Cattle2 Flashcards Preview

FINALS > Cattle2 > Flashcards

Flashcards in Cattle2 Deck (101)
Loading flashcards...
1

How is lepto spread?

Via contact with infected urine or from water/pasture contaminated with urine. products of abortion also source of infection. Venereal transmission possible. not carried by vermin/wildlife. sheep can carry and excrete leptospira.

2

How is leptospirosis destroyed?

Leptospires do not tolerate drying, exposure to sunlight, ph

3

What are the risk factors for lepto?

Open heard, shared bulls
Mixed grazing with sheep
Shared grazing/water courses

4

What are the clinical syndromes seen with leptospira?

Milk drop - 2-7 days after initial infection
Abortion - 3-12 weeks following infection (in last trimester usually)

5

How is leptospirosis diagnosed?

Microscopic agglutination test - used to detect antibodies to lepto hardjo in serum. also ELISA titre. Leptospires in urine following acute infection using dark field micrsocopy or PCR.

6

What are the clinical signs of malignant catarrhal fever?

acute onset illness with depression, anorexia, pyrexia, intense scleral congestion with keratitis erosive stomatitis of mucosa and muzzle, mucopurulent discharge, nervous signs hyperaesthesia and incoordination, diarrhoea.

7

How can MCF be differentiated from other mucosal diseases?

History of sheep and classical clinical signs - central nervous signs are rare with any other mucosal diseases. Differential diagnosis are IBR, BDV, BTV, VSV, FMD. Serological test is available but may not be positive at time of clinical signs, or demonstration of viral genome in blood (PCR).

8

What is sporadic bovine lymphosarcoma (leukosis)

NOT the same as Enzootic bovine leukosis caused by retrovirus !!

Rare and sporadic - juvenile, thymic and skin forms.
In thymic form characteristic massive enlargement of thymus and local LN, thymic mass acuses jugular engorgement, oedema of brisket extending to submandibular region and chronic bloat due to oesophageal compression.
tumour masses can be found in a wide variety of organs including the heart, abomasum, spleen and CNS.

9

What type of virus is BvD?

Pestivirus

10

How is BVD spread?

Nasopharyngeal secretions, urine, aerosol droplets. Faeces not a major source of virus excretion.

11

How does mucosal disease occuR?

When a PI animal becomes superinfected with cpBVD. the CpBVD virus can arise from genetic assortment of Ncpbvd within the PI animal from transfer of genetic material from a heterologous starin to the NCP BVD strain or can arise as an entirely new strain. most cases occur in 6 month to 2 year age group which may coincide with waning of passive immunity.

12

What are the signs of mucosal disease caused by BVD?

Acute onset depresison, pyrexia, anorexia, saliva around muzzle, oral nasal erosions/ulcers, nasal discharnge, profuse diarrhoea/dysentry with shreds of gut mucosa/blood present in terminal stages.

13

How can mucosal disease be diagnosed?

Virus isolation from PM tissues. Normally are antibody negative antigen positive on ELISA test.

14

How can PI calves be confirmed?

Ear notch or blood for persistent viraemia. Ear notch testing can be done at any age. Serum antigen BVDV test accurate from 1 month in the presence of mternal antiboies.

15

How is BVDV screened for in a herD?

Bulk milk or first lactation screens
Calf screen - 5 animals between 9-18 months old from each management group.

16

What did pregsure bvd vaccine cause?

Bovine neonatal pancytopenia

17

What is necrotic enteritis?

Seen almost exclusively in spring born suckled calves and normally affects calves in 2-4 month old age group. Most cases affected are seen at pasture in june/july.

18

What are the clinical signs of necrotic enteritis?

Depression, pyrexia, diarrhoea often profuse and haemorrhagic, tenesmus, abdmoinal pain, respiratory signs, pale mucous membranes, oral and nasal ulcers. Non regenerative neutropenia.

19

What is the cause of winter dysentry?

Bovine coronavirus. Acute highly contagious diarrhoea tht occurs in epizootic fashion in winter housing period. spread by faecal oral route.

20

How is johnes transmitted?

Ingestion of the organism in faeces from infected animals, contaminating food,water or teats. Infection mainly occurs in neonatal animals up to a few months old but occasionally older animals also become infected.

21

What cell does johnes multiply within?

