Diarrhoea in calves Flashcards
Osmotic diarrhoea mechanism and characteristics
Osmotic pull of gut contents cause diarrhoea
Stool osmolality >400mosm (normally 300)
Faecal pH is acidic because bacteria grow in sugary anaerobic environment and produce lactate
Either from diffuse intestinal disease
Or can get with carbohydrate malabsorption (intolerance, overfeeding)
This diarrhoea gets WORSE WITH FEEDING
Secretory diarrhoea causes and characteristics
Due to bacterial enterotoxins, mucosal inflammation, elevated hydrostatic pressure
Stool osmolality nomrla and accounted for by electrolytes
Faecal pH normal/alkaline
What 3 things mediate pathology in neonatal calf diarrhoea
1) enterotoxin production (ETEC, salmonella)
2) inflammation (salmonella, crypto..)
3) villous atrophy (crypto, viruses)
THEN lead to intestinal hypersecrtion, maldigestion/absorption
E coli enterotoxins and mechanism of causing hypersecretion
ETEC heat-labile toxin: activates cAMP to uncouple secretion by crypt cell s
Heat-stabile toxin = same but via c-GMP activation
How does rotavirus mediate hypersecretion
Via NSP4 but unknown mechanism
Why can we still give oral glucose-electrolyte solutions for rehydration during enterotoxin related hypersecretory diarrhoea
Because there is no effect on substrate linked Na+ absorption
When don’t we use oral glucose-electrolyte solutions for rehydration in diarrhoea
Where mucosa destroyed
e.g in inflammation from salmonella, maldigestion with villous atrophy e,g with viruses
Rotavirus characteristics
=dsRNA virus
Peak incidence at 10 days old
See sudden onset in calves, fluid filled guts on PM and lesions from upper jejunum to ileum
Coronavirus characteristics
=ssRNA virus
Similar to rotavirus but more severe disease
COLON ALSO AFFECTED
Corona/rotavirus pathology
Viral infection of villus cells causes atrophy
So get crypt hyperplasia to cover villus cells BUT these are immature
= mainly osmotic diarrhoea due to malabsorption/digestion BUT also some secretory component
+ get acidosis because sugar hypofermentation allows bacteria production of lactate
Why might we give post-closure colostrum feeding in diarrhoea outbreak
Because anti-rotavirus antibodies in gut can give protection
BUT increased risk of Johne’s transmission; may want to vaccinate and harvest from Johne’s free dams
Diagnosis of E coli infection
Demonstration of K99 fimbrial antigen (allows attachment to gut wall)
Pathogenesis + signs
of ETEC diarrhoea
First week of life
= hypersecretory; via effects for toxins
Signs = fluid, malodorous diarrhoea, dehydration, depression, can get death
What is watery green diarrhoea with mucus typical of
Coccidiosis i.e crypto
Pathogenesis of cryptosporidia diarrhoea
Sporozoites hatch and penetrate microvilli; merozoites will reinvade microvillus
Overall: loss of villi so shortened vill, fluid filled gut
Mainly affects distal SI
WHat is persistent peri-weaning calf diarrhoea
Seen in calves after weaning
Unknown cause
- Chronic grey-brown diarrhoea lasting about a month
Could be fungal toxins, giardia may be involved
Which serotype bacteria causes colisepticaemia
EHEC 078
Major risk factor for colisepticaemia
low colostrum intake
signs/PM pathology of coli septicaemia
Acute septicaemia and endotoxaemia
Petechial haemorrhages, polyarthritis, meningitis etc
= congested carcass
Complications of navel ill infection
Joint ill, liver abscensses, valvular endocarditis, meningitis
4 pathogenesis factors in diarrhoea
1) Altered enterocyte transport e.g ETEC secretory diarrhoea
2) Change in strucutre/permeability e.g with villus stunting/crypt hyperplasia in virus infection, inflammation in salmonella
3) Osmotic effects e.g from loss of brush border enzymes so maldigestion
4) Altered motility
Differentiating E coli and Salmonella based on lactose fermentation
Grow on MacConkey’s agar
- E coli = lactose fermenting so goes pink
- Salmonella = non-lactose fermenting so colourless colonies
Which diarrhoea pathogen causes eroded, haemorrhagic surfaces with dysentry
Salmonella
Key difference in pathology location in rotavirus vs coronavirus
Rotavirus = prox/middle SI
Coronavirus = middle/distal SI AND COLON!
