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Farm animal > GIT > Flashcards

GIT Flashcards

1
Q

4 common causes of calf scour within 14 days of age

A
  • Rotavirus
  • Coronavirus
  • E.coli
  • Crypto
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2
Q

What can cause clostridial disease? signs?

A

GIT commensal and ubiquitous => Proliferates due to sudden diet change => Rapid overgrowth and enterotoxin release
Any age pre weaning

  • Haemorrhagic enteritis
  • Intestinal mucosal ulceration
  • Diarrhoea

Clostridia perfringens:
- Signs of peritonitis
- Abomasum ulceration

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3
Q

What does clostridia in an open wound cause

A

Malignant oedema

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4
Q

Clostridia prevention

A

Vaccinate!

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5
Q

How and when do calves get Eimerica (coccidiosis)?

A

Caught from the environment
Risks: Stress, high stocking, mixing age groups, bad weather

  • Calves (3wks to 6m) at most risk
  • Year round disease
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6
Q

Signs of coccidiosis

A
  • Diarrhoea +/- blood mucus
  • Poor DLWG
  • Irritated mucosa = oedema, thickened, inflamed, sloughing
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7
Q

dx for coccidiosis and cryptosporidium

A

McMasters on faecal sample to look for (and speciate) oocyst

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8
Q

Treatment for coccidiosis

A
  • Prevention = Dixlazuril, Toltrazuril
  • Hygiene: bedding management, stocking density
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9
Q

Signs of crypto

A
  • Common cause of scour in youngstock at under 2 weeks
  • Diarrhoea (no blood)
  • Inappetence
  • Abdominal pain
  • Mild pyrexia
  • Reduced growth
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10
Q

Tx for crypto

A
  • Adequate colostrum
  • Maintain good hygiene
  • Prevent faecal-oral transmission (raise feed and water troughs)
  • Older animals can shed so don’t mix age groups
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11
Q

Signs of salmonella

A
  • Enteritis + severe diarrhoea + pyrexia
  • Septicaemia

NB
- Also abortion
- Can also get distal limb necrosis and meningitis
- Risk post partum

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12
Q

Treatment of salmonella

A

TMPS (treats gram -ives)
meloxicam

Prevention:
- Try animal proof feed (difficult)
- Isolate and test new stock

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13
Q

signs of BVD

A

Type one and type two
Acute infection (T1):
- Mild systemic illness
- Immunosuppression
- Reduced repro performance

Acute infection (T2)
- Rare in UK
- Severe, often fatal
- Diarrhoea, haemorrhagic disease, thrombocytopenia

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14
Q

when in pregnancy are PI calves formed

A
  • 1st trimester: Resorption, abortion or still birth. If it survives, it is born a PI calf
  • 2nd trimester = Abortion or still birth
  • 3rd trimester = Normal calf
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15
Q

Blood status of PI calves

A
  • Antigen +++, antibody —
  • Can transmit the disease as always viraemic = large amounts of shedding
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16
Q

what are the two testing methods in calves for BVD

A
  • Test at 8 months: Maternal colostrum antibodies will bind to virus antigen and hide it. Wait until 8 months to test blood for antigen
  • Or can “tag and test” each calf at any age to look for viral antigen in ear tissue, as there are low antibody levels here (better)
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17
Q

testing individuals for BVD

A

Testing individuals:
- Ag presence = could be PI or transient…
- ==> check ABs - PI will have low/no Ab present
- ==>Or do 2 tests, 3 weeks apart to show high antigen remains in PI

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18
Q

how does mucosal disease develop

A
  • PIs can be stunted or normal until they get MD
  • PI animals virus mutates from non-cytopathic => cytopathic
  • Fatal condition
  • weight loss
  • Haemorrhagic diarrhoea, - Dehydration
  • Ulcerated lesions on nose, mouth and interdigital space
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19
Q

Prevention of BVD

A

Prevention:
- Lots of testing (bulk milk + youngstock)
- Identify and remove PI
- Good boundaries and biosecurity as spread by nose-nose contact
- Buy good stock

Vaccination:
- Before first breeding

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20
Q

what bacteria causes Johnes

A

mycobacterium avium paratuberculosis (MAP)

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21
Q

sources of infection for Johnes

A
  • Most infections occur in first month of life (carriers)
  • Most shedding = clinical animals
  • Persistent in the environment
  • Sources of infection: Faeces from cattle/goats/sheep, environment, fomites, colostrum, wildlife
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22
Q

signs of Johnes

A
  • Chronic wasting
  • Diarrhoea
  • Decreased yield
  • +/- oedema (bottle jaw)
  • Normally start showing signs at 2-6 years of age
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23
Q

2 methods to test for Johnes

A

Antibodies (blood /milk)
- Higher sensitivity
- Mostly for individual clinical cases or herd screening
- Cheaper and easier
- Antibodies rise just before clinical signs

