Chronic diarrhoea Flashcards
Small intestinal diarrhoea
Vomiting common
Weight loss common
Polydipsia common
Often appetite increased or reduced
Watery/bulky faeces
Faecal volume increased
Defaecate 1-3 times a day
Faecal fat ± starch may be present
Tenesmus not present
Urgency not present
Mucus not present
If blood present, melaena
Minimal flatulence
Large intestinal diarrhoea
Sometimes vomit (30%)
Usually no weight loss
No polydipsia
Appetite often normal
Faecal type varies
Volume normal or increased
Defaecate > 6 times a day
No faecal fat (unless secondary)
Tenesmus often present
Urgency often present
Mucus often present
If blood present, fresh
Flatulence common
Common dietary causes of chronic SI diarrhoea
Chronic or intermittent scavenging
Chronic dietary intolerance e.g. lactose intolerance, gluten-sensitive enteropathy, other less well-defined food allergies (e.g. as cause of lymphocytic-plasmacytic enteritis)
Common infectious GI causes of chronic SI diarrhoea
e.g. salmonella, campylobacter, trichuris, giardia can particularly become chronic
Common small intestinal disease causes of chronic SI diarrhoea
Chronic inflammatory enteropathy which may be food responsive; antibiotic responsive (“Antibiotic responsive diarrhoea” (ARD)), steroid responsive (idiopathic IBD), or non-responsive/refractory.
SI neoplasia (lymphoma, mast cell tumours, adenocarcinomas)
SI partial obstruction (e.g. FB, intussusceptions - ileo-caeco-colic commonest, then jejuno-jejunal, strictures etc)
Lymphangectasia
Increased permeability due to portal congestion: R-sided CHF, liver disease
Rare brush border enzyme deficits
“Short bowel syndrome” after extensive SI resection (and overgrowth of bacteria particularly if ileocaecocolic valve resected, maldigestion and malabsorption)
Pancreatic causes of chronic SI diarrhoea
exocrine pancreatic insufficiency (EPI); chronic pancreatitis; pancreatic adenocarcinoma
Liver causes of chronic SI diarrhoea
due to portal congestion ± lack of bile salts (-latter actually rare even in cholestatic liver disease)
Renal causes of chrnic SI diarrhoea
due to uraemia ± hypoalbuminaemia/oedema of nephrotic syndrome.
Endocrine causes of chronic SI diarrhoea
hypoadrenocorticism dogs; hyperthyroidism cats
Initial treatment of chronic SI diarrhoea
In many cases, if otherwise bright, hospitalisation for intravenous fluid therapy etc usually not indicated.
Treat any confirmed infections (e.g. giardia, campylobacter, ascarids) and identify/treat extra-GI pathologies (e.g. EPI, pancreatitis etc).
If tests all normal, usually recommend a strict dietary exclusion trial using hypoallergenic or novel protein diet for a minimum of 4 weeks to rule out dietary hypersensitivity/intolerance and/or scavenging (important to prevent scavenging and treats in this time).
You may give a 3-day giardia dose of fenbendazole to rule out intestinal parasitism (as many are intermittently shed and parasitology can therefore be negative) and you may (controversial) elect to give a one month course of metronidazole or tylosin
Otherwise, it is recommended that you do gut biopsies first before a long course of antibiotics.
Radiography for chronic SI diarrhoea
Plain abdominal radiographs for evidence of obstruction (gravel signs, gas-filled loops of bowel), foreign bodies, intussusceptions, abnormalities of other organs.
Plain thoracic radiographs to check for tumour metastases (e.g. pancreatic adenocarcinoma).
Note contrast radiographs (barium follow-through) very limited usefulness in chronic diarrhoea – may be useful for demonstrating partial obstruction (e.g. due to neoplasia or intussusception) but largely replaced by ultrasound.
- Very insensitive to generalised gut wall infiltration.
- Contra-indicated if suspect bowel rupture as barium can cause or exacerbate peritonitis.
Ultrasound for chronic SI diarrhoea
Very useful for evaluating other abdominal viscera, identifying free abdominal fluid, or structural GI pathology (e.g. mass, intusscusceptions etc).
