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Small Ruminants > Diarrhoea in lambs and kids > Flashcards

Diarrhoea in lambs and kids Flashcards

1
Q

What is haematochezia/malodorous faeces likely to be due to

A

Clostridia or Salmonella

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2
Q

What is yellow water diarrhoea likely to be a result of

A

Secretory; i.e crypto, E coli

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3
Q

What is water/brown diarrhoea likely to be caused by

A

Rota virus

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4
Q

What is white/pasty diarrhoea likely to be due to

A

Nutritional

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5
Q

What is nutritional diarrhoea

A

Pastry white diarrhoea in hand/bottle fed lambs due to poor hygiene or poor mixing of milk
> Can get secondary infection later

Also nutritional diarrhoea can be a result of lush pasture or high energy diet changes

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6
Q

Dealing with nutritional diarrhoea in lambs

A

In an individual; withhold milk for a bit to give gut time to rest
+ can give oral electrolytes

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7
Q

Cause of colisepticaemia in young lambs

A

Enterotoxigenic E coli
K99/F5 and F41
-> Produce heat stabile/labile toxin which gives a secretory diarrhoea
–> + can get septicaemia following mucosal damage

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8
Q

Pathogenesis of enterotoxigenic E coli

A

Adhered to the gut at the lower jejunum and ileum; produces toxins
-> Toxins cause secretion of ions; secretory diarrhoea

+ can get septicaemia if there is mucosal damage

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9
Q

Post mortem results in enterotoxigenic E coli infection in lambs

A

Lower jejunum + ileum: hyperaemic mucosa, lacteal distension, neutrophil migration

Colon and caecum are unaffecte

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10
Q

Pathogenesis of watery mouth disaese

A

Non-enterotoxigenic E coli
Ingestion; enteric multiplication; translocation to bloodstream; release of endotoxins; destruction of liver

= ENDOTOXAEMIA

Key factor = HYPOGAMMAGLOBULINAEMIA

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11
Q

Post mortem results from watery mouth in lambs

A

Distension of abomasum with clear acidic fluid
Retained meconium due to gut stasis
Petechial haemorrhages and other septicaemic lesions

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12
Q

Pathogenesis of salmonellosis in lambs

A

Enterotoxins + invasion
-> Get septicaemia

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13
Q

Clinical signs of salmonellosis

A

Foul diarrhoea, septicaemia, pyrexia, abdominal pain, dehydration, shock

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14
Q

Post mortem of lamb with salmonellosis

A

Septicaemia, abomasitis, necrotic enteritis of intestines
+ may see swollen liver and peteichial haemorrhages on organs

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15
Q

What antibiotics could we give to a lamb with enterotoxigenic E coli

A

Systemic tetracyclines, penicillin

NB: oral spectinomycin no longer effective

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16
Q

Cause of lamb dysentery

A

Clostridium perfringens type B

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17
Q

Why is clostridium perfringens especially prevalent in young lambs

A

Because toxins are trypsin sensitive and lambs have low levels of trypsin

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18
Q

Pathogenesis of lamb dysentery (C perfringens type B)

A

Necrotising exotoxins cause ulceration and haemorrhage in intestinal mucosa

Usually death within hours; if they survive a few days get neurological signs

Usually affects well fed singletons

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19
Q

Post mortem findings in C perfringens lamb dysentery

A

Ulceration and haemorrhage of small intestine’ give ‘red guts’
Guts congested/gassy with frothy yellow/red liquid

Swollen, friable liver and kidneys, + mesenteric lymph nodes

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20
Q

What is the causative agent of ‘red gut’

A

C perfringens type B

+ Also have condition by same name due to intestinal torsion

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21
Q

What to do once lamb dysentery identified in a flock

A

Inject all newly born lambs with lamb dysentery anti-serum

Can try penicillin/amoxicillin in those affected

22
Q

Which type of rotavirus usually causes disease in lambs and kids

A

B

23
Q

Pathogenesis of rotavirus infection in lambs/kids

A

Virus replicates in mature villus cells; get villus fusion and thickening; infiltration of immune cells; atrophy of villus
-> Causes diarrhoea of malapsortion (+some secretory element due to crypt cell hyperplasia).

