Diarrhea / Intestinal Pathogens Flashcards

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
Q

Pathogenesis of AEEC

A

Intimin (bacterial virulence factor) —> enterocyte attachment/microvillus distruction —> loss of disaccharides —> loss of absorptive surface area —> malabsorption/maldigestion —> osmotic diarrhea

26
Q

Villus enterocyte necrosis

A

Villus epithelial cell necrosis —> sloughing —> villus contraction —> fusion —> loss of absorptive surface area —> immature replacement cells —> malabsorption/maldigestion —> diarrhea

27
Q

Pathogens that kill villus enterocytes

A

Enteric coronaviruses
Enteric rotavirus
Coccidia parasites

28
Q

Enteric coronavirus

A

Pigs, calves, cows, horses, SA, turkeys, ferrets
Small + large intestine
Severity dependent on viral tropism

29
Q

Transmissible gastroenteritis

A

Enteric coronavirus in swine —> severe villus blunting

30
Q

Pathogens that kill crypt cells

A

“Radiomimetic” viruses (kill replicating cells - crypt cells = stem cells of intestine)

Canine/feline parvoviruses (Feline panleukopenia, Canine parvovirus)
Bovine viral diarrhea virus

31
Q

Pathogenesis of Feline panleukopenia

A

Crypt cell necrosis: villus blunting/fusion —> loss of mucosal barrier —> opportunistic infection —> diphtheritic membranes/septicemia —> slow regeneration with immature replacement epithelium —> malabsorption/maldigestion

32
Q

Clinical signs of parvoviruses in SA

A

Vomiting, diarrhea, dehydration, sepsis

33
Q

Lesions of parvoviruses of SA

A

Necrotizing enteritis + crypt necrosis
Peyer’s patch necrosis
Immune suppression (Panleukopenia in cats, Lymphopenia in dogs/cats)
Teratogenic effects

34
Q

Pathogens that cause crypt hyperplasia

A

Lawsonia intracellular is (swine, equine)

35
Q

Proliferative enteritis

A

Thickening of mucosa
Hyperplasia with reduced maturation of epithelial cells (in crypts)
Cause: Lawsonia intracellularis

36
Q

Mechanisms of exudative/effusive diarrhea

A
  • 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
Q

Viruses causing exudative/effusive diarrhea

A

Salmonella (Zoonotic)
Clostridium perfringens

38
Q

Exudative diarrhea

A

Fibrin, hemorrhage, neutrophils, cell debris (Diphtheritic membranes)

39
Q

Pathogens that kill villus enterocytes and damage lamina propria

A

Salmonella spp.
(Lamina propria capillary invasion —> necrosis —> ulcer/hemorrhage; enterocyte necrosis)

40
Q

Histo of Salmonellosis

A

Mucosal necrosis
Diphtheritic membrane (fibrin, neutrophils, cell debris, bacteria)
Capillary fibrin thrombi

41
Q

Complications of Salmonella

A

Septicemia and intestinal infants due to vascular invasion

42
Q

Clostridium perfringens / difficile (equine)

A

Necrotising to necro-hemorrhagic enterocolitis
Exotoxin ‘burn tissue’ —> vessel damage
Mucosal necrosis with Diphtheritic membranes
(Can look similar to Salmonella)

43
Q

Mechanism of infiltrative disease —> effusion/exudation

A

Lamina propria infiltration —> increased hydrostatic pressure —> decrease absorption —> lacteal dilation —> effusion

44
Q

Causes of infiltrative disease of lamina propria

A

Mycobacterium Adium subspecies paratuberculosis (Johne’s disease) - cattle —> protein losing enteropathy
Diffuse alimentary lymphoma
Diffuse granulomatous enteritis

45
Q

Gross lesions of Johne’s disease

A

Thickened corrugated mucosa
Multi focal mucosal erosions
Enlarged mesenteric lymph nodes

46
Q

Pathogenesis of Johne’s disease

A

Diffuse granulomatous enterocolitis —> inflammation extends —> mesentertic lymphadentiis —> villus blunting/fusion/Lymphangiectasia —> protein losing enteropathy —> hypoproteinemia —> emaciation

47
Q

DDx of Johne’s disease

A

Lymphosarcoma

48
Q

Histo of Johne’s disease

A

Intracellular acid fast bacilli in epitheliod macrophages
Infiltrates of epitheliod mac and multinucleated giant cells
Villus blunting/fusion

49
Q

Types of dysmotility

A

Hypermotility - decreased contact time with mucosa —> maldigestion/malabsorption
Hypomotility - bacterial overgrowth —> toxic substance producers, reduced per mentation —> secondary diarrhea

50
Q

Causes of abnormal motility

A

Physical stimulus/obstruction (i.e. parasite, foreign body, strictures, masses)
Muscular hypertrophy
Peritonitis