Macrophages. It localises in the ileum and gut associated lymph nodes and is phagocytosed by macrophages and may multiply intracellularly.

22

What are the clinical signs of johnes?

Weight loss, emaciation, sub mandibular oedema, coat depigmentation, fall in milk yield. NO FEVER OR TOXAEMIA. appetite and rumenal activity are good. soft faeces or dairrhoea that is thick pea soup with no blood mucous or debris. Small ruminants usually have faeces which remains firm.

23

What do johnes cases usually show on clinical pathology?

Hypoalbuminaemia with normal gammaglobulin levels.

24

What tests are used to diagnose johnes?

Faecal examination for acid fast organisms ZN stain.
Culture of faeces on mycobactin containing media (3 months or more)
PCR to detect quantities of mycobacterial DNA in faeces.

Agar gel immunodiffusion test - not good at detecting subclinical cases.
ELISA - best option though sensitivity still

25

Which species causes dermatophytosis in cattle?

Trichophyton verrucosum.

26

What is the treatment of ringworm?

Griseofulvin in feed - not in UK
Sodium idiode - toxicit
Ringvac vaccine
topical enilconazole, iodine/glycerin

27

What is bovicola bovis?

A biting lice

28

What is haematopinus eurytsternus, linognathus vituli, solenopotes capillatus?

Sucking lice of catle.

29

What is chorioptes bovis?

A surface mite. Lives off epidermal debris. Causes papules, pruritis, alopecia, crusts.

30

Which flies spread summer mastitis?

Hydrotoea irritans.

31

Which flies cause multiple nodules from bites?

Haematobia species. Open wounds/lesions on the lower abdomen, udder and teats can be caused by bites of flies such as haematobia irritans or feeding of hydrotea irritans.
Stomoxys calcitrans (stable flies)
simulium black flies - can cause painful vesicle, mass attack can cause acute syndrome with haemorrhage and oedema
Tabanid horse flies - painful bite

32

Which flies cause blowfly strike?

Lucilia sericata or phormia terranovae.

33

What could be the cause of subcutanoues nodules and cysts along the backs of cattle in spring?

Warble fly larval infestation by hypoderma bovis or h lineatum - notifiable.

34

What is the cause of infectious bovine keratoconjunctivitis?

Moraxella bovis +/- mycoplasmas, flies, dust, IBR.

35

What is the treatment for IBK?

topical antibiotics, subconjunctival injection, systemic oxytet, florfenicol or ceftiofur.

36

What is the cause of ovine infectious keratoconjunctivitis?

Mycoplasma conjunctivae.

37

What are struvite crystals composed of?

Magnesium ammonium phosphate hexahydrate.

38

What is the cause of bacillary haemoglobinuria?

Clostridium haemolyticum (clostridium novyi type D)

39

What is postparturient haemoglobinuria?

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

40

What BCS should a dairy cow be at calving?

2.5-3

41

How can butterfat levels be increased?

By increasing the amount of effective long fibre in the ration > long fibre may be added to the TMR by the inclusion of 0.5kg chopped straw/cow/day . High levels of concentrate feeding will lead to increased propionate production and decreased acetate production in the rumen, leading to a fall in butterfat level Addition of sodium bicarbonnate to buffer rumen and raise acetate production. also inclusion of saturated hard fats will increase butterfat levels, provided their inclusion levels do not exceed 6%. Feeding of protected fats that bypass the rumen will also boost butterfat levels. Milk butterfat responds to changes within days.

42

How can milk protein level be increased?

Increased levels of concentrate feeding, feeding of bypass starch will increase milk protein, Increasing levels of DUP if dietary protein is limiting, maximise DMI during early laxtation to minimise the extent of any NEB, use a mixture of forages/TMR to stimulate intakes and energy supply.

43

What is the optimum pH of the rumen?

6-7.
SARA is defined by the presence of a rumen pH of less than 5.5 in atleast 30% of the animals sampled.

44

What are the clinical signs of poisoning with alkaloid plants e.g yew and laburnum?

Excess salivation, dilation or constriction of the pupil, vomiting, abdominal pain, diarrhoea, incoordination, convulsions and coma.

45

How are cyanogenic glycosides toxic ? e.g linseed and cherry laurel?