24
Q

Which animals does crypto affect

A

Mainly indoor groups
- Kids have higher mortality than lambs (likely due to more artificial feeding)

25
Q

Pathogenesis of cryptosporidium parvum

A

Ileum: infection causes villus atrophy and compensatory crypt hyperplasia
-> Malabsorptive diarrhoea

Infective stage produced within animal so can get autoinfection of new villus tips

Usually self-llimiting

26
Q

Importance of giardia in ruminants

A

Low
BUT zoonotic

27
Q

WHen might we want to give sodium bicarbonate when treating neonatal diarrhoea

A

If there is acidosis present
e.g in Crypto or E coli watery mouth

28
Q

Care to take when giving bicarbonate solutions

A

NOT oral ones with milk as will stop milk clotting
NOT IV with Ca2+ containing solutions; will precipitate

29
Q

How do we protect lambs from clostridium perfringens (lamb dysentery)

A

Give ewes toxoid vaccine 6 weeks before lambing to ensure high quality colostrum

30
Q

What antibiotic would we give for salmonellosis

A

potentiated sulphonamides

31
Q

A-E of clostridia diseases caused

A

A = enterotoxaemia with jaundice
B = lamB dysentery
C = struCk
D = pulpy kiDney disease
E = Enterotoxaemia in calves

32
Q

Which Clostridia toxins are protected by colostrum

A

beta (found in type B and C) = lethal, necrotising toxin

33
Q

Why don’t we see pulpy kidney disease in goats

A

Because less uptake of the epsilon toxin; so just acts a bit in SI to give colic and diarrhoea

34
Q

When do we see ‘Struck’ in lambs

A

6-8 months old lambs at pasture; after changes in diet
Signs are colic, lethargy, convulsion

35
Q

Post mortem of lamb dead from struck (C perfringens type C)

A

Acute haemorrhagic abomasitis, haemorrhagic enteritis, lots of straw-coloured fluid in peritoneum, systemic toxaemia evidence

36
Q

What causes pulpy kidney at post mortem

A

= accelerated post-mortem necrosis due to EXCESS GLUCOSE in kidneys at time of death

> On histopath will see widespread renal necrosis

37
Q

Pathology of Clostridium perfringens type D disease + PM findings

A

Enterotoxaemic disease via GI tract absorption of toxin
> Straw coloured fluid in peritoneum/pericardium
> Petechial haemorrhages of epi/endocardium
Kidneys soft with detachable capsule

38
Q

What disease is associated with eating frosted root crops

A

Brazy - from clostridium septicum
= older group affected compared with clostridium perfringens

39
Q

How do we demonstrate clostridia toxins

A

Via neutralisation test in mice with anti-sera

40
Q

Which Eimeria species are highly pathogenic in sheep

A

E ovinoidalis
E crandalis

41
Q

When do we see coccidiosis

A

In lambs/kids in intesnvei conditions esp at weaning because stressful

42
Q

Eimeria pathogenesis and psot mortem findings

A

Penetration into cells of large intesting, reproduction and exit; damaging mucosa
> See haemorrhagic lesions in caecum and colon, rasied white spots

43
Q

Clinical signs of coccidiosis

A

diarrhoea, haematochezia, mucoid faeces, tenesmus (straining because LI affected), in chronic cases see poor growth

44
Q

How long do eimeria oocysts survive on pasture

A

2 years

45
Q

Which drugs are coccidiocidal (as well as static)

A

Trimethoprim sulphonamide
Amprolium
Toltrazuril

46
Q

Difference with N battus lifecycle compared to other nematodes

A

Reaches infective stage (L3) WITHIN the oocyst
- This egg hatches in response to cool then warming i.e spring; so get disease in young lambs

47
Q

How does red gut (intestinal torsion work)

A

When weaned lambs move to lush pasture/lots of creep
- Relates to change in diet and fermentable carbohydrates

See enlarged intestines with displacement/torsion on PM

48
Q

What is protein engorgement/acidosis

A

acute metabolic disease seen in lambs in autumn being fed cereals indoors

> Diet causes change in bacterial population –> fall in ruminal pH –> increase lactic acid production, inflammation of rumen wall and reduction in bacteria needed to digest fibre

49
Q

What are the signs of protein engorgement/acidosis

A

Depression, bloat, abdominal distension, scour, mucoid foul-smelling diarrhoea, tachycardia, weakness

50
Q

How can we treat protein engorgement/acidosis

A

Lavage rumen via oral tube and give oral antacids and antifoaming agents
- May have to do rumenotomy to remove grain from the stomach.

Small Ruminants (22 decks)

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