GIT Flashcards
4 common causes of calf scour within 14 days of age
- Rotavirus
- Coronavirus
- E.coli
- Crypto
What can cause clostridial disease? signs?
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
What does clostridia in an open wound cause
Malignant oedema
Clostridia prevention
Vaccinate!
How and when do calves get Eimerica (coccidiosis)?
Caught from the environment
Risks: Stress, high stocking, mixing age groups, bad weather
- Calves (3wks to 6m) at most risk
- Year round disease
Signs of coccidiosis
- Diarrhoea +/- blood mucus
- Poor DLWG
- Irritated mucosa = oedema, thickened, inflamed, sloughing
dx for coccidiosis and cryptosporidium
McMasters on faecal sample to look for (and speciate) oocyst
Treatment for coccidiosis
- Prevention = Dixlazuril, Toltrazuril
- Hygiene: bedding management, stocking density
Signs of crypto
- Common cause of scour in youngstock at under 2 weeks
- Diarrhoea (no blood)
- Inappetence
- Abdominal pain
- Mild pyrexia
- Reduced growth
Tx for crypto
- Adequate colostrum
- Maintain good hygiene
- Prevent faecal-oral transmission (raise feed and water troughs)
- Older animals can shed so don’t mix age groups
Signs of salmonella
- Enteritis + severe diarrhoea + pyrexia
- Septicaemia
NB
- Also abortion
- Can also get distal limb necrosis and meningitis
- Risk post partum
Treatment of salmonella
TMPS (treats gram -ives)
meloxicam
Prevention:
- Try animal proof feed (difficult)
- Isolate and test new stock
signs of BVD
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
when in pregnancy are PI calves formed
- 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
Blood status of PI calves
- Antigen +++, antibody —
- Can transmit the disease as always viraemic = large amounts of shedding
what are the two testing methods in calves for BVD
- 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)
testing individuals for BVD
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
how does mucosal disease develop
- 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
Prevention of BVD
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
what bacteria causes Johnes
mycobacterium avium paratuberculosis (MAP)
sources of infection for Johnes
- 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
signs of Johnes
- Chronic wasting
- Diarrhoea
- Decreased yield
- +/- oedema (bottle jaw)
- Normally start showing signs at 2-6 years of age
2 methods to test for Johnes
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
Prevention of Johnes
Goal is to minimise exposure to young stock
- Slurry, colostrum, fomites
- Buy from reliable stock
cause and signs of Winter Dysentry
- Caused my coronavirus
- Highly contagious
- House cattle + close confinement
- Explosive diarrhoea (short lived) due to hypersecretion
How can rumen pH lead to diarrhoea
- 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
What are the two types of Ostertagia disease
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)
Dx fo ostertagia
- Blood tests to look at albumin and pepsinogen
- Worm egg counts not useful as this is a PPP disease
Prevention of ostertagia
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
Treatment for ostertagia and cooperia
- MLs (clear drenches/type 3) like ivermectin
What can lead to abomasa ulcers
- intensively managed herds, fed high energy, acidic diets (think concentrates)
- Long term NSAIDs are a risk
- High yielding dairy cows at risk
signs, dx and tx of abomasa ulcers
CS: Melena, anorexia, bruxism, abdominal pain
Dx: Ultrasound, D-dimers on abdominocentesis
Tx: treat cause, broad ABs, magnesium hydroxide to neutralise
signs of peritonitis
- 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)
treatment options for peritonitis
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
signs of caecal torsion / dilation
- 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
treatment for caecal dilation V torsion
- 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
appearance of Haemorrhagic jejunitis
- Red – dark black blood in faeces
describe the two types of bloat
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)
tx for frothy bloat
- Often fatal
- Anti-foaming agents (Mineral oil, poloxalene)
- Diet management (take off pasture, add long fibre, feed hay before going to grass)
what aged calves is luminal V abomasa bloat seen in
luminal = older (post weaning)
abomasa = pre-weaned (1-3 weeks)
what two areas can vagal indigestion effect
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
LDA ping characteristics
- ICS 9-10 on a line from elbow to tuber coxae.
high pitched
Ruminal bloat ping characteristics
Dorsal paralumbar fossa – more dorsal and caudal than is typical for LDA
low pitched, dull ping
(also palpable per rectum)
how to tell apart LDA ping Vs rumen void ping
Both in similar location
But rumen void = dull
LDA = high pitched
Ping signs of Pneumo-peritoneum
Dorsal, bilateral
Less resonant
Hx of abdominal surgery
Location of RDA ping
And sign it has turned into RA volvulus
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
Caecal dilation / torsion ping characteristics
Paralumbar fossa
can be very large location
Pings of duodenum/SI Vs spiral colon
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
Signs of RAV v RDA
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)
signs of copper toxicity
- Anorexia, depressed, weak
- Diarrhoea
- Abdominal pain
- Jaundice of sclera and skin
- black urine
two common causes of liver cirrhosis
- Subacute liver fluke (nearly always)
- Ragwort poisoning too: Causes direct hepatocellular damage. Chronic ingestion more common due to functional reserve of liver
signs of ragwort poisoning
- Weight loss
- Jaundice
- Photosensitisation
- Diarrhoea
- Hepatic encephalopathy
common cause of liver abscesses
- 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
What age of lambs are effected by e.coli
very young (under 3 days) get watery mouth
signs of Clostridia perfringens Type B;
- Sudden death
- Diarrhoea
- Affects young lambs (under 3 weeks)
aka lamb dysentry
which lambs are most at risk from coccidiosis
- 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
risks for crypto v cocci
cocci: mixing age groups, high stocking density
crypto: poor colostrum, poor hygiene, mixing age groups (worried about faecal contamination)
diarrhoea in crypto v cocci
Cocci = might have mucus and blood
crypto = none
Key goal in managing PGE
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
When does N.batttus emerge
- Hatching: cold period followed by 10 degrees average (spring emergence)
- disease in April to august (caused by larvae burrowing into GIT)
How to treat and test N.battus
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
Which animals should be treated for Teladorsagia (Ostertagia) and Trichostrongylus
Regular FWEC and DLWG monitoring
Only treat animals at threshold of epg
Signs of Ovine Johne’s
- Weight loss
- GIT thickening
- Oedema – Brisket and bottle jaw
Dx of Ovine Johne’s
Diagnosed by faecal exam
- MAP in faeces
- Intermittently shed
PMI
- Rough, thick intestines
Bloods:
- Albumin:globulin = 10
- Low blood albumin (lost across gut wall)
signs of fasciola hepatica
Sub-acute
- Loss of condition (rapid)
- Poor fleece
- Mortality can be high
Chronic
- Very poor condition
- Poor fleece
- Bottle jaw
dx of fasciola hepatica
- 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
tx of fasciola hepatica
Shed for 3 weeks so keep off pasture after giving treatment
- Triclabendazole followed by closantel or nitroxynil is a good approach