They contain an enzyme capable of converting glycosides to hydrocyanic acid. As oxygen transfer to tissues is blocked, venous blood becomes oxygenated with a bright red appearance. HCN is absorbed rapidly and clinical signs including dyspnoea, convulsions, muscle tremors and death occur.

46

How are goitrogenic glycosides toxic? e.g brassicas and white clover

They can cause goitre, reduced growht rates, diarrhoea, sudden onset with rape seed. Glucosinolates in the plants interfere with thyroidhormone synthesis. Thiocyanate goitrogens impair uptake of iodine by the thyroid gland.

47

How are cardiac glycosides toxic to animals? e.g foxglove, lily of the valley and oleander?

They have specific action on the myocardium, increasing contractility and slowing heart rate, moderate intoxication results in bradycardia, depression, regurgitation and diarrhoea, while larger amounts of toxin cause various cardiac irreuglarities including bradycardi athen tachycardia and dysrhythmia.

48

What are causes of primary photosensitisation?

Certain plants such as st johns wort and buckwheat contain photodynamic agents (hypericin and fagoprysim) respectively that ar eabsorbed and carried systemically to the ski

49

What are causes of hepatoenous photosensitisation?

Hepatotoxic plants e.g bog asphodel and ragwort can acuse photosensitsation as biliary excretion of phyloerythren is obstructed due to liver disease.

50

How does blue green algae cause toxicity?

It forms blooms on still water, and contains peptides that are potential hepatotoxins. The toxins are chemically stable and not inactivated by the usual treatments used for drinking water. blue green algae are widespread in inland waters in the UK.

51

What is amanita phalloides?

A toxic mushroom in britain containing aminotoxins. Causes severe abdominal pain, diarrhoea, eventually coma.

52

What are the signs of oak and acorn toxicity?

tannins on oak/acorns bind to protein sand produce astringent reaction in the mouth. Signs of tannin poisoning may not appear for some days after ingestion. Initially there is dullness, anorexia, constipation, cessation of urination. Later there is persistent diarrhoea and dysentery.

53

Which breeds are susceptible to copper toxicity and deficiency?

Texels susceptible to toxicity, blackface susceptible to deficiency.

54

What are the clinical signs of copper deficiency in cattle?

Depigmentation of hair,
Thin dry sparse hair coat
Ill thrift
Anaemia - after prolonged periods
Diarrhoea after turnout onto pastures with high molybdenum concentrations.

55

What is swayback? (enzootic ataxia)

Caused by copper deficiency in pregnant ewes in mid to late gestation. It is associated with mild winters. Two forms are seen; congenital, neurological signs- ataxia, inability to stand, staggering gait, swaying, or delayed - less severe and precipitated by gathering or handling.

56

What are the signs of copper deficiency in sheep?

Depigmentation
Loss of wool crimp, steely wool
Ill thrift

57

What is glutathione peroxidase?

A selenium containing enzyme and is the standard biochemical test for selenium deficiency. As erythrocyte GSHPx levels depend on selenium levels during erythropoiesis and RBCs live for several months, blood GSHPx levels reflect long term selenium status (2-4 months).

58

Which mastitis pathogens are contagious?

Staphylococcus aureus
Streptococcus agalactiae
Streptococcus dysgalactiae
Mycoplasma
Corynebacterium bovis
Coagulase negative staph

59

Which mastitis pathogens are environmental?

E coli
Strep uberis
Pseudomonas auruginosa
Bacillus cereus
Other coliforms
Pasteurella

60

What is lactoferrin

an iron binding protein that is present in relatively high concentrations during the dry period and prevents growth of bacteria by removing iron from udder secretions.

61

What is lactoperoxidase?

An enzyme in milk that is bacteriostatic on gram positive bacteria and bacteriocidal on gram negative bacteria.

62

Straw yards may predispose to which type of mastitis?

Strep uberis

63

What is the normal composition of the proteins in milk?

2.6% casein
3.8% butterfat
4.6% lactose
pH 6.7

64

What is increased in milk during mastitis?

RBCS
WBCS
sodium
chloride
bacteria
pH
milk conductivity

Decreased caesin, lactose, butterfat, protein, calcium, phosphorus.

65

What is the optimal bulk milk SCC?

400 -10ppl

66

What is the optimal bactoscan ?

500 - 5ppl

67

What are the most common type of bacteria that require treatment in the dry period?

