Equine Acute And Chronic Diarrhoea In Adults Flashcards
- How much fluid enters the horse GI tract in 24hrs? - where is it reabsorbed?
- Origin of diarrhoea in the adult horse?
- Origin of diarrhoea in foals?
- 100L - LI.
- LI.
- SI or LI.
Mechanisms of diarrhoea in the adult horse.
Bowel inflammation - colitis.
Inflammation causes diarrhoea mainly via:
- malabsorption e.g. due to damage.
- increased secretion.
- decreased transmit time (abnormal motility).
Diagnostic approach - history taking in the adult horse?
Age.
Acute or chronic.
Dietary change?
Deworming history.
Others affected?
Recent NSAID or ABX use/abuse.
Diagnostic approach - differentials.
Genetic.
Infectious - bacteria, fungi, virus, Protozoa, parasites.
Inflammation.
Neurological.
Autoimmune.
Nutritional.
Developmental.
Degenerative.
Trauma.
HOrmonal
Neoplastic.
Iatrogenic.
Idiopathic.
Cardiovascular.
Chemical or toxic.
Differentials for chronic diarrhoea.
Genetic (granulomatous bowel disease).
Infectious - bacteria (chronic salmonellosis), parasitic (Strongyloides, cyathostomiasis).
Inflammatory - sand.
Auto immune - inflammatory and granulomatous bowel diseases.
Neoplasia (lymphoma most common).
Chemical and toxic / iatrogenic - NSAID use/abuse (right dorsal colitis), antibiotic induced.
- NB some non-GI causes e.g. some liver disease.
Differentials for acute diarrhoea.
Infectious - bacteria (salmonella, clostridia (toxin), rhodococcus (foal).
- parasitic (cyathostomiasis).
- viral (rotavirus).
Nutritional - sudden diet change (shouldn’t be sick).
Idiopathic - most acute colitis.
Chemical and toxic / iatrogenic - NSAID use/abuse (right dorsal colitis), antibiotic-induced.
NB some non-GI causes e.g. some liver disease.
Assessing the effect of the diarrhoea on the individual.
Dehydration:
- HR.
- PCV.
- TP.
Endotoxaemia:
- CE, HR, MMs.
Inflammation:
- fever.
Further testing to assess the effects of the diarrhoea on the horse.
Protein loss - TP and albumin (can have normal TP if high globulin and low albumin — e.g. some cyathostomiasis).
- ventral oedema (not all).
Electrolytes (Acute).
Acid-base (Acute, get acidaemic if severe - test once hydrated).
Test aimed at finding the cause of the diarrhoea.
Faecal sample - for bacteriology.
— serial samples for salmonella (3 x samples every 12-24 hrs).
— Clostridial toxins.
- egg count.
Maybe biopsy:
- IBD.
- neoplasia.
- culture (salmonella).
- encysted cyathostomes.
- rectal — easy, low risk and cheap.
— care when interpreting results .
- intestinal.
— laparoscopy vs laparotomy.
— standing vs GA.
— small vs large.
— can also inspect abdomen.
— generally consider if rectal biopsy was unrewarding.
Abdominoparacentesis:
- neoplasia.
— about 1/4 lymphoma cases and 3/4 SCC cases shed cells.
- inflammatory cells in IBD?
Abdo U/S:
- thickened intestinal wall.
— may see in some cases of:
—> IBD, right dorsal colitis (NSAIDs), neoplasia.
—> fairly poor specificity and sensitivity.
Treatment of chronic diarrhoea in the horse.
Horse usually relatively stable even if underlying cause serious.
Prioritise reaching diagnosis.
Then treat cause.
Treatment of acute diarrhoea in the horse.
Some treatment specific to the cause.
Treatment generally very similar.
Depends on severity.
If dehydration:
- make fluid plan — current dehydration, ongoing losses, maintenance.
- IV fluids usually best.
- monitor.
Feed, spike fluid bags as required and rehydrate to treat electrolyte imbalances.
Hydration to treat acid-base disturbances.
Hypoproteinaemia:
- plasma transfusion.
- may need to repeat.
- expensive.
Endotoxaemia:
- flunixin (NSAID) — judicious as can give colitis in itself.
- Polymyxin B - binds LPS.
- ice feet for laminitis.
Colic:
- Flunixin (with care).
- may need opioids.
- spasmolytics.
Bacteraemia/bacterial overgrowth.