Less useful for evaluating diffuse intestinal disease although can assess gut wall thickness and layering.
May see loss of normal layering with lymphosarcoma whereas this is normally maintained in inflammatory bowel disease, but not invariable.
Endoscopic biopsy for chronic SI diarrhoea
most commonly performed in referral practice
Only duodenum, duodenum, ileum and colon are accessible and samples are generally small and superficial (mucosal/submucosal).
However, multiple biopsies (usually 7-10 from each region) can be taken and under endoscopic guidance so may give a more representative idea of the pathology.
Which part of the instestines cannot be accessed endoscopically?
The jejunum
Laparotomy biopsies for chronic SI diarrhoea
Laparotomy allows visual inspection of other organs including stomach, pancreas, liver and mesenteric lymph nodes and allows full thickness biopsies to be taken from all down gut (although colon usually not biopsied due to risk of dehiscence).
Main disadvantage is the increased invasiveness/morbidity, risk of dehiscence, and often sampling blindly as mucosal lesions not visible externally.
Laparoscopic biopsies for chronic SI diarrhoea
Possible less invasive technique
Pros of endoscopic biopsies
Less invasive
Minimal risk of perforation
Luminal surface can be visualised
Multiple guided biopsies
Inspection/biopsy of stomach, duodenum, oesophagus, colon, ileum possible
Cons of endoscopic biopsies
Technically challenging
Requires expensive equipment
Requires starvation +/- KleanPrep & enema preparation
Partial thickness
More difficult to differentiate IBD and lymphoma
Pros of surgical biopsies
Assessment/biopsy of jejunum and other ogans possible
Full thickness and larger biopsies
More reliable to differentiate IBD and lymphoma
No special equipment needed
Cons of surgical biopsies
More invasive
Increased morbidity and post operative pain
Risk of dehiscence and peritonitis
Fewer samples taken and pathology may not be visible from serosal surface
Oesophagus not accessible and colon not usually biopsied
Chronic inflammatory enteropathis (CIE, IBD)
Small intestine, large intestine, stomach or all three.
Often patchy/focal esp small intestine ± colon.
The aetiology of chronic inflammatory enteropathies in dogs and cats probably represent complex interactions between host genetics mucosal immunity and the intestinal microbiota.
Work in man and lab animals suggests genetic inherent susceptibility to gut immune dysregulation.
Subdivisions of CIE
- Food-responsive enteropathy (FRE)
-ruled out using exclusion hydrolyzed or novel-protein diet >6weeks - Antibiotic-responsive diarrhoea/enteropathy (ARD/ARE)
– ruled out using an appropriate antibiotic trial - Steroid/immunosuppressant-responsive enteropathy (often referred to as idiopathic inflammatory bowel disease, IBD)
- Non-responsive or refractory enteropathy
Food-responsive enteropathies
True food allergy is rare but “food-responsive enteropathy” in general is
common.
SI diarrhoea may improve non-specifically using a low allergy diet because it is very digestible - does not imply there is an allergic basis to the disease.
Most cases of confirmed food allergy in dogs and cats produce pruritic skin diseases rather than GI signs but can (more common in cats).
Which hypersensitivity types are implicated in allergic SI disease?
Types I, III, and IV
Diagnosis of food allergies
generally diagnosed clinically on a good response to an exclusion diet and recurrence on re-challenge
Blood tests and other tests very unreliable.
Antibiotic responsive diarrhoea (ARD)
Defined as cases of diarrhoea with no other cause diagnosed which respond to antibiotic therapy and require long term use to maintain clinical remission.
may have increased numbers of bacteria (whatever that may mean) or may more represent an abnormal host immune response to normal bacteria.
Small intestinal bacterial overgrowth (SIBO)
no longer really described as such.
It was defined on results of duodenal juice culture; defined overgrowth based on standard culture methods.
HOWEVER PCRs now show many more bacteria in small intestine than previously thought (many do not grow in traditional cultures) so it is not really clear what normal bacterial population in dogs and cats is and no real over-lap between dogs with classical SIBO and dogs which respond to antibiotics.
