Bacterial GI infections Flashcards

1
Q

Major causal species of bacterial gastroenteritis

A
  • GN bacilli: E coli (commensal, C), vibrio (not C), salmonella (not C), shigella (not C), campylobacter jejuni (not C), yersinia enterocolitica (not C)
  • GP cocci: Staph (C)
  • GP bacilli: bacillus anthracis and bacillus cereus (not C), clostridium (C)
  • Campylobacter and salmonella are most common cause in US (both associated w/ poultry)
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2
Q

Diarrhea

A
  • Due to increased secretion or reduced absorption of fluids
  • Inflammatory: large number of WBCs (PMNs and mononuclear)
  • Non-inflammatory: absence of large amounts of WBCs
  • RBCs may be incidental, except hemorrhagic E coli (EHEC) infections
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3
Q

Types of E Coli GI infections 1

A
  • ETEC: enterotoxigenic E Coli, cause of 1/3 of bacterial-induced traveler’s diarrhea (most common for traveler’s)
  • Does this by enterotoxin production in SI (either heat stable or heat labile)
  • Heat labile enterotoxin activates AC (like cholera) and stimulates fluid secretion
  • Heat stable enterotoxin activates GC and inhibits fluid absorption
  • Non-inflammatory diarrhea, (-RBCs)
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4
Q

Types of E Coli GI infections 2

A
  • EPEC: enteropathogenic E Coli adhere to epithelial cells in SI and prevent fluid absorption
  • Risk higher for non-breast fed infants (epidemic infantile diarrhea)
  • Causes inflammatory diarrhea but few WBCs (-RBCs)
  • EAEC: enteroaggregative E Coli aggregate and adhere to epithelial lining in SI and prevent fluid absorption
  • Causes inflammatory diarrhea but few WBCs (-RBCs)
  • EPEC and EAEC both cause production of IL8
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5
Q

Types of E Coli GI infections 3

A
  • EIEC: enteroinvasive E Coli invades and destroys the epithelial lining of the colon
  • Destruction of epithelial cells causes inhibition of fluid absorption
  • Causes inflammatory diarrhea w/ lots of WBCs (+ RBCs)
  • EHEC: enterohemorrhagic E Coli: produces a shigella-like toxin that destroys (but doesn’t invade) the epithelial lining of the colon
  • Destruction of epithelial cells causes inhibition of fluid absorption
  • Can cause hemolytic uremic syndrome
  • Causes inflammatory diarrhea w/ no WBCs but lots of RBCs
  • DAEC: diffusely adherent E Coli, affects SI
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6
Q

Overview of E Coli pathogenesis mechanisms

A
  • EPEC and EAEC prevent fluid absorption by destroying epithelial cells via adherence (SI)
  • EIEC prevent fluid absorption by destroying epithelial cells via invasion (LI)
  • EHEC prevent fluid absorption by destroying epithelial cells via shiva-like toxin (LI)
  • ETEC can prevent fluid absorption by destroying epithelial cells via heat stable toxin that activates GC (SI)
  • ETEC can also cause increased fluid secretion by heat labile toxin that activates AC (SI)
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7
Q

Other GN bacterial gastrointestinal infection etiologies 1

A
  • Vibrio cholera: binary toxin that increases fluid secretion via AC stimulation
  • Found in shell fish, causes rice water diarrhea
  • 3 types of vaccines: killed, live attenuated, toxoid
  • Salmonella typhi: can cause typhoid fever (systemic, characterized by rash)
  • Survives phagocytosis and can replicate intracellularly
  • Shigella: F-O, produces shiga toxin, can replicate intracellularly
  • Characteristic bloody, mucoid stools
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8
Q

Other GN bacterial gastrointestinal infection etiologies 2

A
  • Campylobacter: associated w/ undercooked poultry, causes bloody (inflammatory) diarrhea
  • Complication: guillan-barre (Th1 and Th2) syndrome due to cross reaction of Abs to bacterial wall and nerve myelin
  • Yersinia enterocolitica: inflammatory diarrhea, can cause pseudo appendicitis syndrome
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9
Q

Food poisoning causes

A
  • Can be due to Staph aureus, B cereus, clostridium botulinum
  • Food poisoning due to preformed toxins, leading to early illness (1-6 hr) that is often emetic (+/- ab pain, diarrhea)
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10
Q

Staph aureus and B cereus

A
  • Staph aureus: from improper food handling, expresses several enterotoxins and a heat stable toxin (responsible for food poisoning)
  • B cereus: spore forming, emetic illness associated w/ recooked rice, diarrheal illness associated w/ undercooked foods
  • Food poisoning (emetic form) due to preformed heat stable toxin, live cells not required (YES vomiting, +/- diarrhea)
  • Also has diarrheal form (1-24hr incubation): due to overgrowth of cells in intestine that produce enterotoxin (NO vomiting, YES diarrhea)
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11
Q

Clostridium sp

A
  • Clostridium difficile: spore former, can be commensal but overgrows w/ ANTIBIO Rx (nosocomial)
  • Produces enterotoxin and cytotoxin (both increase inflammatory response
  • Overgrowth of C Dif due to antibio Rx can lead to diarrhea, pseudomembranous colitis
  • Clostridium perfringens: produces many toxins that can cause food poisoning (diarrhea, no N/V)
  • Cooking kills bacteria but not spores, spores germinate in cooled foods and when ingested produce enterotoxins
  • Associated w/ smoked/cured meats (sausage, dear)
  • Commensal, but can lead to food poisoning, soft tissue infections (gas gangrene), septicemia
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12
Q

Clostridium botulinum 1

A
  • Spores and preformed toxins are transmitted into improperly prepared foods
  • Foodborne botulism: inadequately preserved canned goods allow botulinum spores to germinate, bacteria multiply and produce toxin under anaerobic conditions
  • Bacteria cannot multiply in healthy adult GI tract, toxin is what causes food poisoning and Sx
  • Toxin inhibits ACh release at NMJs leading to flaccid paralysis, blurred vision
  • Also causes diarrhea, N/V
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13
Q

Clostridium botulinum 2

A
  • Infant botulism: HONEY contaminated w/ botulinum spores is ingested by baby
  • Bacteria multiple (less competing microflora) and toxin is produced in vivo
  • Sx: constipation, poor breast feeding, lethargy, floppy baby
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14
Q

Helicobacter Pylori

A
  • Established infections in pyloric region of stomach cause gastritis, gastric and duodenal ulcers
  • Gastric ulcers may lead to gastric CA due to chronic inflammation
  • May be a cause of MALT B cell lymphoma
  • cagA gene is correlated w/ gastric CA, possibly inactivates tumor suppressor proteins (p53 and RUNX3)
  • Is commensal but virulence factors can make it pathogenic
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15
Q

H Pylori virulence factors

A
  • Heat shock protein: induces expression of urease
  • Urease: neutralizes gastric acidity by producing ammonia, breaks down unstirred layer
  • Mucinase and phospholipase: disrupts gastric mucus
  • Acid inhibitory protein: prevents production of stomach acid
  • Catalase and superoxide dismutase: prevents phagocytosis
  • VacA: helps w/ intracellular replication
  • Overall there is an increased amount of gastric acid secretion, since the inflammatory response leads to hyper secretion of acid
  • There is also increased gastrin
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