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Microbiology Exam III > Bacterial Infections of the GI Tract III > Flashcards

Bacterial Infections of the GI Tract III Flashcards

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1
Q

Vibrio spp. (Disease-Causing spp.)

A

1) Vibrio cholerae (Gastroenteritsi, Bacteremia)
2) Vibrio parahaemolyticus (Gastroenteritis, Bacteremia, Wound infection)
3) Vibrio vulnificus (Bacteremia, Wound infection)

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2
Q

Virbio spp. (Characteristics)

A
  • Gram negative, facultative anaerobes
  • COMMMA (curved) shaped
  • Free-living in water
  • Broad temperature range of growth
  • REQUIRE SODIUM CHLORIDE for growth
  • Grow at a WIDE RANGE of pH (susceptive to stomach acid, high infectious dose ~10^9)
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3
Q

Vibrio cholerae (Small Intestine) (Disease)

A

Cholera

  • Asymptomatic –> severe WATERY diarrhea
  • 2-3 day incubation
  • Up to 7 day duration
  • 5 to 25% of infected individuals develop SEVERE WATERY diarrhea (abrupt onset, ~17 liters/4.5 gallons in a 150 lb person, Rice water stool, can kill within HOURS via dehydration)
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4
Q

Vibrio cholerae (Small Intestine) (Epidemiology)

A
  • Spread through CONTAMINATED WATER
  • Infection = LONG-TERM IMMUNITY (appears to be O antigen specific)
  • Associated with epidemics and pandemics
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5
Q

Vibrio cholerae (Small Intestine) (Typing and Epidemiology)

A

1) Based on O-antigens (O1 to O200+)
2) O1 = cholera toxin-producing
- Epidemic and Pandemic cholera caused by O1 serotype
a) Pandemics 1-6 caused by classic biotype
b) Current pandemic (#7) caused by El Tor biotype
- Less severe disease (1 symptomatic to 30-100 asymptomatic)
- Duration of carriage longer than classic strain
- Survives better in the environment (carried longer, shed longer)

O-antigens change = Patients no longer immune

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6
Q

Vibrio cholerae (Small Intestine) (Virulence Factors (2 of them) and Pathogenesis)

A

1) Toxin co-regulated pilus (TCP)
- Mediated adherence to intestinal epithelial cells
* Binds to cell*

2) Cholera Toxin
- AB toxin
- Activation of adenylate cyclase –> INCREASE cAMP –> massive efflux of watery secretions
- NO significant cell damage done by toxin
- Very similar effect to ETEC LT toxin (structure and function)
- Encoded on CTXo (PROPHAGE/BACTERIOPHAGE)

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7
Q

Vibrio cholerae (Small Intestine) (Diagnosis and Treatment)

A

Diagnosis:
-Culture (differential media; in places where cholera is not common)

Treatment:

  • Rehydration therapy - IV and oral
  • Without rehydration therapy, mortality can be as high as 90%
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8
Q

Vibrio parahaemolyitcus (Small Intestine) (Disease and Virulence)

A

Disease:
-Explosive watery diarrhea, nausea, vomiting, abd cramps, low grade fever

Virulence:

  • KANAGAWA HEMOLYSIN* (VIRULENCE FACTOR)
  • Induces chloride secretion, thus watery diarrhea
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9
Q

Vibrio parahaemolyitcus (Small Intestine) (Epidemiology and Treatment/Prevention)

A

Epidemiology:

  • Associated with consumption of RAW SHELLFISH
  • Most common cause of:
    1) Bacterial gastroenteritis in Japan and Southeast Asia
    2) Seafood associated gastroenteritis in the US

Treatment and Prevention:

  • Self-limiting
  • Proper cooking of shellfish
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10
Q

Yersinia enterocolitica (Small Intestine) (Characteristics)

A
  • Gram negative coccobacilli

- Related to Yersinia pestis (Causative agent of Bubonic Plague)

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11
Q

Yersinia enterocolitica (Small Intestine) (Epidemiology)

A

Widespread in NATURE and ANIMALS

  • Most isolates are AVIRULENT
  • Spread by ingestion of CONTAMINATED WATER, FOOD (e.g. improperly cooked PORK)
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12
Q

Yersinia enterocolitica (Small Intestine) (Symptoms)

