Week2: Bacterial GI infections Flashcards

1
Q

List the most common bacterial species that cause gastroenteritis.

A
Gram neg bacilli
-E coli: commensal
-Vibrio spp.
-Salmonella spp.
-Shigella spp.
-Campylobacter jejuni
-Yersinia enterocolitica
Gram positive Cocci
-Staphlococcus spp.: commensal
Gram positive bacili
-bacillus anthracis, B. cereus
-Clotridium spp. : C. dificil is comensal
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2
Q

Non inflammatory vs. inflammatory diarrhea

A
Non inflammatory/secretory
-no WBCs or RBCs
-local inflammation may be present: Il-8 and PMNs
Inflammatory diarrhea
-presence of WBCs: pmns and lymphocytes
-may or may not have RBCs
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3
Q

Bacterial virulence factors

A
  1. exotoxins
    -enterotoxins: alter intestinal secretory mechanism
    -cytotoxins: destroy intestinal mucosal cells
  2. Invasion
    -allows intracellular replication
    can pass cells lining GI and spread systemically
  3. Endotoxin
    -gram neg bacteria. Induces Il1 Il6 and TNFa
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4
Q

Top 5 pathogens causing GI infections and hospitalizations

A
  • Hospitalizations: Salmonella (nontyphoidal)> norovirus > Campylobacter spp.> toxoplasma gondii > E coli (STEC) O157
  • food borne illness: Norovirus, salmonella, clostridium perfringens, campylobacter, staph. aureus
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5
Q

Describe 6 types of pathogenic E. coli and their virulence factors

A

INFLAMMTORY Diarrhea
1. EPEC: Enteropathogenic. adherence to epithelial cells lining small intestine. Prevents absorption.
2. EAEC: enteroaggregative -aggregative adherence to epithelial cells, prevents fluid absorption
3. EIEC: Enteroinvasive-invasion, replication, destruction of epithelial cells. inv genes. Large intestines.
4. EHEC: enterohemorrhagic-shiga like toxin, destroy epithelial cells. HUS. systemic absorption. large intestine.
SECRETORY Diarrhea
5. ETEC: Enterotoxigenic- heat stable and/or heat labile enterotoxins inhibit intestinal uptake and stimulate hyper secretion of fluids respectively. Most common cause of traveller’s diarrhea (O157:H7)
EMETIC disease
6. DAEC: Diffuse adherent

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6
Q

General E. coli features

A
  • Gram neg bacilli, facultative anaerob, lactose positive
  • classified based on O (cell wall polysaccharide), H (flagellar), and K (capsular) antigens
  • 1/3 traveler’s diarrhea caused by ETEC
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7
Q

Vibrio cholerae

A
  • gram neg baciili
  • marine environments
  • causes severe rice water diarrhea
  • cholera toxin causes hyper secretion of water and electrolytes through accumulation of cAMP. Binary toxin: B for binding and A for active component
  • pili is a virulence factor
  • Rx supportive therapy Antibiotics can be used to reduce severity
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8
Q

Salmonella spp.

A
  • gram neg bacilli
  • s. typhi and paratyphoid are exclusively human pathogens. transmitted via food/water contamination
  • animal reservoir for others
  • causes inflammatory diarrhea, and enteric fever
  • virulence: adherence factors and invasion factors, survives phagocytosis, acid tolerance response
  • always require hospital treatment
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9
Q

Shigella spp.

A
  • gram neg bacilli
  • human reservoir. person to person fecal oral transmission
  • don’t nee many organisms to establish infection
  • disease: diarrhea with RBCs, WBCs, mucus
  • virulence: adherence and invasion factors, survives phagocytosis, Shiga toxin interferes with mRNA translation
  • Rx antibiotics
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10
Q

Campylobacter jejuni

A
  • gram neg bacilli
  • flagella
  • animal reservoir
  • found in 50% of retail poultry
  • diarrhea with blood and leukocytes, nausea, vomiting ab pain
  • virulence: adhesins, cytotoxic enzymes, enterotoxins
  • complication: Guillan-Barre syndrome because of antibody cross reactivity between olisaccharides and glycospingolipids in neural tissue
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11
Q

yersinia enterocolitica

A
  • gram neg bacilli
  • water, raw milk, animal reservoir
  • enterocolitis: inflammatory diarrhea
  • virulence: invasion factors (chromosome), enterotoxin, heat-stable, resistance to complement mediated phagocytosis, resistance to antibody mediated complement (plasmid)
  • rx supportive therapy
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12
Q

Which bacterial toxins cause food poisoning?

A
  • Staph aureus: food contaminated by handler. boiling kills bacteria but doesn’t inactivate toxin. Egg products, institutionalized food
  • b. cereus
  • clostridium
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13
Q

B cereus: emetic vs. diarrhea illness

A

gram pos baccili. ubiquitous in environment.

  • Emetic: from heat stable enterotoxin in reheated rice.short duration 9hr.
  • Diarrheal form: undercooked food containing bacteria producing heat labile enterotoxin. 24 hr duration. Toxin affects adenyl cyclase. meat and veggies.
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14
Q

Clostridium difficile

A
  • gram pos. bacilli. anaerobic
  • spore former
  • Antibiotic associated diarrhea: C. difficile is a commensal. In person with altered intestinal flora (antibiotics), C difficile can compete and establishes overgrowth.
  • antibiotic associated colitis (pseudomembranous colitis)
  • Toxin A=enterotoxin causes hyper secretion of fluid and chemotaxis of granulocytes
  • Toxin B=cytotoxin, induces depolymerization of actin with resultant loss of cytoskeleton in leukocytes and epithelial cells. Increases inflammatory response.
  • Rx with vancomycin or metronidazole.
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15
Q

Foodbourne vs. infant botulism

A
  • caused by clostridium botulinum- gram pos bacilli, anaerobic. spore forming
  • Foodborne botulism: inadequately preserved canned food. Toxin type A-flaccid paralysis. Blurred vision and speech are first symptoms.
  • Infant botulism: contaminated honey. Ingested spores germinante in GI tract of baby, bacteria multiply, toxin produced in vivo. Constipation, difficulty swallowing, floppy baby.
  • spores ingested by adults may germinate, but growth is suppressed by competing microflora.
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16
Q

Helicobacter pylori virulence factors

A
  • heat shock protein: induces expression of urease
  • urease: neutralizes gastric acidity
  • mucinase and phospholipase: disrupts gastric mucus
  • acid inhibitory protein: prevents production of stomach acid
  • catalase and superoxide dismutase: interferes with phagocytosis
  • VacA-allows intracellular replication
17
Q

Correlation between H. pylori and gastric cancer

A
  • chronic infection leads to inflammatory response
  • cagA gene in bacteria has been correlated to gastric cancer and possibly acts to inhibit or inactivate tumor suppressor proteins p53 and RUNX3