MAP in faeces
- Intermittently shed
- Usually PCR
- Mostly confirmatory

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24
Q

Prevention of Johnes

A

Goal is to minimise exposure to young stock
- Slurry, colostrum, fomites
- Buy from reliable stock

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25
Q

cause and signs of Winter Dysentry

A
  • Caused my coronavirus
  • Highly contagious
  • House cattle + close confinement
  • Explosive diarrhoea (short lived) due to hypersecretion
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26
Q

How can rumen pH lead to diarrhoea

A
  • SARA = repeated bouts of low pH in the rumen
  • can lead to mild diarrhoea
    due to
    1. insufficient fibre => decrease rumination + saliva
    2. Excess starch => rapid VFA fermentation
    3. Or decreased DMI
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27
Q

What are the two types of Ostertagia disease

A

Overwintered larvae encountered in spring

  • Type 1: Wet summers cause eggs to hatch  disease in same season (July to October)
  • Type 2: Dry summers means eggs hatch in Autumn = hypobiois within lambs and mass emerge in spring = SEVERE disease + death
    (feb to April / towards end of winter housing)
28
Q

Dx fo ostertagia

A
  • Blood tests to look at albumin and pepsinogen
  • Worm egg counts not useful as this is a PPP disease
29
Q

Prevention of ostertagia

A

Type 1: Graze youngstock on different pasture and pre-treat with anthelmintic

Type 2: Worm at housing time with anthelmintic… shouldn’t routinely do this

30
Q

Treatment for ostertagia and cooperia

A
  • MLs (clear drenches/type 3) like ivermectin
31
Q

What can lead to abomasa ulcers

A
  • intensively managed herds, fed high energy, acidic diets (think concentrates)
  • Long term NSAIDs are a risk
  • High yielding dairy cows at risk
32
Q

signs, dx and tx of abomasa ulcers

A

CS: Melena, anorexia, bruxism, abdominal pain

Dx: Ultrasound, D-dimers on abdominocentesis

Tx: treat cause, broad ABs, magnesium hydroxide to neutralise

33
Q

signs of peritonitis

A
  • Gloving during rectal exam is indicative (rectum sticking to arm)

Acute: abdominal discomfort, pyrexia +/- toxaemia, altered faecal output

Chronic: non-specific clinical signs (Hanging back in parlour, not eating lots ect)

34
Q

treatment options for peritonitis

A

Immediate (for ileus):
- Fluid therapy
- NSAIDs
- Antibiotics (Amoxicillin or OxyTet, long course)

Surgical:
- Challenging. Severe damage from adhesions may require euthanasia
- Debridement, lavage and drainage

35
Q

signs of caecal torsion / dilation

A
  • Right sided ping but dorsally and caudally displaced (paralumbar fossa)
  • Off food and milk drop (signs of a sick cow)
  • Pain in abdomen (kick)
  • Depressed, lethargic
  • Can’t defecate or faeces scant with blood/mucus
36
Q

treatment for caecal dilation V torsion

A
  • Can surgically correct (empty and reposition with purse-string suture)
  • Oral fluids + calcium
  • NSAIDs and antibiotics

if only dilated, treat with NSAIDs (Ketoprofen) + calcium boroglucanate

37
Q

appearance of Haemorrhagic jejunitis

A
  • Red – dark black blood in faeces
38
Q

describe the two types of bloat

A

Frothy bloat = primary
- Froth in the rumen due to diet change
- Usually clover-rich pasture or legumes
Gas bloat = secondary
- Inability to eructate secondary to other condition (HypoCa, obstruction, tetanus, vagal nerve damage)

39
Q

tx for frothy bloat

A
  • Often fatal
  • Anti-foaming agents (Mineral oil, poloxalene)
  • Diet management (take off pasture, add long fibre, feed hay before going to grass)
40
Q

what aged calves is luminal V abomasa bloat seen in

A

luminal = older (post weaning)
abomasa = pre-weaned (1-3 weeks)

41
Q

what two areas can vagal indigestion effect

A

Anterior functional stenosis:
- Omasum paralysis  ingesta/fluid can’t flow into omasum  rumen distends

Pyloric outflow failure:
- Ingesta accumulates in abomasum and omasum  content enters rumen  distension + decreased motility

42
Q

LDA ping characteristics

A
  • ICS 9-10 on a line from elbow to tuber coxae.

high pitched

43
Q

Ruminal bloat ping characteristics

A

Dorsal paralumbar fossa – more dorsal and caudal than is typical for LDA

low pitched, dull ping

(also palpable per rectum)