What is necrotising enteritis
Condition of unknown origin in beef suckler calves of a few months old
May be mycotoxin,BVD-like virus
REsembles BVD (but test negative)
Severe ulcerative lesions in GI tract and oral lesions
Why is it hard to isolate bacteria post-mortem from guts
Detach from mucosa within 30 mins of death
How does diarrhoea lead to acidosis
Loss of ECF so contraction of blood volume; lower renal perfusion so less H+ excretion
+ some contribution from more anaerobic metabolism producing lactate
Electrolye changes with diarrhoea
ACidosis
Hyponatraemia
(K+ changes but differ based on stage)
Using base deficits to assess level of acidosis
Range from 0 (normal) to 20mmol/l which is close to death
IV correction of acidosis
Spike of bicarbonate 200-400mmol of HCO3-
What to do to manage osmotic diarrhoea (acidic faeces) with fluids etc
Withdraw milk because no villi to absorb it well
- Can give oral fluids
NB: if calves DO WANT TO SUCK; give more dilute milk to reduce osmolality
Key difference in faeces b/w osmotic and secretory diarrhoea
Osmotic = acidic faeces
Secretory = neutral/alkaline faeces
Managing secretory diarrhoea - fluids/food?
Absorptive mechanisms still in tact so don’t withdraw milk
Rehydrate with oral fluids based on % dehydration
Managing diarrhoea from inflammation with fluids?
May avoid oral glucose as it could feed bacteria and make inflammation worse
- IV may be solution
Which alkalinising agent is most effective at counteracting acidosis
Bicarbonate
Want to give oral fluids with 40-80mmol/L
Things to be careful with when giving bicarbonate fluid
DO not give with calcium containing fluids as will precipitate
Don’t use when milk being fed as interfered with digestion (would give another alkalinising agent)
ALkalinising agents for maintenance vs resuscitation
acetate, lactate
Options of IV fluids to correct acidosis
1) Lactated ringers; corrects acidosis via lactate; inadequate for SEVERE cases
2) Saline + bicarbonate
Effect of fluid administration of blood K+ levels
= an extracellular ion so will get increased secretion
– Should supplement to avoid hypokalaemia complication
Which lactate isomer is not metabolised
D
What does faeces from ruminal acidosis look like
Pale and pasty
What does faeces look like in cases of endotoxaemia (e.g mastitis/metritis)
Dark, watery
What does diarrhoea with air bubbles suggest
Maldigestion e.g Johne’s
Salmonella strains
S Dublin = adapted to cattle; main one; can be carriers
S Typhi = ubiquitous
Clinical signs of salmonellosis
+ pathology
Signs: pyrexia, profuse diarrhoea progressing to dysentery
Pathology: enteritis, severe and haemorrhagic with shreds of mucosa in lumen
+ paratyphoid nodules = focal granulomas in liver/spleen
What are the main economic effects of BVD
Immunosuppressive
Reproductive
Acute BVD infection
Usually asymptomatic, mild diarrhoea, transient milk drop
Can get severe disease
Cause of black disease
Clostridium nevyi bacterial infection of necrotic tracts in liver
Post mortem findings with fasciolosis
Liver fibrosis esp ventral lobe
Compensatory dorsal hypertrophy
Calcification into pipe stem lesions
Clinical signs of liver fluke
ILl thrift, anaemia, sub mandibular oedema, weight loss
Causative agent of Johne’s disease
Mycobacterium avium subspecies paratuberculousis
- Animals pick it up in first month of life; but don’t get disease until >3 years old
Signs of Johne’s disease
chronic diarrhoea with bubbly scour, weight loss, ill thrift, malabsorption with hypoproteinaemia (albumin conc = 15g/L vs 30g/L)
Pathology of Johne’s disease
stunted, thickened villi full of macrophages, thickened/granular ileum = cobblestone gut
How does Johne’s disease work
INtracellular mycobacteria are taken up by M cells covering peyer’s patches; get cellular infiltrate into villi causing malabsorption
See thickened ileum full of macrophages + giant cells and lymphocytes
Why is Johne’s disease vaccination only allowed under special Defra license
Can affect TB test results
Cause of winter dystentery
Bovine coronavirus mainly
= explosive herd outbreaks; repeatedly seen when immunity wanes
Agent causing malignant catarrhal fever
Ovine herpes virus 2 (carried by healthy sheep)
Signs of malignant catarrhal fever
Pyrexia, erosive stomatitis, muzzle crusting, red lesions of gums/palate, constipation then diarrhoea
FATAL
What is the pathology mechanism of malignant catarrhal fever
type III hypersensitivity and immune complex deposition in small capillary beds
Renal amyloidosis pathogenesis
Amyloid = anti-parallel beta sheets which body struggles to degrade
Get protein deposition in blood vessels including glomeruli in kidneys; get plasma protein loss in urine
–> Hypoproteinaemia –> oedema
Kidneys = double usual size with waxy granular surface
Diagnosing renal amyloidosis
Marked proteinuria (>3000mg/L) severe hypoalbuminaemia <10g/L
