Diarrhoea in Horses and Foals Flashcards

1
Q

adult vs foal - large vs small intestine

A

adult - LI only

foal - can be both

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2
Q

DDx - neonates

A
Foal heat diarrhoea 
Viral especially Rotavirus 
Salmonella 
Clostridia 
Necrotizing enterocolitis 
Sepsis 
Nutritional diarrhoea 
Parasitic diarrhoea – Strongyloides westeri 
Gastroduodenal ulceration
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3
Q

DDx - older foals (10-12 months)

A

Cryptosporidiosis
Parasitic diarrhoea – Strongylus vulgaris, cyathostomins
Proliferative enteropathy - Lawsonia intracellularis
Rhodococcus equi colitis
Viral, especially Rotavirus
Salmonella
Clostridia
Sepsis
Nutritional diarrhoea
Gastroduodenal ulceration
Parasitic diarrhoea – Strongyloides westeri

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4
Q

DDx - adults

A
Salmonellosis
Clostridiosis
Parasitism (Larval cyathostominosis, strongylosis) 
Antimicrobial-associated diarrhoea 
NSAID toxicity (right dorsal colitis) 
Sand enteropathy 
Carbohydrate overload 
Inflammatory or infiltrative disorders – IBD 
Dietary: abnormal fermentation 
Neoplasia – Lymphoma 
Peritonitis, Abdominal abscessation
undiagnosed
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5
Q

what is acute diarrhoea

A

Acute onset febrile diarrhoea

Clinical signs of hypovolaemia, endotoxaemia

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6
Q

acute diarrhoea - causes

A
Salmonellosis 
Parasitism (Larval cyathostominosis,strongylosis) 
Clostridiosis 
antimicrobial-associated diarrhoea 
NSAID toxicity (right dorsal colitis) 
Sand enteropathy 
Carbohydrate overload
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7
Q

chronic diarrhoea - causes

A

Salmonellosis
Parasitism (Larval cyathostominosis, strongylosis)
Sand enteropathy
NSAID toxicity (Right dorsal colitis)
Inflammatory of infiltrative disorders – IBD
Dietary: abnormal fermentation
Neoplasia – Lymphoma, Peritonitis, Abdominal abscessation

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8
Q

why try to make definitive diagnosis?

A

specific treatment

contagious +/- zoonosis

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9
Q

principles of therapy

A

address fluid loss
Address inflammation and endotoxaemia
Address specific cause

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10
Q

fluid therapy

A

check deficit
maintenance of fluid levels
ongoing losses need to be factored in

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11
Q

what is endotoxin

A

Part of the outer membrane of gram negative bacteria Released during cell death or rapid growth

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12
Q

where does endotoxin come from

A

Horse GIT normally has large numbers of G-ve bacteria in lumen - fermentation/digestion
Normal mucosal barrier prevents access to circulation
mucosal barrier breakdown = endotoxaemia

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13
Q

effects of endotoxaemia

A

Interacts with cells eg macrophages
Initiates systemic inflammation
Clinical signs of endotoxaemia
CV and GI dysfunction, shock, organ failure, death

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14
Q

endotoxaemia - clinical signs

A
Depression 
tachycardia 
Tachypnoea 
fever 
Colic 
Diarrhoea 
Hyperaemic ‘toxic’ mucous membranes
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15
Q

endotoxaemia - diagnosis

A

clinical signs
low white cell count
low neutrophil count
immature band neutrophils

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16
Q

endotoxaemia - treatment

A
  1. Prevent movement of endotoxin into the circulation
  2. Neutralize endotoxin before it interacts with inflammatory cells
  3. Prevent synthesis, release or action of inflammatory mediators
  4. Prevent endotoxin-induced cellular activation
17
Q

endotoxaemia - prevent access to circulation

A

remove dead tissue with exposed mucosa

18
Q

endotoxaemia - drugs

A

Polymixin B
Hyperimmune plasma
Pentoxyfilline
Flunixin

19
Q

foals and endotoxaemia

A

Similar effects as in adult horses
Usually associated with bacteraemia/sepsis
Large colon less well developed
gram negative bacteria population smaller?
Concern regarding nephrotoxicity - polymixin B, flunixin
Treatments - plasma, antibiotics

20
Q

foals on fluids

A

smaller volumes
intermittent, freq boluses or seperate mare + foal for continuous fluids
labour intensive

21
Q

treat vs refer

A

If horse/foal can keep up with fluid requirements by drinking, then probably OK to treat at home
Best to be over cautious with foals as they can deteriorate very rapidly
Contagious?
Isolation facilities can be provided at a hospital