
\* Doesn't tend to refill
\* Parturition at full term possible
\* Treatment: termination of pregnancy: corticosteroids, prostaglandins; Caesarean section: with supportive treatments
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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
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What are the antibiotics used with DCT? What must you always consider with treating production animals?
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Who is the most common patient with a vaginal prolapse? Treatment?
Fat, old beef cows BEFORE they've calved
\* Treatment: epidural, lubrication and replacement, purse string suture, perivaginal buttons
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What do you need to determine with uterine torsion?
\* Determine rotation direction and degree
\* Manual rotation, detorsion rod, using chains, rolling the cow, laparotomy
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Indications for a Caesarean section in a cow? Approaches?
\* Live, viable calf but foeto-pelvic disproportion
\* Valuable calf
\* elective pre-parturient
\* Foetal monsters
\* Dead, emphysematous calf
\* Uterine torsion
\*\* Surgical approaches: standing-- LEFT FLANK (rumen won't come out-- too big) & don't use right flank (intestines will come out); recumbent-- flank & paramedian (good for fully exteriorizing uterus of a rotten calf) & ventral midline (BAD IDEA- full anaesthetic with the cow on its back)
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What type of anaesthesia for caesarian section in a cow?
\* Caudal epidural (last sacral, first and second coccygeal-- 4-5 mL of lidnocaine)... keeping tail out of surgical wound (tie with hair or someone can hold)
\* Regional anaesthesia (more common): personal preference between the 3: inverted L (can extend if you need to cut further down), line block, lumbar paravertebral (T13, L1, L2-- if you don't do it right-- can't as easily extend)
\* Tocolytic: Clenbuterol (Planipart)-- anti-contraction meds, Isoxsuprine??
(two hands back from last rib for surgical wound-- not too low or too high in terms of how high inverted L anaesthesia is around the surgical incision-- do not do the inverted L behind the incision, you're just separating the surgical wound from the anus)
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Post operative care of a cow after C-section
\* (some people put a pessary in-- off label), Oxytocin, penicillin, wound management (clean blood off, attracts flies, fly repellent)
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What do you check with the calf after birth?
What do you check with the cow?
\* respiration, colostrum, swollen head or tongue, fractures, paralysis, facial tears
\* Twins?, lacerations of uterus, cervix, vagina, vulva, haemorrhage, other disease: hypocalcaemia, paralysis, dislocations
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Strep dysgalactiae as a cause of mastitis?
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Mycoplasma as a cause of mastitis?
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Risk factors for uterine prolapse? Treatment?
\* Usually skinny dairy cows after they've calved
\* Old, multiparous, hypocalcaemia, dystocia, big calf, prolonged labour, sloped bedding
\* Treatment: epidural, frogleg, oxytocin, replacement, purse string sutures
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What causes Schistosomus reflexus? Should we cull her? Can we expect more? My wife is pregnant, is she at risk?
Anything that causes an insult at the stage of fusion-- failure to zip up
\* No, unlikely she will have another
\* No, usually just one offs, if you get two or three more-- tell us and we will start heading down the genetic path
\* I'm not a doctor, go and get a medical opinion, but as a veterinarian there is no evidence that it is zoonotic-- the insult occurred 8 months ago
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Pseudomonas aeruginosa as a cause of mastitis
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Arcanobacterium pyogenes as a cause of mastitis
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General treatment of mastitis, clinical case
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Significance of Mastitis?
\* Reduced milk production
\* Loss of body condition (poor fertility, disease susceptibility)
\* Inferior milk quality- reduced payment for milk
\* Cost of treatment (antibiotics, discarded milk, time)
\* Loss of cattle due to disease
\* Culling of chronically infected cattle
\* Cost of preventive measures (teat disinfectants)
\* Possible antibiotic contamination of milk/ meat residues
\* Cost of control program
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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
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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
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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
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Teat blockage causes
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Problems and causes of haemolactia?