Staph aureus and strep uberis. The ones that most commonly become established during the dry period are strep uberis and E coli.

68

which antibiotics have good udder penetration?

Tylosin
Cefquinome (cobactin)
Fluoroquinolones (marbocyl)

69

What is the cause of summer mastitis?

Arcanobacterium pyogenes
Peptostreptococcus indolicus
Streptococcus dysgalactiae
Act synergistically to cause summer mastitis. the major factor in transmission is thought to be the head fly (hydrotea irritans).

70

What are thermoduric bacteria?

BActeria that withstand pasteurisation and thus high levels are indicative of a wash up problem.

71

What are psychotrophic bacteriA?

They are found in dust and grow best at low temperatures. the value gives an indicative of poor premilking teat disinfection.

72

What is the cause of herpes mamillitis?

bovine herpes virus 2

73

What are the clinical signs of acetonaemia?

wasting form - losing condition, refusal to eat, sudden drop in milk yield, firm and waxy appearance to faeces.
Nervous form - hypoglycaemic encephalopathy - jumpy, frenzied, head pressing, circling, wandering, licking at objects, salivation.

Hypoglycaemia, mobilisation of body fat (NEFA levels >0.7mmol) and accumulation of Ketone bodies - acetone, acetoacetate and B hydroxybutyrate.

74

What are the clinical signs of hypocalcaemia?

Loss of appetite
dullness
lethargy
normal or slightly depressed rectal temperature
initial hypersensitivity and hyperaesthsia
grinding and msucle tremors
stiffness of legs
recumbency with lateral S bend in the neck
Increased HR, dilated pupils, gut stasis, constipation,
eventually comatose >death

75

How does hypomagnesaemia result in hypocalcaemia?

Low magnesium may interfere with the release of PTH, the ability of PTH to act on its target tissues and hydroxylation of vitamin D3 in the liver > hypomagnesaemia during dry period may result in milk fever due to critical need for magnesium in calcium homeostasis.

76

How can hypocalcaemia be prevented?

Dietary calcium restriction during the dry period - limit the amount of calcium in dry cow diet in 3-4 weeks prior to calving.
Manipulation of the dietary cation anion balance - metabolic alkalosis predisposes cows to milkf ever, as the raised PH Prevents PTH from acting on its receptor, thus blocking mechanisms of PTH dependent calcium mobilisation. lowering the Ph stops this lack of response to PTH and releases of cations from bones.

77

What ions have the strongest effect on acid base balance?

DCAB = Na and K minus Cl and S

Urine pH should fall to 5.5-6.5 if the ration is successful.

78

What are the clinical signs of hypocalcaemia in ewes?

Rapid respiratory rate, passive reflux of ruminal contents down the nose.

79

What are the clinical signs of hypomagnesaemia?

Sudden death - with paddling in soil around

Acute - apprehension, nervousness, hyperaesthesia, incoordination, collapse, convulsions.

80

What is the most reliable way of diangosing hypomagnesaemia in a post mortem?

In CSF - in freshly dead animals only
In aqeous humour - in freshly dead animals
In vitreous humour - stable for 48 hours post mortem.

81

List When the Placenta takes over progesterone production in the pregnancy of the Pig, goat, dog, rabbit, cow, horse, sheep and cat.

Source of progesterone during mid and late pregnancy;
for pig, goat, dog, rabbit - CL produces progesterone throughout pregnancy.

In cow - placenta takes over 210
In horse - plcenta takes over day 70
In sheep - placenta takes over day 50
In cat - placenta takes over day 50

82

What type of placenta does the cow, sheep, dog, cat, pig and horse have?

Diffuse, epitheliochorial = horse and pigs
Cotyledonary, (syndesmochorial)= ruminants
Zonary, endotheliochorial -= dog and cat
Discoid, hemochorial = monkeys, rodents

83

What can be use to terminate a pregnancy in a cow?

Major source of progesterone untilday 150 is the CL. Use of prostaglandin up to 120-150 days will terminate pregnancy. Beyond day 150 the corpus luteum isn't the sole source of progesterone, which is produced by the oarian stroma, the placenta and the adrenals. Loss of the corpus luteum beyond day 150 Wont necessarily terminate the pregnancy. combination of PG and corticosteroid needed.
If close to normal gestation - inject with short acting corticosteroid.
Between 150-270 days - use dexamethasone and PGf2a.
If

84

What is interferon tau?

