Colitis
Neonate
Differential diagnoses
Foal heat diarrhoea
Viral especially rotavirus
Salmonella
Clostridia
Necrotising enterocolitis
Sepsis
Nutritional diarrhoea
parasitic diarrhoea
Strongyloides westeri
Gastroduodenal ulceration
Foals (up to about 10-12 months)
Differential diagnoses
Cryptosporidiosis
Parasitic diarrhoea e.g. strongyles vulgaris, cyathostomins
Proliferative enteropathy e.g. Lawsonia intracellularis
Rhodococcus equi colitis
Viral especially Rotavirus
Salmonella
Clostridia
Sepsis
Nutritional diarrhoea
Gastroduodenal ulceration
Parasitic diarrhoea e.g. Strogyloides westeri
Adults
Acute
Chronic
Clinical signs: hypovolaemia, endotoxaemia
1 week duration to >1 month duration
Salmonellosis
Parasitism (Larval cyathostominosis, strongylosis)
Clostridiosis
Antimicrobial associated diarrhoea
NSAID toxicity (right dorsal colitis)
sand enteropathy
Carbohydrate overload
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
signs of endotoxaemia
Depression
Tachycardia
Tachypnoea
Fever
Colic
Diarrhoea
Hyperaemic (toxic) mucous membranes
Usually see low white cell count, low neutrophil count, immature 'band' neutrophils
Treatment: polymyxin b, hyperimmune plasma, pentoxyfilline, flunixin
Moxidectin, fenbendazole
Can cause a plaque of oedema on ventral abdomen
Associated clinical signs
Colic due to pain
Muscle weakness and fasciculation's due to electrolyte loss (from intestinal mucosal ulceration causing plasma and blood loss)
Protein loss
weight loss and ventral oedema
Endotoxaemia
Vaculopathy
Laminitis
Ventral oedema
Pyrexia, depression, extended CRT, sweating
Tachycardia, altered mucous membrane colour, increased skin tenting (also caused by dehydration)
The increased borborygmi and diarrheic faeces is from decreased intestinal transit time and reduced water absorption from intestinal contents
Most cases in late winter and early spring
More common in younger animals (1-5 years old)
Approach to diagnosis
Clinical pathology
Red cell parameters considered in conjunction with protein concentrations will help to determine the extent of any dehydration
Anaemia
parasitic colitis
Gastric ulceration
White cell parameters
Extent of any endotoxaemia
Salmonellosis
Clostridiosis
Peritonitis
Total protein and albumin concentrations
Increased as a consequence of dehydration
decreased as a result of protein loss into the intestinal tract
Globulin concentrations may be increased as a result of dehydration or a chronic inflammatory response
Serum protein electrophoresis
helpful in distinguishing parasitic colitis, where an elevation in beta1 globulins may be appreciated
Severe diarrhoea will result in electrolyte losses
Sodium, potassium, calcium and bicarbonate especially
Direct visual inspection of faeces or microscopic examination of a wet preparation of faeces
often allow identification of cyathostome larvae in cases of parasitic colitis
Faecal worm egg count results should be interpreted with caution
the pathogenic stage of both large and small strongyles primarily involves immature parasites (not acquired ability to lay eggs)
both cyathostomosis and strongylosis may not be associated with a significant faecal worm egg count
faecal culture = vital step in identification of bacterial enteritis
e.g. salmonellosis, clostridiosis
Advisable to collect multiple samples over a period of at least 3 days
Does not mean cultured pathogenic bacteria is causative e.g. in cases of chronic diarrhoea where salmonella species are often cultured in association with a separate primary enteropathy
Rectal biopsy
samples should be collected from 10 and 2 o'clock positions to avoid the larger blood vessels in the dorsal midline of the rectum
Ultrasonography
Percutaneously through abdominal wall or per rectum
Sugar absorption tests
To assess small intestinal absorptive function
Most cases of diarrhoea involve changes to large intestine, but some involve small intestinal changes
Can be seen in some cases of parasitic colitis and intestinal lymphosarcoma and the infiltrative bowel diseases
Administer 1g/kg bodyweight of glucose via a stomach tube and then measure blood glucose concentrations over the following 4 hours
In a normal horse the blood glucose concentration reaches a peach of approx. double the baseline concentration at 2 hours
a reduced peak indicates a state of malabsorption and in an adult horse with diarrhoea, this suggests that there are significant changes present in both the small and large intestine
Surgical bowel +/- lymph node biopsy
histopathological examination of full thickness intestinal wall biopsies
can only be taken at laparotomy and usually requires general anaesthesia to allow samples to be collected from multiple sites along the intestinal tract
alternative: collect mesenteric lymph nodes biopsies (may reflect the pathological changes present in adjacent intestine)
can be performed laparoscopically in the standing animal
Initial pyrexia, depression and colic prior to onset of diarrhoea
profound leucopenia present at the acute stage
Salmonellosis often associated with previous stress or intercurrent disease
highly infectious and has zoonotic potential
isolate and barrier nurse
Rarely a cause of chronic diarrhoea
consider underlying disease process
often associated with start (or cessation) of antimicrobial therapy
other stresses e.g. transport, GA, withholding roughage may be risk factors
Both C perfringens and C difficile have been identified
Often younger animals (1-5) but can be seen in elderly
Weight loss may occur prior to diarrhoea
Usually occurs late winter and spring
Initial pyrexia and leucopenia are variable and faecal worm egg counts are often negative. Macroscopic faecal (or rectal glove) examination may identify larvae. Elevated Alpha and beta globulin concentrations may be seen.