Probably not total numbers which are important but host response and types of bacteria there: some gut bacteria can cause disease, some are protective and some are neutral so absolute numbers probably not important.
Reasons for ARD
Commonest form is “primary” in young, large breed dogs especially GSDs.
- Probably result of aberrant host immune response – defects in innate immunity have been demonstrated in GSDs.
- Defective immune response probably predisposes/progresses to inflammatory bowel disease.
Deranged SI/gastric motility e.g.” gastric dumping”, SI ileus
Increase in unabsorbed nutrients e.g. in EPI, chronic inflammatory enteropathies
Reflux of bacteria from colon if ileocaecocolic valve has been surgically removed – these cases may need long term antibiotics to prevent diarrhoea.
Reduced gastric acid secretion – rare in small animals unless they are on omeprazole
Clinical signs of ARD
chronic diarrhoea (classically steatorrhoea with some largeintestinal character due to fat maldigestion), weight loss and may also be vomiting and reactive increase in hepatocellular enzymes in some.
Mild changes on histology of SI - normal in 60%.
30% show partial villus atrophy and mild lymphocytic-plasmacytic infiltrate
How does ARD cause clinical signs?
Bacterial deconjugation of bile salts reducing fat emulsification so digestion. It is particularly bacteroides species which do this in man (anaerobes) and they also bind B12. Deconjugated bile salts cause colonic irritation and secretory diarrhoea.
Bacterial breakdown of fat to hydroxy fatty acids which also cause secretory diarrhoea in colon (and smell!).
Interference with brush border enzymes and enterocyte function.
Potential for certain bacterial antigens to cause aberrant immune responses which may predispose to inflammatory bowel disease?
Diagnosis of ARD
Best diagnostic tests are to rule out everything else (including endoscopic gut biopsies) + trial of antibiotics (ARD).
N.B. Faecal cultures no help as only give colonic flora!
Treatment of ARD
Antibiotics: 4-8 weeks or longer of metronidazole 10 mg/kg bid or tylosin 10 mg/kg tid or oxytetracycline 10-20 mg/kg bid.
Low fat diet recommended - fat not an essential dietary component except need a small amount as vehicle for fat soluble vitamins and to provide EFAs.
Easily digestible diet important - to reduce undigested nutrients left in lumen for bacteria to work on ± dietary fructo-oligosaccharides may encourage normal flora.
Usually rapid resolution of diarrhoea with treatment but may need to treat for months/years if no obvious precipitating factor e.g. GSD.
Often try to discontinue due to concerns over responsible anti-biotic use but can relapse and require long-term treatment.
Steroid responsive enteropathies
Chronic (>3 weeks) persistent or recurrent GI signs
Histopathological evidence of mucosal inflammation
Exclusion of other causes of the inflammation (such as infectious or food allergic)
Inadequate response to dietary, antibiotic and anthelmintic therapies alone
Clinical response to anti-inflammatory or immunosuppressive agents
Types of IBD found on biopsy
Lymphocytic-plasmacytic enteritis (+/- gastritis +/- colitis)
Eosinophilic enteritis (+/- gastritis +/- colitis)
Lymphocytic-plasmacytic enteritis (± gastritis ± colitis)
commonest form of
inflammatory bowel disease in dogs and cats
However, L-P infiltrate may also occur secondary to other conditions e.g. ARD, giardia, and possible confusion between severe L-P enteritis and lymphosarcoma on biopsy so beware!
Severe cases show protein-losing enteropathy.
Some breed-associated L-P enteritis
Eosinophilic enteritis (± gastritis ± colitis)
usually more severe condition than L-P enteritis ± protein-losing enteropathy.
Need to rule out intestinal parasitism and will produce eosinophilic infiltrate.
Note cats may suffer eosinophilic enteritis as part of more generalised hyper-eosinophilic syndrome involving liver, spleen, mesenteric lymph nodes, kidneys, adrenals ± lungs, skin and other organs - these need life long high doses of steroids and prognosis poor.