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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)
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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
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Cowpox- exotic to Australia and rare in rest of world-- spread by direct and indirect contact, erythma--\> vesicle--\> scabs
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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
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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
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Mastitis affect on milk quality
\* Lactose decreases (resulting in an influx of sodium and chloride ions to maintain osmotic pressure-- causes a bitter and slightly salty taste and increases electrical conductivity of milk which can be used to diagnose mastitis)
\* Casein decreases (but albumins and globulins increase)- protein level remains stable but composition changes-- it is the coagulation of casein that is important as a starting process for cheese and yoghurt production
\* Plasmin increases-- an enzyme that is not destroyed by pasteurization and remains active in refrigerated milk, will continue to decompose casein in stored milk
\* Lipase is present in high levels in mastitic milk. Lipase degrades milk fats into their fatty acid components imparting a rancid flavour-- leading to inhibition of cheese and yoghurt starter cultures
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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
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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)
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Two broad categories of mastitis pathogens
\* contagious (cow associated) and Environmental (non-contagious, non cow associated)
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Risk factors in cattle for mastitis
\* Age- prevalence increases with age
\* Stage of lactation- first month/ dry period
\* Teat conformation- wide teat canal
\* Teat condition- lesions harbour bacteria
\* Production- high production more susceptible
\* Existing prevalence in herd
\* Environment- mud and faecal contamination
\* Seasonal conditions- heat, humidity, wet, and muddy conditions
\* Selenium and Vitamine E status- when these levels are very low, they can influence the defence mechanisms of the udder
\* Milking practices
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Clinical changes in milk
\* Clots, wateriness, blood, serum, gas, odour
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Pathogenesis of bacterial mastitis
\* From the teat canal, the invading bacteria can reach the cistern and infection can occur-- inflammation follows and the follow on effects depend on the bacterial species virulence (e.g. endotoxins can cause systemic effects), host reponses (immune response, CMI)
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Sub-clinically, what is the most significant abnormality with mastitis? What is a healthy cow parameter?
\* increase in somatic cell count (macrophages, lymphocytes, neutrophils, epithelial cells)
\* Healthy cows produce milk with somatic cells in the order of 10^5 cells/mL
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What are the different classifications of mastitis based on severity?
\* Peracute mastitis- severe inflammation with both marked heat and swelling of the effected quarters or gangrene, can be fatal (with gangrene, it may be cold)
\* Acute mastitis- less marked systemic reaction, mastitic quarter is severely inflamed
\* Subacute- the inflammation of the mammary gland is mild
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Examination of udder
\* Visualize
\* Palpate
\* Strip milk samples: compare quarters, use black background, cannot usually make aetiological diagnosis
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Between 10 and 40% of cultures may return a value of "no growth," what are some of the reasons for this?
\* Elimination of infection by defence mechanisms
\* Bacteria present in concentration too low for lab detection
\* Presence of antibiotics in the sample due to prior treatment of the cow
\* Unusual pathogen such as anaerobes, fungi or Mycoplasma which do not grow on normal culture media
\* Non bacterial causes of mastitis
\* Bacteria which are usually considered to be non pathogenic are not reported by the lab (e.g. coagulase negative Staph's)
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An ICCC above what suggests infection of at least one quarter?
\* Above 250,000 cells per mL
\* It should be assumed that any cow with a single count above 250,000 cells per mL is sub-clinically infected-- S. aureus and S. uberis are the main pathogens and tend to persist in the udder inducing variable inflammatory responses throughout lactation
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What is the BMCC? What is the correlation between BMCC and overall production of the herd?
Somatic cell count of the herd as sampled from the vat. Companies pay a premium to farmers who produce milk with a BMCC less than 250,000 cells/mL
\* Severe penalties if over 600,000 or 750,000 cells/mL depending on factoring but considered poor if \> 400,000 (EU not fit for humans)
\*\* production decreases 2.5% for every 100,000 cells/mL above 100,000
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Which cows to culture?
\* Select range of cows representative of problem
\* If high number of high ICCC cows, collect from these
\* If high number of clinical, collect these
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Why do you freeze clinical samples of milk for a cow with suspected mastitis?
\* Freezing increases detection of S. aureus
\* All pathogens survive freezing except Nocardia
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What are ICCCs best used for?
