Chronic diarrhoea/enteropathies Flashcards
what factors influence the development of chronic enteropathies?
what happens to the microbiome of dogs with chrinic enteropathies?
- comorbidities
- genetices
- environment
- immune response
- microbiome
- diet
reduced diversity and richness of the microbiome
what are the major differntials for chronic enteropathies?
- Food responsive enteropathy (FRE)
- Dysbiosis (previously called Antibiotic responsive enteropathy - ARE)
- Steroid responsive enteropathy – SRE (IBD?)
- Non-responsive enteropathy (NRE)
- Protein Losing Enteropathy – e.g. lymphangiectasia
- Exocrine pancreatic insufficiency (EPI)
- Neoplasia
- (Irritable bowel disease/syndrome)
- (Non-GI causes)
- Rarely from clinical signs alone can you differentiate between these
what is the difference between food allergy reactions and food intolerance reactions?
- Food allergy reactions refer to an immunologically mediated adverse reaction to food unrelated to any physiological effect of the food or food additive. Relapse when specific antigens from previous diet are reintroduced (distinguishes from intolerance)
- Food intolerance reactions refer to any abnormal physiologic response to a food that is not believed to be immunologic in nature and may include food poisoning, food idiosyncrasy, pharmacologic reaction, toxicological reaction or metabolic reaction.
how do food responsive enteropathies normaly present?
Usually chronic small or mixed intestinal diarrhoea
* Can see large intestinal signs which may be due to unconjugated bile acids and other maldigested SI products
Vomiting can be seen
Maybe skin signs in some cases
how do you diagnose a food responsive enteropathy? what are the components of the diet they should have?
Food trial
* Needs to be accepted by patient and owner
* Offending antigen excluded (often don’t know what this is)
* For GI disease no need for longer than 3 weeks
◦ Signs of improvement noted very quickly compared with skin
* Reintroduction of diet should lead to relapse – rarely does this happen unless an accident.
Home-cooked or commercial
* Novel intact or hydrolysed proteins (care with osmolarity)
* Single or limited protein source
* High digestibility
* Reduced fat
* Avoid high protein
* Moderate amount of fermentable fibre (prebiotic)
Diagnosis – by response to food trial – how many – lots! This is the main diagnostic test
food specific serum-immunoglobin - No evidence that measuring antibodies aids with diagnosis of food hypersensitivity or identifying offending antigens
why shoul dantibiotics not be used with chronic enteropathies?
the antibiotics will temporarily fix the diarrhoea but will push the microbiome in a direction that is further away than normal, this will then cause the diarrhoea to relapse in the future (like sticking a plaster on it)
Dysbiosis may be seen as primary condition in susceptible breeds due to:
* Poor tolerance of normal microflora - Abnormalities in innate immune system, abnormal flora, mucosal barrier defects
what breed is predisposed to dysbiosis as a primanry condition and why is whis?
GSD in particular – possible IgA deficiency, genetic susceptibility, loss of tolerance to endogenous bacteria
what are the consequences of dysbiosis?
- Utilise nutrients/interfere with absorption
- Damage epithelium and microvillar enzyme dysfunction
- Increase mucosal permeability/fluid loss
- Deconjugate bile acids
- Hydroxylate fatty acids
- Stimulate colonocyte secretion
causes
* Chronic diarrhoea - small intestinal usually
* Weight loss/failure to thrive
* Vomiting/borborygmus/appetite changes
what vitamin is often low and needed to be supplemented in cases of dysbyosis?
Vitamine B12 (cobalamin) - needs supplementation
folate is also often low
how is dysbiosis managed?
Dietary manipulation
◦ Highly digestible diet
◦ Low fat (unclear of efficacy for dysbiosis cases but may help)
‣ Dysbiosis leads to hydroxylation of fats and diarrhoea
‣ Caution as calorie restriction will reduce weight recovery
* Prebiotics - Alter colonic flora in cats but no current evidence that alter small intestinal numbers in dogs
* Probiotics - Increasing evidence for this impacting the microbiome in a positive way (Prokolin enterogenic)
- Treat primary cause if there is one (eg EPI treatment – bacterial numbers fall)
- Cobalamin supplementation - Essential to improve recovery rate
- Antibiotics were used in the past, but this is not considered justifiable
(If no other approaches are working with careful conversations can use
◦ for 4-6 weeks, review after 2 weeks may need to change type
‣ Oxytetracycline, Tylosin, Metronidazole)
what is steroid responsive enteropathy?
Persistent/recurrent GI signs with histopathological evidence for inflammation
* Non-dietary responsive disease (can partially respond)
* Assumed as idiopathic condition
* Mucosal infiltration with inflammatory cells
* Characterised by cellular infiltrate
◦ Eosinophilic (worse?), Lymphocytic-plasmacytic (breed variants e.g. SCWT, Basenji enteropathy)
◦ Granulomatous, Neutrophilic
◦ Regional (only in one part of intestine)
*variable serverity/length of SI affected - Can see regional signs – gastroenteritis, enterocolitis, gastroenterocolitis
* Triaditis in cats - Also difficult to determine between SRE and small cell lymphoma in cats.
- Currently suspected that this a syndrome comprising a group of disorders with similar characteristics
what is the pathogenesis of steroid responvie enteropathy?
- Mucosa controls exposure of luminal antigens to GALT (GALT must be immunocompetent but also tolerant of non-pathogenic resident flora and food)
◦ Loss of tolerance is critical to development of disease
‣ Via breakdown of mucosal barrier – excessive exposure of antigens
‣ Dysregulation of immune response
* Altered TLR expression
* Altered lymphocyte populations
* Acute phase protein increase is variable
* Consequence is uncontrolled inflammation and products thereof
◦ Altered architecture
what is the signalment, clinical signs of steroid responsive enteropathy?
what is felt on physical exam?
Middle aged animals mainly - Uncommon in dogs < 12months
Cats of any age are reported but mostly middle aged
- Chronic diarrhoea common- SI in character but if prolonged or involving colon can be mixed
- Vomiting more common in cats - can be haemorrhagic (esp cats)
- Weight loss with more severe mucosal disruption
- Appetite very variable – increased, decreased, no change
- Abdominal discomfort – variable and concomitant signs (can see motility abnormalities)
- Physical examination
◦ Thin, thick gut loops, abd LN palpable? [CAT]
◦ Ascites/oedema
how is steroid responsive enteropathies diagnosed?
Minimum database should include specPLI and TLI, folate, cobalamin, UPC, full faecal analysis
Diagnostic imaging - Radiographs and Ultrasound
‣ Rule out other disease e.g. chronic FB/intussusception
‣ Evaluate wall layering with ultrasound – mucosal speckling/striations
‣ Can see fluid with both - clearer with US
* Biopsies
◦ Endoscopic vs. full thickness
◦ endoscopic biopsy is first line in dogs - but the endoscope can only get to proximal duodenum, therefore can miss a lot of the disease as it is in jejunum for ilium
Histology can be subjective
* WSAVA criteria makes classification and diagnosis more consistent
* Increased inflammatory cells in lamina propria – mild/moderate/severe
* Often multiple cell lines, diagnosis based on predominant cell type.
◦ Lymphoplasmacytic (LPE)
◦ Eosinophilic
◦ Neutrophilic component could suggest superimposed infection/acute inflammatory response (FISH?)
◦ Regional granulomatous form rare
‣ Thickened, stenotic segment of bowel
‣ DDx granulomatous inflammation/neoplasia
what is the most common adn second most common types of steroid responsive enteropathies?
1st - Lymphoplasmacytic enteritis (LPE)
2nd - eosinophilic enteritis