Treatment of chronic inflammatory enteropathies
Hypoallergenic diet (properly designed and adhered to!).
May give fenbendazole to rule out giardiasis/intestinal parasitism.
Consider probiotics/prebiotics (or antibiotics as above but controversial)
If the above are curative, then strictly speaking, it is not IBD (!) – if not add in immunosuppressives.
Immunosuppressives for chronic inflammatory enteropathies
Typically start with steroids: 1-2mg/kg prednisolone once a day.
May also add in a second immunosuppressive such as cyclosporine or chlorambucil to allow long term control with minimal side effects.
Try to wean off slowly.
Many dogs are stable long term on very low doses as long as you are careful with diet.
NB: IF CONSIDERING BIOPSY, THIS SHOULD BE PERFORMED PRIOR TO STARTING PREDNISOLONE/ IMMUNOSUPPRESSION.
Prognosis of chronic inflammatory enteropathies
Quite variable
Good for many but some may relapse or fail to respond
Several negative prognostic indicators reported including:
§ Hypoalbuminaemia
§ Hypocobalaminaemia - should be supplemented
§ High CIBDAI or CCECAI score
§ Hypovitaminosis D - consider supplementing
Familial protein-losing enteropathy/nephropathy
In soft-coated Wheaten terriers
Combined LP enteritis and protein-losing nephropathy and food allergy may be involved in both as respond to diet trials.
Gluten enteropathy
Reported most commonly in Irish setters.
Probably immune-mediated (mechanisms still incompletely understood).
Susceptible setters show signs 4-7 months old - diarrhoea and weight loss which resolves on gluten-free diet (rice, potatoes).
Tests show increased intestinal permeability which continues even when clinically normal on gluten-free diet.
If exposure to gluten is delayed in susceptible animals until over 1 year of age less likely to develop clinical problems.
Biopsy of SI shows partial villus atrophy + lymphocytic mucosal infiltrate.
Worst in proximal SI.
Immunoproliferative enteropathy
Basenji dogs
A generally severe disease with autosomal recessive inheritance.
Gastric mucosal hypertrophy, LP enteritis (most severe proximally) and polyclonal increase in serum IgA.
These dogs need immunosuppressive doses of prednisolone to control the clinical signs and diet is less important, so thought to be primarily an immunological dysfunction.
Histiocytic colitis
Occurs in boxers
Infectious causes of chronic diarrhoea
Giardia and Tritrichomonas probably most relevant infectious causes of chronic diarrhoea
Role of bacterial infectious agents unclear as most commonly cause acute diarrhoea.
Fungal disease (e.g. histoplasmosis, pythiosis) not really seen UK but occur in other parts of the world so may be seen in patients with travel history (e.g. the US).
Viral causes are uncommon except for perhaps FeLV and FIV which may cause chronic or recurrent GI signs as part of a more systemic disease process.
Tritrichomonas foetus
Single-celled highly motile flagellate protozoa
Important causes of predominantly LI diarrhoea in cats but can also be found in normal cats and those with other causes of diarrhoea
Not zoonotic
Esp. common in younger cats (<1yr), pedigrees, and multi-cat households
Clinical signs of Tritrichomonas foetus
Usually LI diarrhoea
Weight loss, lethargy etc. are uncommon
Diagnosis of Tritrichomonas foetus
Direct smears positive in 5/36 (similar to giardia trophozoites but more jerky motion)
Culture positive in 20/36
PCR positive in 34/36 - but intermittent shedding and sensitivity variable depending on method (colonic flush or faecal loop>diarrhoea faecal sample>solid faeces).
Treatment of Tritrichomonas foetus
Ronidazole only “effective” drug but risk of neurotoxicity and not licensed. Important to warn the owner carefully of the risks.
Cats may improve clinically but may remain PCR positive and relapses can occur in <25%.
Start by treating concurrent infections and parasites - many cats will self-resolve.
Litter tray hygiene etc, ideally affected cats should be isolated.
Often difficult to know what to do in multi-cat households – generally only clinically affected animals treated.