44
Q

how to tell apart LDA ping Vs rumen void ping

A

Both in similar location
But rumen void = dull
LDA = high pitched

45
Q

Ping signs of Pneumo-peritoneum

A

Dorsal, bilateral
Less resonant
Hx of abdominal surgery

46
Q

Location of RDA ping
And sign it has turned into RA volvulus

A

ICS 10-13 on a line from elbow to tuber coxae.
Dorsal
usually >10 cm

More cranial ping (rib 8) = medial displacement of liver = RA volvulus

47
Q

Caecal dilation / torsion ping characteristics

A

Paralumbar fossa
can be very large location

48
Q

Pings of duodenum/SI Vs spiral colon

A

DSI: Paralumbar fossa, variable location and pitch
Usually <10cm

SC: Multiple areas within paralumbar fossa – may extend over last 2 rib spaces dorsally
variable pitch
Usually <10cm

49
Q

Signs of RAV v RDA

A

RAV (Vs RDA)
- Dehydrated (V hydrated)
- Signs of pain (V none)
- High HR (V normal)
- High RR (v normmal)
- BOTH = low rumen turnover
- Reduced., mucoid faeces (V normal/reduced)
- Abnormal MM (red) (V normal)
- High lactate (normal)

50
Q

signs of copper toxicity

A
  • Anorexia, depressed, weak
  • Diarrhoea
  • Abdominal pain
  • Jaundice of sclera and skin
  • black urine
51
Q

two common causes of liver cirrhosis

A
  • Subacute liver fluke (nearly always)
  • Ragwort poisoning too: Causes direct hepatocellular damage. Chronic ingestion more common due to functional reserve of liver
52
Q

signs of ragwort poisoning

A
  • Weight loss
  • Jaundice
  • Photosensitisation
  • Diarrhoea
  • Hepatic encephalopathy
53
Q

common cause of liver abscesses

A
  • Often from grain overload damaging the rumen
  • Rumenitis = acidosis = bacteria enter portal circulation = form emboli n liver (commonly fusobacterium or A.pyogenes)
  • Emboli form abscesses in the liver
54
Q

What age of lambs are effected by e.coli

A

very young (under 3 days) get watery mouth

55
Q

signs of Clostridia perfringens Type B;

A
  • Sudden death
  • Diarrhoea
  • Affects young lambs (under 3 weeks)

aka lamb dysentry

56
Q

which lambs are most at risk from coccidiosis

A
  • Lambs 3-12 weeks at most risk
  • also later born lambs
  • First born lambs = exposed to low level from ewe and overwintered = develop immunity = oocysts multiply in lambs and shed = later born lambs encounter higher challenge of infectious oocysts
57
Q

risks for crypto v cocci

A

cocci: mixing age groups, high stocking density

crypto: poor colostrum, poor hygiene, mixing age groups (worried about faecal contamination)

58
Q

diarrhoea in crypto v cocci

A

Cocci = might have mucus and blood

crypto = none

59
Q

Key goal in managing PGE

A

reducing worm burden to enable immunity

Animals develop immunity during the first grazing season (except Haemonchus and Fluke)
High challenge = disease, but no challenge = naive, vulnerable animals
Aim to reduce worm burden so animals develop immunity

60
Q

When does N.batttus emerge

A
  • Hatching: cold period followed by 10 degrees average (spring emergence)
  • disease in April to august (caused by larvae burrowing into GIT)
61
Q

How to treat and test N.battus

A

Test: can’t do FWEC as PPP disease

Treat:
- Strategic treatment based on larval peak with white drenches (benzimidazoles like albendazole, fenbendazole)
- Keep inside to miss peak

62
Q

Which animals should be treated for Teladorsagia (Ostertagia) and Trichostrongylus

A

Regular FWEC and DLWG monitoring
Only treat animals at threshold of epg

63
Q

Signs of Ovine Johne’s

A
  • Weight loss
  • GIT thickening
  • Oedema – Brisket and bottle jaw
64
Q

Dx of Ovine Johne’s

A

Diagnosed by faecal exam
- MAP in faeces
- Intermittently shed

PMI
- Rough, thick intestines

Bloods:
- Albumin:globulin = 10
- Low blood albumin (lost across gut wall)

65
Q

signs of fasciola hepatica

A

Sub-acute
- Loss of condition (rapid)
- Poor fleece
- Mortality can be high
Chronic
- Very poor condition
- Poor fleece
- Bottle jaw

66
Q

dx of fasciola hepatica

A
  • Requires faecal egg flotation
  • Bloods: Low albumin AND low globulins

PMI
- Acute = pale liver (due to blood loss death)
- Chronic = thick tracts = damages bile ducts

67
Q

tx of fasciola hepatica

A

Shed for 3 weeks so keep off pasture after giving treatment
- Triclabendazole followed by closantel or nitroxynil is a good approach

Farm animal (7 decks)

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