A

Fever, abd cramps, watery –> bloody diarrhea

-Last 1-2 weeks

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13
Q

Yersinia enterocolitica (Small Intestine) (Pathogenesis)

A
  • Poorly understood
  • Binds to and invades M-cells in the terminal ILEUM (similar to Salmonella spp. , but via separate mechanism)
  • Involves T3SS and injection of Yops (Yersinia outer proteins)
  • Produces HEAT-STABLE ENTEROTOXIN (main reason symptoms manifest as diarrhea)
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14
Q

Yersinia enterocolitica (Small Intestine) (Diagnosis and Treatment)

A

Diagnosis
-Stool culture

Treatment:
-Self-limiting

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15
Q

Clostridium difficile (Large Intestine) (Characteristics)

A
  • Gram positive anaerobe
  • Non-invasive
  • SPORE FORMING
  • Emerging pathogen (Nosocomial, HAI)
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16
Q

Clostridium difficile (Large Intestine) (Disease and Symptoms [Vary])

A

Asymptomatic carriage –> CDAD (C. diff Associated Diarrhea) –> Pseudomembrane colitis –> fulminant colitis with TOXIC MEGACOLON

Forms large plaques on top of intestinal epithelium, reducing uptake of water

17
Q

Clostridium difficile (Large Intestine) (Pathogenesis)

A

Toxin A and Toxin B

-Caused DAMAGE to the MUCOSA by disrupting the host cell CYTOSKELETON and causing diarrhea

18
Q

Clostridium difficile (Large Intestine) (Diagnosis, Treatment, and Prevention)

A

Diagnosis:

  • Toxin detection in the stool
  • Culture is NOT HELPFUL (as C diff is part of normal microbiota in 5-10% of population)

Treatment:
-Oral Vancomycin or Metronidazole

Prevention:
-Fecal Transplant

19
Q

Clostridium difficile (Large Intestine) (Epidemiology and Risk Factors)

A

Mainly seen in patients in the HOSPITAL for a SURGICAL PROCEDURE or being treated with BROAD SPECTRUM ANTIBIOTICS that alter normal microbiota

20
Q

EHEC (Large Intestine) (Characteristics)

A
  • Gram negative, facultative anaerobe
  • O157:H7 (a lot of news coverage)
  • Animal reservoirs** = *Cattle or other ruminants (Animals are ASYMPTOMATIC; will not know they have it unless cultured)
  • Generally non-invasive

Mnemonic: EHEC –> “H” = Hamburger

21
Q

EHEC (Large Intestine) (Epidemiology)

A

Sporadic cases and outbreaks mainly in the developed world

-Associated with contaminated ground beef (HAMBURGER) and vegetables (washed with water from rivers/streams)

22
Q

EHEC (Large Intestine) (Disease)

A
  • HEMORRHAGIC COLITIS = blood diarrhea (MARKED blood)
  • No fever, marked abdominal tenderness
  • Sequelae –> HEMOLYTIC UREMIC SYNDROME (HUS) = Anemia and kidney failure
23
Q

EHEC (Large Intestine) (Pathogenesis)

A
  • Attaching and Effacing lesions like PEEC (***Uses TYPE III system to inject protein in)
  • Shiga-like toxin (Verotoxin)
  • –> Blocks translation by cleaving part of the 60S subunit of the ribosome
24
Q

EHEC (Large Intestine) (MOA)

A
  1. E. coli O157:H7 binds to brush border of intestinal mucosa
  2. E. coli O157:H7 produces VEROTOXIN that destroys microvilli
  3. Verotoxin (i.e. Shiga-like Toxin [Stx]) enters blood, causing vascular endothelial damage and increased platelet aggregation
  4. Platelet-Fibrin thrombi form causing ischemic damage to colon, kidneys, and other tissues
    - Hemorrhagic Colitis
    - Hemolytic Uremic Syndrome (HUS)
25
Q

What causes kidney damage in EHEC patients?