Will also usually resolve spontaneously in untreated cats although this can take several months or longer.
Protein losing enteropathies (PLE)
Rather than a specific disease, any process causing marked increase in permeability can cause PLE including some infections, portal hypertension, congestive heart failure, ulceration and chronic
intussusceptions/obstructions/foreign bodies.
Commonest causes of PLE
Chronic inflammatory enteropathies/IBD
Intestinal lymphosarcoma (and other neoplasms)
Lymphangiectasia
GI Haemorrhage
Impact of low plasma proteins
pre-dispose to development of ascites ± oedema
also have serious deleterious effects on the gut which may prolong diarrhoea and pre-dispose to wound breakdown after biopsy
protein malnutrition reduces turnover of enterocytes and brush border enzymes, reduces local gut immunity, increases risk of bacterial translocation into the blood, and delays tissue repair.
Diet for dogs with PLE
Do not restrict dietary protein
Feed plenty of high quality, digestible protein to help restore plasma level
May need feeding tube placement
Surgery and PLE
If surgery considered in animal with significantly reduced albumin, can consider preoperative transfusion with human albumin (plasma transfusion could be considered if not available and provides additional anti-thrombin 3 which may help reduce risk of
thromboembolism but relatively low concentration of albumin).
Chronic inflammatory enteropathies/IBD with PLE
Tend to have a much poorer prognosis, more aggressive intervention is usually required
in severe cases, dietary
modification, fenbendazole and immunosuppression are often recommended from the outset due to the risk of treatment delays
Lymphangiectasia
Relatively uncommon
Primary or secondary
Loss of lymph to gut
Primary lymphangiectasia
Seen in Yorkshire Terriers, Rottweilers, Lundehunds
Secondary lymphangiectasia
e.g. chronic inflammatory enteropathy, lymphoma, portal hypertension
Acquired show blockage, dilation, leakage and rupture of lymphatics with surrounding granulomatous inflammation but underlying cause usually unknown.
Clinical signs of lympangiectasia
Major clinical signs are weight loss ± ascites/pleural effusion/ oedema - diarrhoea (steatorrhoea) variable - not always present.
lymph contains a lot of fat (triglycerides as chylomicrons), protein and lymphocytes, so affected dogs have low total proteins (albumin and globulin), lymphopenia and hypocholesterolaemia.
Lipogranulomatous lymphangitis.
Diagnosis of lymphangiectasia
Laboratory changes may be suggestive but are not diagnostic.
Dilated lacteals may be visible on ultrasound (radial mucosal hyperechoic striations) or endoscopy (white spots over duodenal mucosa) in severe cases.
Often full thickness biopsy may be required.
Treatment of lymphangiectasia
Little and often low fat, high quality protein diet: reducing dietary fat reduces lymphatic flow so reducing protein loss.
Could also consider adding medium chain triglycerides (MCTs) to increase energy density of diet e.g. coconut oil.
○ Don’t overdose as can cause osmotic diarrhoea and don’t use in liver disease as can worsen encephalopathy.
○ Avoid use in cats can cause vomiting/neuro signs.
○ MCTs also cannot carry fat soluble vitamins.
Prednisolone (anti-inflammatory dose if primary lymphangiectasia, or immunosuppressive dose if underlying IBD) or ciclosporin can also help to address concurrent/consequent inflammation.
Prognosis generally poor.
Intestinal lymphoma
Large cell, high grade lymphoma has poor prognosis (more common in dogs)
Small cell, low grade (more common in cats) can do reasonably well with prednisolone + chlorambucil
May be localised to the GI tract or also affect lymph nodes/other organs
Either alone or as part of multicentric lymphoma in cats or dogs.
Focal or diffuse.
Endoscopic changes indistinguishable from IBD
Clinical signs of intestinal lymphoma
Requires biopsy or cytology
Differentiating from IBD can be difficult
PARR or immunohistochemistry can help but not always clear cut
Intestinal thickening +/- loss of wall layering, muscularis thickening, lymphadenopathy etc. may be seen on ultrasound but are non-specific
Colonic anatomy
ascending, transverse and descending colon, rectum, anus.