It is secreted from the blastocyst >15mm diameter normally by day 15 until around day 20. it inhibits oxytocin receptor expresison in the endometrium which prevents rostaglandin production by the endometrium and therefore preents luteolysis.

85

What bacteria are most likely to be isolated from metritis in a cow?

A pyogenes, bacteroides, fusibacterium.

86

What is the definitiion of metritis?

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

87

What is the definition of clinical endometritis?

Clinical endometritis is characterised by the presence of purulent >50% pus uterine discharge detectable in the vagina 21 days or more after parturition. There is no systemic illness.

88

What factors predispose to developing endometritis?

Dystocia/assisted calving
RFM
Dirty calving environment
Premature calving
Delay in return of pp cyclicity
Over fat at calving/fatty liver syndrome
Nutritional deficiency e.g selenium.

89

What is the treatment for endometritis?

Prostaglandin injection - requires responsive CL. (also treatment for pyometra)
Intra uterine pessaries/washouts.
antiseptic washouts - lugols iodine or chlorhexidine, irritant to endometrium and cause PGF2a release which may have curative effect.

90

What is the difference between metritis, endometritis and pyometra?

. Endometritis occurs three weeks or more after calving and it should not be confused with the more severe condition of acute metritis which occurs immediately post-partum. Chronic metritis (pyometra) persists over a long period and generally, the cow is not really visibly ill of it, usually she has a good appetite. Pyometra is the accumulation of purulent material within the uterine lumen in the presence of a persistent CL and a closed cervix.

91

What is the definition of puerperal metritis/

An abormally enlarged uterus and a fetid watery red brown uterine discharge, associated wth signs of systemic illness, decreased milk yield, dullness and other signs of toxaemia and fever >39.5.

92

What is a cyst?

Fluid filled structure >2.5cm diameter present for >ten days on one or both ovaries in absence of a corpus luteum. Follicular cyst is thin walled and non progesterone producing. Luteal cyst is thicker walled and progesterone producing.

93

What is the treatment for cystic ovaries in cows?

If luteal - PG
If follicular - PRID/CIDR or GnRH
If unsur e- GNRH + PG or PRID with PG.

94

Describe the ovsynch regime?

Day 0 - 2.5ml GnRH
Day 7 - Prostaglandin inj
Day 9 - 2.5ml GnRH
day 10 - AI

This synchronises cows but pregnancy rates may be poor with this regime.

95

What is camypolbacter foetus var venerealis?

The natural habitat is the prepuce, glans penis and distal urethra. IT is transmitted venereally. there is no systemic illness. females experience a mild endometritis and cervicitis, with mucopurulent vaginal discharge. cases present as a repeat breeder which eventually holds, abortion & rfm at 4-7 months or pregnancy survives to term.

96

What anaesthetic technique should be used for sheep C section?

Distal paravertebral anaesthesia or lumbosacral high extradural injection

97

Which factors are implicated in the aetiology of vaginal prolapse?

Excess body condition, multigravid uterus, high fibre diets particularly those containing root crops, limited exercise in housed ewes, lameness leading to prolonged periods in sternal recumbency, steep fields, hypocalcaemia.

98

Which anaesthetic technique should be used to replace a vaginal prolapse?

Sacroccygeal extradural injection

99

What is the earliest a cow can be Pregnancy diagnosed on rectal palpation?

Transrectal scanning - 25-30 days post insemination, sex foetus 55 days
Manual rectal palpation - 6-8 weeks post insemination.

30-45 days - membrane slip, amniotic vesicle
75 days - placentomes present
90 days - foetus present
Fremitus on ipsilateral horn - 105 days
Bilateral fremitus -5-7 months

100

What is the target for the following;
Voluntary waiting period
Calving interval
Calving to 1st service interval
Calving to conception interval

Voluntary waiting period - 42-50 days
Calving interval - 365 days for block calving herds, for up to 10,000 litre lactation 400 days, for 7000-8000L lactation 375 days
Calving to 1st service interval- 60 days
Calving to conception interval - 85 'days open'

101

What health tests are statutory for bulls?

TB, Brucella, trichomonas foetus, IBr, campylobacter fetus, EBL, BVD, are statutory. some studs will do johnes, lepto and Q fever additionally.