Diarrhea / Intestinal Pathogens Flashcards
Acute intestinal reaction to injury
- Mucoid (catarrhal exudate)
- Hemorrhagic exudate
- Diphtheritic membranes
- Villus blunting
Subacute intestinal reaction to injury
- Villus fusion
- Crypt abscesses
- Crypt hyperplasia
- Epithelial attenuation
Chronic intestinal reaction to injury
- Fibrosis
- Granulomatous inflammation
- Lymphangiectasia
- Muscular hypertrophy
Sequelae of fibrosis (as chronic reaction to intestinal injury)
Bowel stenosis —> altered peristalsis —> abnormal micro flora proliferation —> dysmotility
Lymphangiectasia —> protein exudation / effusion
Decrease digestion/absorption —> malabsorption/maldigestion
Lymphangiectasia
Dilated lymphatic ducts and lacteals (tiny lymphatic ducts within villi)
Caused by: chronic/infiltrative disease (granulomatous, neoplastic), fibrosis, increased hydrostatic pressure/decreased lymphatic drainage, protein losing enteropathy
Sequelae of intestinal muscle hypertrophy
Persistently altered peristalsis —> predisposition to obstruction —> rupture
Enteritis
Inflammation of small intestine
Ileitis
Inflammation of ileum (of small intestine)
Colitis
Inflammation of colon (large intestine)
Typhlitis
Inflammation of cecum
Gastroenteritis
Inflammation of stomach and small intestine
Enterocolitis
Inflammation of small intestine and colon
Typhlocolitis
Inflammation of cecum and colon
Proctitis
Inflammation of rectum
Definition of diarrhea
Secretion of abnormally fluid feces with
- increased volume of feces
- increased frequencey
Basic mechanisms of diarrhea
- Hypersecretion
- Malabsorption/maldigestion
- Exudation/effusion
- Deranged intestinal motility
Diarrhea from hypersecretion
Architecturally normal intestine (i.e. functional change only)
Rapid recovery upon elimination of pathogen
Mechanism: bacteria colonize epithelial surface, FIP Rae bind membrane receptors —> enterotoxin —> activates cAMP/cGMP —> increase fluid secretion
Hypersecretion pathogen
Enterotoxigenic E. coli (ETEC)
Gross signs of hypersecretion
dehydration, perineal staining, fluid-distended SI loops
Histo of hypersecretion
Normal small intestine
Bacteria on apical border - attached by frimbriae
Causes of malabsorptive/maldigestive diarrhea
- Microvillus damage
- Absorptive enterocyte necrosis/loss
- Crypt cell necrosis/loss
- Crypt hyperplasia —> epithelial attenuation
Gross lesions of malabsoption/maldigestion
Dehydration
Watery diarrhea/fecal staining
Histo lesions of malabsorption/maldigestion
Loss of microvillus border
Villus enterocyte degeneration sloughing
Pathogens that damage microvilli
Attaching and Effacing E. coli (AEEC)
Cryptosporidium (zoonotic!)
Pathogenesis of AEEC
Intimin (bacterial virulence factor) —> enterocyte attachment/microvillus distruction —> loss of disaccharides —> loss of absorptive surface area —> malabsorption/maldigestion —> osmotic diarrhea
Villus enterocyte necrosis
Villus epithelial cell necrosis —> sloughing —> villus contraction —> fusion —> loss of absorptive surface area —> immature replacement cells —> malabsorption/maldigestion —> diarrhea
Pathogens that kill villus enterocytes
Enteric coronaviruses
Enteric rotavirus
Coccidia parasites
Enteric coronavirus
Pigs, calves, cows, horses, SA, turkeys, ferrets
Small + large intestine
Severity dependent on viral tropism
Transmissible gastroenteritis
Enteric coronavirus in swine —> severe villus blunting
Pathogens that kill crypt cells
“Radiomimetic” viruses (kill replicating cells - crypt cells = stem cells of intestine)
Canine/feline parvoviruses (Feline panleukopenia, Canine parvovirus)
Bovine viral diarrhea virus
Pathogenesis of Feline panleukopenia
Crypt cell necrosis: villus blunting/fusion —> loss of mucosal barrier —> opportunistic infection —> diphtheritic membranes/septicemia —> slow regeneration with immature replacement epithelium —> malabsorption/maldigestion
Clinical signs of parvoviruses in SA
Vomiting, diarrhea, dehydration, sepsis
Lesions of parvoviruses of SA
Necrotizing enteritis + crypt necrosis
Peyer’s patch necrosis
Immune suppression (Panleukopenia in cats, Lymphopenia in dogs/cats)
Teratogenic effects
Pathogens that cause crypt hyperplasia
Lawsonia intracellular is (swine, equine)
Proliferative enteritis
Thickening of mucosa
Hyperplasia with reduced maturation of epithelial cells (in crypts)
Cause: Lawsonia intracellularis
Mechanisms of exudative/effusive diarrhea
- increased capillary or epithelial permeability (e.g. vascular necrosis, vasculitis, mucosal erosion/ulcer) - viral causes
- lymphatic obstruction —> protein losing enteropathy - infiltrative diseases (granulomatous, neoplastic)
Viruses causing exudative/effusive diarrhea
Salmonella (Zoonotic)
Clostridium perfringens
Exudative diarrhea
Fibrin, hemorrhage, neutrophils, cell debris (Diphtheritic membranes)
Pathogens that kill villus enterocytes and damage lamina propria
Salmonella spp.
(Lamina propria capillary invasion —> necrosis —> ulcer/hemorrhage; enterocyte necrosis)
Histo of Salmonellosis
Mucosal necrosis
Diphtheritic membrane (fibrin, neutrophils, cell debris, bacteria)
Capillary fibrin thrombi
Complications of Salmonella
Septicemia and intestinal infants due to vascular invasion
Clostridium perfringens / difficile (equine)
Necrotising to necro-hemorrhagic enterocolitis
Exotoxin ‘burn tissue’ —> vessel damage
Mucosal necrosis with Diphtheritic membranes
(Can look similar to Salmonella)
Mechanism of infiltrative disease —> effusion/exudation
Lamina propria infiltration —> increased hydrostatic pressure —> decrease absorption —> lacteal dilation —> effusion
Causes of infiltrative disease of lamina propria
Mycobacterium Adium subspecies paratuberculosis (Johne’s disease) - cattle —> protein losing enteropathy
Diffuse alimentary lymphoma
Diffuse granulomatous enteritis
Gross lesions of Johne’s disease
Thickened corrugated mucosa
Multi focal mucosal erosions
Enlarged mesenteric lymph nodes
Pathogenesis of Johne’s disease
Diffuse granulomatous enterocolitis —> inflammation extends —> mesentertic lymphadentiis —> villus blunting/fusion/Lymphangiectasia —> protein losing enteropathy —> hypoproteinemia —> emaciation
DDx of Johne’s disease
Lymphosarcoma
Histo of Johne’s disease
Intracellular acid fast bacilli in epitheliod macrophages
Infiltrates of epitheliod mac and multinucleated giant cells
Villus blunting/fusion
Types of dysmotility
Hypermotility - decreased contact time with mucosa —> maldigestion/malabsorption
Hypomotility - bacterial overgrowth —> toxic substance producers, reduced per mentation —> secondary diarrhea
Causes of abnormal motility
Physical stimulus/obstruction (i.e. parasite, foreign body, strictures, masses)
Muscular hypertrophy
Peritonitis