Proximal colon closely anatomically associated with stomach and left limb pancreas (so inflammation in
this area has direct effect on colon).
Physiology of colon
salt and water absorption maximal ascending colon - facilitated by
retroperistalsis and rhythmic segmentation in this area slowing down forward motion of
ingesta.
Colonic and gastric function intimately related - unabsorbed nutrients reaching colon (particularly fat and bile) causes reflex slowing of gastric emptying (under hormonal control).
Reflex may be disrupted after colectomy resulting in diarrhoea.
In chronic colitis, presence of food in stomach stimulates abnormal
increase in colonic giant migrating contractions.
Where does maximal salt and water absorbtion occur
The ascending colon
Dietary fibre and the colon
LI bacterial flora larger than SI (and more anaerobes and G+ves in LI).
Bacteria ferment fibre to short chain fatty acids (SCFAs) - important colonic nutrient source, especially
butyrate which provides 50% of the calorie requirements for colonocytes.
High fibre diets are particularly indicated in chronic colitis.
Fibre
plant polysaccharides and lignin resistant to hydrolysis by digestive enzymes
Fermentable (soluble) fibre
fibre which is fermented by LI bacteria to SCFAs: largely butyrate, propionate and acetate
Fermented to butyrate which provides 50% of energy requirements of colonocytes. Important for colonic health
Fermented to SCFAs which lower colonic pH favouring beneficial bacteria and reducing ammonia absorption
Binds water which renders faeces more solid
Binds bile acids so reducing their enterohepatic circulation but also reducing colonic mucosal irritation
Non fermentable (insoluble) fibre
fibre which is resistant to bacterial degradation and passes through unchanged
Stretches colon and encourages normal motility in both constipation and diarrhoea
Contraindications and cautions with high fibre diets
Contra-indicated in SI diarrhoea as impair nutrient absorption and brush border enzyme activity
Contra-indicated in pancreatic disease (EPI and pancreatitis) - interfere with pancreatic enzyme function and stretch stomach so increasing pancreatic enzyme release in pancreatitis (beware! EPI and chronic pancreatitis can produce colitis secondary to fat maldigestion)
Contraindicated in gastritis as soluble fibre delays gastric emptying.
Feed with plenty of fluids or causes constipation
Binds minerals so potential for deficiency especially in young/marginal diets. Commercial high fibre diets supplemented with extra minerals. Also increase taurine requirement in cats
Common dietary causes of chronic LI diarrhoea
indiscretion, intolerance, allergy, foreign body
Chronic inflammatory colitis
lymphocytic-plasmacytic
eosinophilic
granulomatous (seen in Boxers and French Bulldogs, actually caused E. coli)
histiocytic
Infectious causes of chronic LI diarrhoea
particularly parasitic/protozoal (e.g. Tritrichomonas in cats, giardiasis, Trichuris whipworms etc).
Chronic bacterial or viral infection? (e.g. campylobacter, salmonella, clostridia, E.coli, FeLV, FIV, FIP etc)
Chronic LI diarrhoea secodary to SI fat malabsorption/maldigestion
EPI, ARD, CIE, chronic pancreatitis, bile salt deficiency (severe cholestatic liver disease)
Common extra GI causes of chronic LI diarrhoea
Uraemic colitis
Secondary to local irritation e.g. peritonitis (pancreatitis, prostatitis), extra-colonic mass (e.g. prostate)
Other causes e.g. renal disease, liver disease, hypoadrenocorticism etc possible but usually cause SI or mixed diarrhoea.
Differentiation of colitis and constipation
Tenesmus + frequency important features of LI diarrhoea but also occur with constipation.
May be difficult for owners to differentiate the two, especially in cats.
Note in constipation, passage of hard faeces often followed by liquid faeces - normal due to altered colonic motility + mucosal irritation by impacted faeces - but owners often describe this as diarrhoea.
May also have fresh blood and mucus with constipation.
Faecal samples for colitis
gross appearance; culture; flotation +/- antigen testing for giardia, nematodes; undigested fat may suggest secondary to fat maldigestion.