\* Choosing which cows to culture
\* Not to decide who to treat (only helpful with S. agalactiae)
\* Best used to segregate infected cows from non-infected cows
\* Whose milk does not go into the vat
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What does high incidence of mastitis in heifers mean?
Infectious mastitis (if 20% have ICCCs over 250,000 cells/mL)
\* high incidence in old cows but heifers free of infection-- infection is not spreading
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How often should ICCC testing be conducted?
\* Bimonthly or monthly-- used to help detect individual cases, sub-clinical cases, used to manipulate BMCC
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What do you do if no response to treatment?
\* Treat for longer
\* Try different antibiotic regime (culture?)
\* Dry off quarter
\* Chemically dry off quarter (5% Copper Sulphate)
\* Dry off cow (DCT- dry cow therapy)
\* Cull
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Treatment for gangrenous mastitis
\* Tribactral IV
\* Finadyne IV (or other NSAID such as Tolfenic acid or Meloxicam)
\* +/- IV fluids
If the cow has another quarter infected:
\* Oxytocin IV- to milk out quarter
\* Ampiclox intramammary treatment
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What is the part of the milking machine that attaches to the teats? That brings the milk to the vat?
\* Cluster & milk transfer line (also the wash line to wash out the cluster after)
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Pulsation of a milking machine purpose? What is the pulsation rate? What is the pulsation ratio?
\* Maintains circulation in teat
\* Vacuum changes in pulsation chamber cause massage of teat by liner
\* Cycles 50 to 60 times per minute (pulsation rate)
\* Milk out phase to the massage phase (pulsation ratio)- 60:40
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Why are emollients added to disinfectant? What are some examples?
\* Keep teats soft and supple, help prevent cracking
\* Glycerine most common, Sorbitol and Lanolin
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What is Dry Cow Management?
\* Aimed at treating infections either not cured or not detected during lactation & aimed at reducing number of infections over dry period-- effect of AM (intrammary) & formation of keratin plug
\* DCT gives high cure rates because a high dose of sustained release antibiotic is delivered to each quarter
\* Minimum of six weeks required to allow udder tissue to regenerate
\* With no dry period milk production will be reduced following lactation
\* A keratin teat plug seals teat canal at the start of the drying period
\* Formation of keratin plug aided by DCT
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What is DCT teat sealant?
\* Teat seal contains bismuth sub-nitrate in a paraffin base- provides physical barrier (sometimes used with DCT)
\* Does not cure infections but prevent infections over dry period (100 days)
\* As good at preventing infections as DCT
\* More expensive than antibiotic preparations
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Which cows should be dried off? Where should they go?
\* Cows producing less than 5 litres/day
\* 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
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In a mastitis program, which cows do you cull?
\* Important part of mastitis control- chronically infected cows-- cows with 3 or more clinical cases in a lactation
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S. aureus considerations with mastitis
\* Common in Australia (that and S. uberis)
\* Most sub-clinical-- micro abscesses-- very difficult to cows with antimicrobials + resistant to many AMs-- very difficult to cure during lactation
\* Reservoir- infected udders and skin of teats if damaged
\* Spread at milking by contaminated milk-- found on liners 6 to 8 cows after infected cow is milked
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Staph aureus control program
\* Culture 20 cows if possible
\* ID chronically infected cows by use of cell counts
\* Correct machine and milking problems
\* Teat disinfection
\* Separate high cell count cows
\* Blanket DCT
\* Cull chronically infected cows
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Strep agalactiae mastitis? What type of AM and treatment?