A

Glomeruli are rich in toxin glycolipid receptor Gb3, which binds to Shiga-like toxin (Verotoxin), causing thrombi to form and cause ischemic damage to the kidney

26
Q

EHEC (Large Intestine) (Diagnosis)

A
  • Presumptive –> bloody diarrhea WITHOUT fever*
  • Culture
  • PCR (NAAT): Detection of stx gene that encodes toxin
  • Rapid diagnostic test kits
27
Q

EHEC (Large Intestine) (Treatment)

A
  • Supportive therapy
  • Antibiotic therapy not beneficial and may be harmful
    a) Antibiotic use –> bacterial cell damage –> lysogenic phage (Stx) –> lytic cycle –> increased toxin production –> increase in HUS rate
  • Antibiotic therapy is contraindicated*
28
Q

EHEC (Large Intestine) (Prevention)

A

-Properly cook hamburger, raw vegetables

29
Q

Shigella spp (Large Intestine) (Characteristics)

A

Gram negative rods, facultative anaerobe
Intracellular pathogens
Dysentery

30
Q

Shigella spp (Large Intestine) (Epidemiology)

A

~150 million cases, 600,000 deaths per year worldwide

  • Humans are the ONLY RESERVOIR
  • Transmission through FECAL-ORAL ROUTE
  • Extremely low infectious dose, < 10 organisms
  • Incidence directly related to hygiene (poor sanitary infrastructure, crowded healthcare systems; DAY CARE CENTERS)
31
Q

Shigella spp (Large Intestine) (Global Species Distribution)

A

1) S. soneii: DevelopED countries
2) S. flexneri: DevelopING countries
3) S. dysentariae: underdeveloped tropical areas (most severe infections due to HIGH SHIGA TOXIN production)

32
Q

Shigella spp (Large Intestine) (Clinical Manifestations of Shigellosis)

A
  • 1 to 3 days post-ingestion
  • Disease usually self-limiting, 2 to 5 days post-manifestation
  • Generally strain-specific
    a) S. sonneii:
  • -Fever, malaise, and watery diarrhea
    b) S. flexerni and S. dysenteriae:
  • -Dysentery: fever, malaise, watery diarrhea, abdominal cramps, tenesmus (frequently feeling the need to defecate), frequent bloody and pus-filled stools
  • -S. dysenteriae- potential for HEMOLYTIC UREMIC SYNDROME (HUS)
  • HIGHLY INFLAMMATORY DISEASE*
33
Q

Shigella spp (Large Intestine) (Pathogenesis Part I)

A
  • Acid resistant***
  • Adhere selectively to and pass through M-cells (Similar to Salmonella***)
  • Phagocytosis by macrophages
  • Rapid escape from phagosome (Unknown mechanism)
  • Rapid in induction of macrophage apoptosis
  • Leads to a lot of inflammation and pus production*
34
Q

Shigella spp (Large Intestine) (Pathogenesis Part II)

A
  • Interact with basolateral face of enterocytes
  • Induce uptake via T3SS (injection of Ipa proteins; cytoskeletal rearrangement)
  • Lysis of endocytic vacuole (unknown mechanism)
  • Spread to neighboring cells via actin polymerization at a pole (hijacking of host actin; evasion of host defenses)

Can jump between cells like Listeria

35
Q

Shigella spp (Large Intestine) (Pathogenesis Part III)

A
  • Enterocytes escape/invasion leads to cell death
  • Ulcers*** form in infected areas
  • Diarrhea primarily from severe inflammation
  • Shiga toxin production (Stx)
    1) Binds host Gb3 receptor
    2) Inhibits translation = cell death = tissue damage
    3) Glomerular endothelial cells rich in Gb3 (Hemolytic Uremic Syndrome HUS)
36
Q

Shigella spp (Large Intestine) (Diagnosis)

A

Stool culture

Serological tests to confirm species

37
Q

Shigella spp (Large Intestine) (Treatment and Prevention)

A

Treatment:

  • Rehydration therapy
  • Antibiotic treatment (shorten duration of illness and/or limit disease severity; Ampicillin resistance is common; Ampicillin choice dependent on susceptibility profile)

Prevention;

  • No vaccine
  • Improved sanitation and personal hygiene
  • Infection does not confer immunity* (Can get it over and over again)
38
Q

Enteroinvasive E. coli (Large Intestine)

A
  • Very uncommon
  • Same as Shigella infection EXCEPT NO SHIGA TOXIN
  • Appears E. coli obtained pathogenicity island from Shigella spp. via horizontal gene transfer

***Certain sexual acts associated with increased risk: oral to anal contact (transmission of Salmonella spp. Campylobacter jejuni, and Shigella spp.)

Microbiology Exam III (9 decks)

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