Histopathological examination of a rectal mucosal biopsy can be diagnostic
Strongylosis usually a cause of colic or ill thrift. The condition may be associated with diarrhoea as a result of changes to blood supply in the large intestine. Faecal worm egg count may be negative.
Peritonitis
Diagnosis is confirmed by abdominal paracentesis and peritoneal fluid analysis. Aggressive treatment required.
Prognosis depends on underlying cause e.g. gut perforation, abscess, neoplasia
Lymphosarcoma
Typically insidious onset and slow progression and primarily affect small intestine.
Concurrent malabsorption and weight loss often occur.
Thickened bowel may be seen on rectal exam or USS
Dx - histopath of bowel wall or LN biopsy
Prognosis poor, but horse may respond to high-dose corticosteroids.
Hypoproteinaemia and hypoalbuminaemia develop rapidly and may present before the onset of diarrhoea
Usually causes an impaction colic
Diarrhoea often mild and intermittent
Acute deterioration associated with bowel wall inflammation and perforation
Sand is present in faeces and may be identified using sand sedimentation test.
Treatment
Maintain fluid and electrolyte balance once fluid deficit corrected
Fluid deficit (litres) = percentage dehydration x bodyweight (kg)
Maintenance fluid requirement (litres/day) = 0.05 litres/kg/bodyweight/day
The initial fluid deficit should be replaced within 4-12 hours and represents an extracellular fluid loss
Replacement with a balanced polytonic crystalloid fluid such as lactated Ringer's solution is most suitable.
In acute, severe cases, hypertonic saline may be used, but it is essential this is followed by an appropriate volume of polytonic crystalloid fluid to replace the extravascular extracellular fluid
If profuse diarrhoea continues more than 12 hrs
monitor calcium and potassium balance and supplement intravenous fluids if necessary
In severe cases of colitis, the loss of intravascular plasma proteins and reduced oncotic pressure results in fluid accumulation in the interstitial tissues (oedema) and it becomes difficult to maintain crystalloid fluids in the intravascular space
treatment = colloidal solution such as hetastarch or plasma
expensive tho
Caution with intravenous catheter care in diarrheic animals, as they are at an increased risk of complications e.g. jugular phlebitis and thrombosis
Continue until diarrhoea stops or fluid maintained with voluntary drinking.
Minimise endotoxaemia
reduce absorption of endotoxin
activated charcoal administered at 0.5 - 1g/kg by stomach tube once or twice daily.
Limit the effects of circulating endotoxin
Flunixin meglumine
0.25mg/kg intravenously 3x a day
Polymixin B
Endotoxin specific IgG
Prolong intestinal transit time
Codeine phosphate up to 3mg/kg orally 3x a day
Bismuth subsalicylate
up to 4 litres/500kg orally 2x a day
Antisecretory agents
Loperamide 0.1-0.2mg/kg orally 4x daily
Reduce bowel inflammation
NSAIDs
Flunixin (0.5-1.1mg/kg IV)
Corticosteroids
Dexamethasone 0.05mg/kg IV or IM
Nutritional support
Alfalfa or similar hay ad libitum
High protein and energy concentrate
Mineral supplementation
Turnout to grass can be beneficial in some instances
make all dietary changes gradually
General nursing
Isolation and barrier nursing if salmonella species or C difficile is suspected
Limb bandages/supports to prevent oedema accumulation
Tail protection
Perineal cleaning and protection with petroleum jelly to prevent scalding
Laminitis prophylaxis with frog supports and topical nitroglycerine
Specific therapy
Cyathostomosis/strongylosis
Anthelmintics
Fenbendazole (7.5-10mg/kg orally once daily for 5 consecutive days)
Ivermectin
0.2mg/kg orally
moxidectin
0/4mg/kg orally
Clostridiosis
Metronidazole 15mg/kg orally 3x a day
probiotics/yoghurt may be beneficial
Grain overload
nasogastric intubation to allow gastric decompression
Epsom salts (magnesium sulphate) 1g/kg by stomach tube
Aspirin 10mg/kg orally or IV once daily
Sodium bicarbonate intravenously if indicated by blood gas analysis
Laminitis prophylaxis (frog supports and topical nitroglycerine)
Peritonitis
Broad spectrum bactericidal antimicrobials 3 x daily in combination with gentamicin 2.2mg/kg IV 3x daily or 6.6mg/kg IV once daily
Sand enteropathy
Psyllium mucilloid 0.25-0.5kg for a 500kg horse in 4-8 litres of water by stomach tube
Ispaghula husk 300-400g for a 500kg horse in 4 litres of water by stomach tube
NSAID toxicity
Psyllium mucoid 30-60g administered in feed for 3-6 months
Misoprostal orally
decrease gastric acid secretion and increase recovery of the ischaemia-injured equine jejunum
Sucralfate 22mg/kg orally 2 or 3x daily
Metronidazole 10-15mg/kg orally 2x daily
Potomac horse fever
Tetracyclines 6/6mg/kg slowly IV once daily for 3-5 days
Prognosis
Better
Worse
Intermittent diarrhoea
Soft or cow pat faecal consistency
No or mild endotoxaemia
