Diarrhea / Intestinal Pathogens Flashcards

(50 cards)

1
Q

Acute intestinal reaction to injury

A
  1. Mucoid (catarrhal exudate)
  2. Hemorrhagic exudate
  3. Diphtheritic membranes
  4. Villus blunting
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2
Q

Subacute intestinal reaction to injury

A
  1. Villus fusion
  2. Crypt abscesses
  3. Crypt hyperplasia
  4. Epithelial attenuation
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3
Q

Chronic intestinal reaction to injury

A
  1. Fibrosis
  2. Granulomatous inflammation
  3. Lymphangiectasia
  4. Muscular hypertrophy
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4
Q

Sequelae of fibrosis (as chronic reaction to intestinal injury)

A

Bowel stenosis —> altered peristalsis —> abnormal micro flora proliferation —> dysmotility
Lymphangiectasia —> protein exudation / effusion
Decrease digestion/absorption —> malabsorption/maldigestion

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5
Q

Lymphangiectasia

A

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

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6
Q

Sequelae of intestinal muscle hypertrophy

A

Persistently altered peristalsis —> predisposition to obstruction —> rupture

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7
Q

Enteritis

A

Inflammation of small intestine

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8
Q

Ileitis

A

Inflammation of ileum (of small intestine)

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9
Q

Colitis

A

Inflammation of colon (large intestine)

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10
Q

Typhlitis

A

Inflammation of cecum

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11
Q

Gastroenteritis

A

Inflammation of stomach and small intestine

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12
Q

Enterocolitis

A

Inflammation of small intestine and colon

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13
Q

Typhlocolitis

A

Inflammation of cecum and colon

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14
Q

Proctitis

A

Inflammation of rectum

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15
Q

Definition of diarrhea

A

Secretion of abnormally fluid feces with
- increased volume of feces
- increased frequencey

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16
Q

Basic mechanisms of diarrhea

A
  1. Hypersecretion
  2. Malabsorption/maldigestion
  3. Exudation/effusion
  4. Deranged intestinal motility
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17
Q

Diarrhea from hypersecretion

A

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

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18
Q

Hypersecretion pathogen

A

Enterotoxigenic E. coli (ETEC)

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19
Q

Gross signs of hypersecretion

A

dehydration, perineal staining, fluid-distended SI loops

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20
Q

Histo of hypersecretion

A

Normal small intestine
Bacteria on apical border - attached by frimbriae

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21
Q

Causes of malabsorptive/maldigestive diarrhea

A
  • Microvillus damage
  • Absorptive enterocyte necrosis/loss
  • Crypt cell necrosis/loss
  • Crypt hyperplasia —> epithelial attenuation
22
Q

Gross lesions of malabsoption/maldigestion

A

Dehydration
Watery diarrhea/fecal staining

23
Q

Histo lesions of malabsorption/maldigestion

A

Loss of microvillus border
Villus enterocyte degeneration sloughing

24
Q

Pathogens that damage microvilli

A

Attaching and Effacing E. coli (AEEC)
Cryptosporidium (zoonotic!)

25
Pathogenesis of AEEC
Intimin (bacterial virulence factor) —> enterocyte attachment/microvillus distruction —> loss of disaccharides —> loss of absorptive surface area —> malabsorption/maldigestion —> osmotic diarrhea
26
Villus enterocyte necrosis
Villus epithelial cell necrosis —> sloughing —> villus contraction —> fusion —> loss of absorptive surface area —> immature replacement cells —> malabsorption/maldigestion —> diarrhea
27
Pathogens that kill villus enterocytes
Enteric coronaviruses Enteric rotavirus Coccidia parasites
28
Enteric coronavirus
Pigs, calves, cows, horses, SA, turkeys, ferrets Small + large intestine Severity dependent on viral tropism
29
Transmissible gastroenteritis
Enteric coronavirus in swine —> severe villus blunting
30
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
31
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
32
Clinical signs of parvoviruses in SA
Vomiting, diarrhea, dehydration, sepsis
33
Lesions of parvoviruses of SA
Necrotizing enteritis + crypt necrosis Peyer’s patch necrosis Immune suppression (Panleukopenia in cats, Lymphopenia in dogs/cats) Teratogenic effects
34
Pathogens that cause crypt hyperplasia
Lawsonia intracellular is (swine, equine)
35
Proliferative enteritis
Thickening of mucosa Hyperplasia with reduced maturation of epithelial cells (in crypts) Cause: Lawsonia intracellularis
36
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)
37
Viruses causing exudative/effusive diarrhea
Salmonella (Zoonotic) Clostridium perfringens
38
Exudative diarrhea
Fibrin, hemorrhage, neutrophils, cell debris (Diphtheritic membranes)
39
Pathogens that kill villus enterocytes and damage lamina propria
Salmonella spp. (Lamina propria capillary invasion —> necrosis —> ulcer/hemorrhage; enterocyte necrosis)
40
Histo of Salmonellosis
Mucosal necrosis Diphtheritic membrane (fibrin, neutrophils, cell debris, bacteria) Capillary fibrin thrombi
41
Complications of Salmonella
Septicemia and intestinal infants due to vascular invasion
42
Clostridium perfringens / difficile (equine)
Necrotising to necro-hemorrhagic enterocolitis Exotoxin ‘burn tissue’ —> vessel damage Mucosal necrosis with Diphtheritic membranes (Can look similar to Salmonella)
43
Mechanism of infiltrative disease —> effusion/exudation
Lamina propria infiltration —> increased hydrostatic pressure —> decrease absorption —> lacteal dilation —> effusion
44
Causes of infiltrative disease of lamina propria
Mycobacterium Adium subspecies paratuberculosis (Johne’s disease) - cattle —> protein losing enteropathy Diffuse alimentary lymphoma Diffuse granulomatous enteritis
45
Gross lesions of Johne’s disease
Thickened corrugated mucosa Multi focal mucosal erosions Enlarged mesenteric lymph nodes
46
Pathogenesis of Johne’s disease
Diffuse granulomatous enterocolitis —> inflammation extends —> mesentertic lymphadentiis —> villus blunting/fusion/Lymphangiectasia —> protein losing enteropathy —> hypoproteinemia —> emaciation
47
DDx of Johne’s disease
Lymphosarcoma
48
Histo of Johne’s disease
Intracellular acid fast bacilli in epitheliod macrophages Infiltrates of epitheliod mac and multinucleated giant cells Villus blunting/fusion
49
Types of dysmotility
Hypermotility - decreased contact time with mucosa —> maldigestion/malabsorption Hypomotility - bacterial overgrowth —> toxic substance producers, reduced per mentation —> secondary diarrhea
50
Causes of abnormal motility
Physical stimulus/obstruction (i.e. parasite, foreign body, strictures, masses) Muscular hypertrophy Peritonitis