\* Obligate parasite, however can survive on milking machines, milker's hands and clothes
\* Very rapid spread
\* Infected cows shed very large number of bacteria
\* High rate of clinical with some sub clinical cases
\* Penicillin sensitive + DCT will cure 100% of cases
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Strep agalactiae control program
\* ID bacteria up to 20 milk cultures
\* Farmer must be prepared to make changes with machines/ milking technique
\* Can spread very rapidly
\* Thoroughly investigate: milking techniques, milking machines, teat disinfection
\* Separate cows based on ICCC and clinical mastitis status
\* Blitz therapy- treat all or part of herd during lactation
\* Use DCT on entire herd
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Strep uberis as a cause of mastitis
\* leading cause of clinical and subclinical mastitis in dairy herds in AUS
\* Found in the enviroment, esp mud and faeces
\* Shed in the faeces of infected cows (can survive up to 2 weeks in manure/ mud)
\* Udders can act as reservoir and contaminate milking machines-- esp wet or dirty teats
\*Infection usually in late dry period/ periparturient period or early lactation
\* Usually clinical mastitis- very high incidence rates-- can become chronic
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Strep uberis control
\* Important to treat cases early and aggressively based on sensitivity testing
\* Combination of intramammary and parenteral antibiotics
\* Reduce contamination (faecal shedding maintains S. uberis in environment)
- calving pads/paddocks
- laneways
- water in dairy
\* Put cups on clean dry teats
\* Reduce lead feed energy intake if dry cows are running milk
\* Teat spray cows prior to calving
\* Milk cows as soon as possible after calving
\* DCT- long acting product plus teat sealant to provide immediate seal
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Coliform mastitis? Treatment?
\* E. coli most common by far, teat skin contaminated by the environment, infection may occur at any time including milking-- most prone to infection around time of calving (induced cows or milk fever most at risk)
\* Most infections localized in teat sinus, disease is caused by toxins
\* Toxins can cause serious systemic disease
\* Treatment- mild cases treated by frequent stripping of quarter with the aid of oxytocin
- More severe cases systemic antibiotic, anti-inflammatory, and fluid therapy
- to treat cases of mastitis in cows assume may be coliform mastitis and treat aggressively
- intramammary treatment: Ampiclox (Ampicillin and Cloxacillin) + Cefuroximime (Cepravin)
- Parenteral antibiotics: Trimethoprim/ Sulpha combination Oxytocin
- Flunixin meglumide (Finadyne) or other NSAID
- Control similar to Strep uberis= hygiene!
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If you have a muddy herd, what might you do before milking?
Cleaning + Pre-dipping
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Teat dilation- what do you do?
\* Sedate cow (Xyalzine)
\* Tail jack, leg rope
\* indicated for teat peas, black spot, fibrous tissue resulting from infection or slow milkers
\* will increase risk of mastitis, use sterilised teat dilator, aseptic technique
\* Cow on antibiotics prophylactically for 3 days
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Approach to herd mastitis problem
\* Questionnaire from CDDU
\* Cultures (past and present)
\* Machine test (dry)- AMMTA-- performance testing of milk machines
\* Look at hygiene, yards
\* Look at the udders- conformation, damage, etc.
\* Behavior
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What is stripping?
The process of removing three to four streams of milk from each teat before milking is known as stripping-- important for mastitis control and assists in milk let down... cows and quarters with mastitic milk should be identified with stripping
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When are dairy herds most susceptible to mastitis? Why?
\* early and late dry period-- but really throughout the dry period
\* when they are first dried off and going out into the paddocks-- more susceptible and when they are about to start calving and letting down their milk also very susceptible
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Supplementary skin tests in cattle
\* Swabs for microbiology
\* Skin scrapings
\* Biopsy or impression smears
\* Haematology/ biochemistry
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Australian cattle mange
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Two common causes of mange exotic to Australia
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Secondary?
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\* 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
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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.
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Skin diseases of calves
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Ticks that cause problems in Australia
\* Boophilus microplus (cattle tick)
- one host tick (3 weeks on host, 1 month egg laying)
- heavy infestations \> "tick worry"
- important vector of disease (Babesiosis & Anaplasmosis)
- Control: chemical control of ticks, resistance in cattle (Bos indicus), vaccine- expensive
\* Haemaphysalis longicornis (NZ cattle tick)
- Three host tick
- found in relatively low numbers in Australia (QLD, NSW, VIC)
- Less significant
\* Ixodes holocyclus (paralysis tick)
- can cause paralysis esp in calves
- sporadic, in wetter coastal regions of Eastern AUS
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Is lumpy skin disease in Australia?
No- pseudo lumpy skin disease is though which is Bovine Herpes Virus Type 2
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