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Lent term fourth year > Diarrhoea in calves > Flashcards

Diarrhoea in calves Flashcards

1
Q

Osmotic diarrhoea mechanism and characteristics

A

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

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2
Q

Secretory diarrhoea causes and characteristics

A

Due to bacterial enterotoxins, mucosal inflammation, elevated hydrostatic pressure

Stool osmolality nomrla and accounted for by electrolytes
Faecal pH normal/alkaline

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3
Q

What 3 things mediate pathology in neonatal calf diarrhoea

A

1) enterotoxin production (ETEC, salmonella)
2) inflammation (salmonella, crypto..)
3) villous atrophy (crypto, viruses)

THEN lead to intestinal hypersecrtion, maldigestion/absorption

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4
Q

E coli enterotoxins and mechanism of causing hypersecretion

A

ETEC heat-labile toxin: activates cAMP to uncouple secretion by crypt cell s
Heat-stabile toxin = same but via c-GMP activation

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5
Q

How does rotavirus mediate hypersecretion

A

Via NSP4 but unknown mechanism

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6
Q

Why can we still give oral glucose-electrolyte solutions for rehydration during enterotoxin related hypersecretory diarrhoea

A

Because there is no effect on substrate linked Na+ absorption

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7
Q

When don’t we use oral glucose-electrolyte solutions for rehydration in diarrhoea

A

Where mucosa destroyed
e.g in inflammation from salmonella, maldigestion with villous atrophy e,g with viruses

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8
Q

Rotavirus characteristics

A

=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

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9
Q

Coronavirus characteristics

A

=ssRNA virus
Similar to rotavirus but more severe disease
COLON ALSO AFFECTED

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10
Q

Corona/rotavirus pathology

A

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

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11
Q

Why might we give post-closure colostrum feeding in diarrhoea outbreak

A

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

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12
Q

Diagnosis of E coli infection

A

Demonstration of K99 fimbrial antigen (allows attachment to gut wall)

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13
Q

Pathogenesis + signs
of ETEC diarrhoea

A

First week of life
= hypersecretory; via effects for toxins
Signs = fluid, malodorous diarrhoea, dehydration, depression, can get death

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14
Q

What is watery green diarrhoea with mucus typical of

A

Coccidiosis i.e crypto

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15
Q

Pathogenesis of cryptosporidia diarrhoea

A

Sporozoites hatch and penetrate microvilli; merozoites will reinvade microvillus

Overall: loss of villi so shortened vill, fluid filled gut

Mainly affects distal SI

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16
Q

WHat is persistent peri-weaning calf diarrhoea

A

Seen in calves after weaning
Unknown cause
- Chronic grey-brown diarrhoea lasting about a month
Could be fungal toxins, giardia may be involved

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17
Q

Which serotype bacteria causes colisepticaemia

A

EHEC 078

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18
Q

Major risk factor for colisepticaemia

A

low colostrum intake

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19
Q

signs/PM pathology of coli septicaemia

A

Acute septicaemia and endotoxaemia
Petechial haemorrhages, polyarthritis, meningitis etc
= congested carcass

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20
Q

Complications of navel ill infection

A

Joint ill, liver abscensses, valvular endocarditis, meningitis

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21
Q

4 pathogenesis factors in diarrhoea

A

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

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22
Q

Differentiating E coli and Salmonella based on lactose fermentation

A

Grow on MacConkey’s agar
- E coli = lactose fermenting so goes pink
- Salmonella = non-lactose fermenting so colourless colonies

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23
Q

Which diarrhoea pathogen causes eroded, haemorrhagic surfaces with dysentry

A

Salmonella

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24
Q

Key difference in pathology location in rotavirus vs coronavirus

A

Rotavirus = prox/middle SI
Coronavirus = middle/distal SI AND COLON!