Animal able to maintain fluid balance
Voluntary drinking and eating continues
good response to correction of fluid/electrolyte imbalances
Diarrhoea resolves within 48 hours
Albumin concentration maintained
no secondary complications develop
Persistent diarrhoea
liquid faecal consistency
severe endotoxaemia
animal unable to maintain fluid balance
voluntary drinking and eating ceases
fluid/electrolyte balances continue
diarrhoea continues beyond 48 hours
hypoalbuminaemia develops
secondary complications such as thrombophlebitis, laminitis and septicaemia develop
Ventral oedema (increased hydrostatic pressure and vascular permeability, decreased oncotic pressure and lymphatic drainage)
Oxytetracycline only early in disease process, once colon inflamed it increases the permeability of the vasculature
Intracellular bacteria therefore penicillin/gentamicin will not work
Identification by bacterial culture or PCR analysis
103 colony-forming units/g feces or intestinal contents; demonstration of enterotoxin or cytotoxin A or B (for C difficile)
Slower onset, oral cavity ulcers; early ventral edema associated with hypoproteinemia; gastric or intestinal ulceration
Abdominal discomfort from intraluminal sequestration of fluid or gas, or 2ry to inflammatory mediator activity
Can be mild e.g. recumbency or inappetence or severe such as rolling and thrashing
Neorickettsia risticii is the causative agent which causes biphasic fever, laminitis, and colitis of variable severity
N risticii-associated colitis may be supported by comparing paired serum titers using immunofluorescence assay testing techniques
Diagnosis confirmed using antigen detection by identification of N risticii morulae in WBCs during the acute phase of the disease, isolation of the organism from WBCs or PCR testing of WBCs or faeces
Equine coronavirus can be a cause of acute equine colitis, and faecal PCR for equine coronavirus should be included in the screening process
Horses with acute colitis absorb large quantities of endotoxin across the disrupted intestinal mucosal barrier
High risk for developing laminitis, thrombophlebitis and disseminated intravascular coagulation
digital pulses should be monitored 3-4x daily until systemic signs of colitis abate
Endosperm is a hyperimmune serum obtained from horses vaccinated against salmonella typhimurium Re mutant (diluted in sterile isotonic saline or lactated ringers solution)
dilution at 1:10 or 1:20 to minimise the risk for immune mediated hypersensitivity reactions
Risk potential for nephrotoxic effects so use with care and not recommended in azotaemic horses
recommended to prevent endotoxin-induced prostanoid synthesis in horses
Compared to other NSAID regimens it has a lower risk of adverse effects including gastrointestinal ulceration, ileus and renal papillary necrosis
Firocoxib (cyclooxyrgenase-2 inhibitor drug)
fewer adverse effects
Antiinflammatories and analgesics
Flunixin meglumine (1.1mg/kg, IV, every 12 hours)
Phenylbutazone (2.2mg/kg, IV, every 12 hours)
can contribute to further damage of the intestinal epithelial barrier, so lower and less frequent does should be considered
Firoxocib
selective cyclooxyrgenase 2 inhibitor so safer in horses with similar beneficial anti-inflammatory effects
Must balance need for analgesic effects of non selective NSAIDs against the possibility of further bowel damage induced by blocking the protective effects of intestinal mucosal prostaglandins
Endogenous prostaglandins are important inhibitors of intestinal inflammation, an blocking these agents with nonselective NSAIDs may slow recovery and healing of inflamed intestinal mucosa
Analgesic combination with minimal effects of gastrointestinal motility
butorphanol (0.96-0.1mg/kg IM) and detomidine (0.01-0.02mg/kg IM)
Antimicrobials
Broad spectrum antimicrobials may be considered for profound/persistent neutropenia and risk for complications associated with sepsis, such as peritonitis, pneumonia, cellulitis, thrombophlebitis and disseminated intravascular coagulation.
Potassium penicillin G + gentamicin common regimen for horses with ongoing systemic disease
Oral broad spectrum antimicrobials are not recommended due to potential for further disruption of intestinal microbial population
Oral administered metronidazole (10-15mg/kg every 8hrs) may be indicated in horses in which Clostridium app are suspected to play a pathogenic role in disease
May have local anti-inflammatory effects and can cause loss of appetite in some horses
Most horses with acute colitis are partially or completely inappetent and lose protein due to cachexia and protein losing enteropathy
Partial or total parenteral nutrition may be indicated in horses that remain inappetent for more than 3-4 days
Frequent complications include laminitis, thrombophlebitis, debilitation and marked weight loss