- antibiotics - do you? Don’t you?
— if sick/toxic —> penicillin, gentamicin, metronidazole.
— if not, take faecal and blood culture first.
— watch for thrombophlebitis.
What is transfaunation?
Filter faeces from a healthy horse from the sick horse’s home environment.
NG tube.
After omeprazole to raise pH?
Several times.
Treatment - encouraging blood flow to the colon wall.
For healing of inflamed colon.
Including colonic ulceration.
Will also help gastric ulceration.
Oral sucralfate (currently made as a special).
Oral misoprostal (human drug).
- used to induce abortion in humans so be careful!
Both PG agonists.
Extras:
- Biosponge.
- Yeasacc.
- Probiotics? — no evidence for their efficacy at the moment.
4 clinical syndromes of salmonella enterica.
Inapparent infections with latent or active carrier states.
Depression, fever, anorexia, neutropenia, without diarrhoea or colic.
Acute enterocolitis with diarrhoea.
Septicaemia with or without diarrhoea.
- Route of salmonella infection?
- What if immunocompromised (e.g. stress or illness)?
- Risk of having carriers or infected horses?
- Faecal-oral route. Can persist in the environment.
- Carriers can get diseased.
Easier to get infected - Nosocomial infection.
Zoonosis.
Features of acute enterocolitis caused by salmonella.
Severe inflammation, ulceration, even infarction.
First clinical signs usually fever and anorexia.
Endotoxaemia:
- due to inflammation, bacteria/LPS can cross to bloodstream.
- endotoxic shock (fever, tachycardia, congested MMs, weakness, organ failure).
- risk laminitis.
- risk thrombophlebitis.
Diarrhoea 24-48hrs after onset of pyrexia.
- severe, very dehydrated, mild/moderate colic, PLE.
Neutropenic early on - as all gone to gut.
Isolate if has any 2 of:
- pyrexia, depression, diarrhoea, leukopenia (even if not unwell).
Dx of salmonella.
Clinical suspicion.
Faecal sample:
- 3-5 serial samples.
— 3 negatives can confirm negative.
— if have a positive, need 5 negatives to confirm negative.
— PCR can help.
— can culture rectal biopsy.
Px of salmonella.
Need aggressive treatment.
High risk of complications.
Can become carriers.
Can develop into chronic salmonellosis.
Poor if persists more than 4-5 weeks.
Clostridia causing diarrhoea.
Clostridia is part of the normal gut flora.
But those producing enterotoxin are not part of normal.
Toxin-producing clostridia can be triggered by antibiotic administration.
High numbers of clostridia and toxin on faecal culture.
Presentation similar to other causes of colitis.
Lawsonia intracellularis causing diarrhoea.
Proliferative response of intestinal mucosa.
- alters absorption of nutrients.
- alters fluid secretion.
— by disrupting villi architecture.
— by altering maturation of epithelial cells into absorptive cells.
Inflammatory response.
Malabsorption:
- diarrhoea.
- severe weight loss.
- PLE.
- Lawsonia intracellularis clinical signs.
- Lawsonia intracellularis clinical pathology.
- Lawsonia intracellularis on U/S.
- Weaning foals 4-6 months old.
I’ll-thrift.
Weight loss.
Peripheral oedema.
Diarrhoea.
Colic. - Moderate to often severe hypoalbuminaemia.
Hyperfibrinogenaemia.
Anaemia. - Marked thickening and oedema of intestinal wall.
Diagnosis of Lawsonia intracellularis?
Serology of blood and PCR of faeces.
Take both to increase sensitivity and specificity.
Definitive diagnosis with histopathology of affected tissue.
- Treatment of Lawsonia intracellularis?
- Prognosis?
- Supportive - may include plasma transfusion.
Doxycycline.
Until clinical signs (hypoproteinaemia, ultrasonograpic evidence of intestinal thickening) resolve. - Depends on:
- duration of disease.
- degree of fibrosis and destruction of the intestinal architecture.
Cyathostome life cycle.
Migration of 4th stage larvae through mucosa of large intestine.
Can encyst (hypobiosis).
Emergence due to unknown stimulus (spring, late summer).
- causes inflammation of the colon.
— causing diarrhoea and PLE.
Younger horses tend to have higher burden.
Usually acute diarrhoea which can then become chronic.
Weight loss.
Ventral oedema.
Intermittent pyrexia.
Intermittent colic.