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25
Q

What is necrotising enteritis

A

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

26
Q

Why is it hard to isolate bacteria post-mortem from guts

A

Detach from mucosa within 30 mins of death

27
Q

How does diarrhoea lead to acidosis

A

Loss of ECF so contraction of blood volume; lower renal perfusion so less H+ excretion

+ some contribution from more anaerobic metabolism producing lactate

28
Q

Electrolye changes with diarrhoea

A

ACidosis
Hyponatraemia
(K+ changes but differ based on stage)

29
Q

Using base deficits to assess level of acidosis

A

Range from 0 (normal) to 20mmol/l which is close to death

30
Q

IV correction of acidosis

A

Spike of bicarbonate 200-400mmol of HCO3-

31
Q

What to do to manage osmotic diarrhoea (acidic faeces) with fluids etc

A

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

32
Q

Key difference in faeces b/w osmotic and secretory diarrhoea

A

Osmotic = acidic faeces
Secretory = neutral/alkaline faeces

33
Q

Managing secretory diarrhoea - fluids/food?

A

Absorptive mechanisms still in tact so don’t withdraw milk

Rehydrate with oral fluids based on % dehydration

34
Q

Managing diarrhoea from inflammation with fluids?

A

May avoid oral glucose as it could feed bacteria and make inflammation worse
- IV may be solution

35
Q

Which alkalinising agent is most effective at counteracting acidosis

A

Bicarbonate

Want to give oral fluids with 40-80mmol/L

36
Q

Things to be careful with when giving bicarbonate fluid

A

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)

37
Q

ALkalinising agents for maintenance vs resuscitation

A

acetate, lactate

38
Q

Options of IV fluids to correct acidosis

A

1) Lactated ringers; corrects acidosis via lactate; inadequate for SEVERE cases
2) Saline + bicarbonate

39
Q

Effect of fluid administration of blood K+ levels

A

= an extracellular ion so will get increased secretion
– Should supplement to avoid hypokalaemia complication

40
Q

Which lactate isomer is not metabolised

A

D

41
Q

What does faeces from ruminal acidosis look like

A

Pale and pasty

42
Q

What does faeces look like in cases of endotoxaemia (e.g mastitis/metritis)

A

Dark, watery

43
Q

What does diarrhoea with air bubbles suggest

A

Maldigestion e.g Johne’s

44
Q

Salmonella strains

A

S Dublin = adapted to cattle; main one; can be carriers
S Typhi = ubiquitous

45
Q

Clinical signs of salmonellosis
+ pathology

A

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

46
Q

What are the main economic effects of BVD

A

Immunosuppressive
Reproductive

47
Q

Acute BVD infection

A

Usually asymptomatic, mild diarrhoea, transient milk drop
Can get severe disease

48
Q

Cause of black disease

A

Clostridium nevyi bacterial infection of necrotic tracts in liver

49
Q

Post mortem findings with fasciolosis

A

Liver fibrosis esp ventral lobe
Compensatory dorsal hypertrophy
Calcification into pipe stem lesions

50
Q

Clinical signs of liver fluke

A

ILl thrift, anaemia, sub mandibular oedema, weight loss

51
Q

Causative agent of Johne’s disease

A

Mycobacterium avium subspecies paratuberculousis
- Animals pick it up in first month of life; but don’t get disease until >3 years old

52
Q

Signs of Johne’s disease

A

chronic diarrhoea with bubbly scour, weight loss, ill thrift, malabsorption with hypoproteinaemia (albumin conc = 15g/L vs 30g/L)

53
Q

Pathology of Johne’s disease

A

stunted, thickened villi full of macrophages, thickened/granular ileum = cobblestone gut

54
Q

How does Johne’s disease work

A

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

55
Q

Why is Johne’s disease vaccination only allowed under special Defra license

A

Can affect TB test results

56
Q

Cause of winter dystentery

A

Bovine coronavirus mainly
= explosive herd outbreaks; repeatedly seen when immunity wanes

57
Q

Agent causing malignant catarrhal fever

A

Ovine herpes virus 2 (carried by healthy sheep)

58
Q

Signs of malignant catarrhal fever

A

Pyrexia, erosive stomatitis, muzzle crusting, red lesions of gums/palate, constipation then diarrhoea
FATAL

59
Q

What is the pathology mechanism of malignant catarrhal fever

A

type III hypersensitivity and immune complex deposition in small capillary beds

60
Q

Renal amyloidosis pathogenesis

A

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

61
Q

Diagnosing renal amyloidosis

A

Marked proteinuria (>3000mg/L) severe hypoalbuminaemia <10g/L

Lent term fourth year (38 decks)

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