Blood samples for colitis
less important in LI disease but useful to rule out extra-GI causes.
B12, folate and TLI ± other SI tests indicated if suspect secondary to fat maldigestion or suspect diffuse intestinal pathology.
Radiography of colitis
plain films often normal but important to rule out obvious neoplasia (colonic, rectal or peri-colonic), foreign bodies (e.g. bones causing abrasive colitis), megacolon.
Contrast films often more helpful: pneumoncolonogram possible without full evacuation.
Barium enema needs careful removal of ALL faeces first - any remaining faeces results in confusing appearance
Ultrasound of colitis
can be useful particularly in assessment of colonic masses (+ disease or metastases other organs) although unable to evaluate intra-pelvic colon.
Colonoscopy/proctoscopy and biopsy
Under GA.
Usually performed with flexible endoscope but descending colon possible using rigid endoscopy (with care!).
Careful preparation with 24-48h starvation + laxative (usually KleanPrep per os over preceding 24 hours) and enemas first.
Assess gross appearance of colon and multiple endoscopic biopsies (mucosa and submucosa).
In dogs the ileum can usually also be intubated and biopsied and, in cats, it is usually possible to take blind biopsies via the ileo-caecal-colic junction.
Chronic inflammatory colitis/IBD
Commonest cause of chronic colitis in dogs, perhaps less common in cats.
May be isolated colonic pathology or part of a more diffuse inflammatory enteropathy.
Usually lymphocytic-plasmacytic (L-P) infiltrate but may also be other cell type (e.g. eosinophilic).
Any age or breed, but higher incidence 6 months to 4 years old and GSDs, rough collies and Labradors.
Diagnosis of chronic inflammatory colitis/IBD
clinical signs of chronic colitis and rule out other causes.
Endoscopy may show grossly thickened (“cobblestone”) and erythematous mucosa + lose visualisation of submucosal vessels.
Ulcerative changes are generally more common with eosinophilic and granulomatous subtypes.
Definitive diagnosis on biopsy (but note some lymphocytes and plasma cells normal in colon).
Treatment of chronic inflammatory colitis/IBD
Dietary modification most important
- hypoallergenic with added fibre (mix of soluble and insoluble)
Steroid/immunosuppressives
- usually preds first line
- chlorambucil and ciclosporin can be added in
Antibiotics
- commonly used but not really indicated in most cases
Granulomatous colitis (AKA Histiocytic ulcerative colitis)
Boxers and French bulldogs
Uncommon disease recognised in young boxer dogs (usually < 3 years old).
Diagnosis of granulomatous colitis
Clinical signs of colitis - may be more severe than usual and may be concurrent weight loss and anorexia (unusual with colitis).
Colon grossly thickened and ulcerated on proctoscopy.
Definitive diagnosis on histology: severe colonic mucosal ulceration with infiltration of submucosa and lamina propria with periodic acid-Schiff positive macrophages.
Cause of granulomatous colitis
due to an adherent-invasive E.coli with a genetic susceptibility for invasion in boxers and French bulldogs.
Treatment of granulomatous colitis
responsive to enrofloxacin but important to treat for long enough to prevent resistance – recent concerning reports of boxers developing resistance to fluoroquinolones in up to 43% of cases.
Prognosis of granulomatous colitis
typically good and most respond quickly. Incomplete or lack of response can suggest resistance and poor prognosis
Irritable bowel syndrome (IBS)
Poorly defined in dogs but may be very common
particularly working and excitable breeds
primarily motility defect
affects ileum ± jejunum as well as colon - colitis is the main feature
Diagnosis of exclusion
Control rather than cure, reduce stress and modify diet
Colonic neoplasia
40-60% of all GI tumours in dog and 10-15% of GI tumours in cats.
Dogs: commonest are benign adenomatous polyps. Also adenocarcinoma, lymphoma and others.
In cats, adenocarcinoma, lymphosarcoma and mast cell tumour commonest.
Commonly rectal in dogs and ileocaecocolic in cats.
Best prognosis if can be surgically resected
