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Module 5: GI > Microbiology: Lower GI > Flashcards

Microbiology: Lower GI Flashcards

1
Q

What are some general types of lower GI infections caused by enteric Gram-negative Rods?

A

- Secretory Diarrhea
Watery diarrhea
absence of PMNs
Mediated by enterotoxin(s)

- Inflammatory Diarrhea
PMNs in stool
Dysentery
Mediated by bacterial invasion
Damage to enterocytes

- Hemorrhagic Colitis
Bloody diarrhea w/ or w/o inflammation

**- Enteric Fever**
 Systemic infection (intestinal origin)
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2
Q

What is dysentery?

A

Small volume stools with blood and pus

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3
Q

What are characteristics of Enterobacteriaceae? What are some examples?

A

Characteristics:
Gram neg rods
Glucose fermenters
Oxidase negative
Facultative Anaerobes
Grow on MacConkey agar

Examples:
Shigella sp.
Salmonella sp.
Yersinia sp.
Escherichia coli
ETEC
EIEC
EPEC
EHEC/STEC
EAEC

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4
Q

How does lactose fermentation differ in Eneterobacteriaceae?

A

It is used to distinguish some pathogenic species from commensal E. coli:

Non-lactose fermenters:
(colorless MacConkey agar)
Shigella sp.
Salmonella sp.

Lactose fermenters:
(pink colonies on Mac agar)
E. Coli (except EIEC)
Commensal and pathogenic
ETEC
EPEC
EHEC
EAEC

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5
Q

What is the shigella classification system?

A

Group A: Shigella dysenteriae
Most severe disease
Type 1 produces Shiga toxin

Group B: Shigella flexnerii
Most common in developing countries

Group C: Shigella boydii
rare

Group D: Shigella sonnei
Most common in US

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6
Q

How can a patient present with Shigella disease?

A

Asymptomatic

Watery Diarrhea

Bacillary (colonic) dysentery
Abdominal pain
Tenesmus
Fever
Low volume stools:
bloody, mucoid
fecal leukocytes

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7
Q

What are possible complications of Shigella disease?

A

Reiter’s syndrome - reactive arthritis

Hemmolytic uremic syndrome (HUS)
(for Shiga toxin producing strains)
Hemolytic anemia
Acute Kidney Failure
Low Platelet count

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8
Q

What is the pathogenesis of Shigellosis?

A
  1. Enters through the M cells in the intestine
  2. Causes apoptotic killing of macrophages, eliciting an inflammatory response

–> This causes transmigration of PMNs through the epithelial lining and facilitation of bacterial access to basolateral pole of epithelial cells

  1. Bacteria enter enterocytes and spread from cell to cell

(Shigella virulence factors allow the bacteria to utilize the cell’s actin monomers to “shoot” it from cell to cell to facilitate spread)

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9
Q

What are the four Fs of Shigella transmission?

A

Feces, Fingers, Fomites, Flies

Often Found in:
Institutions (prisons, asylums)
Day care centers
POW camps, refugee camps
Latrines
Cruise Ships
Public pools

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10
Q

What are characteristics of Shigella sp?

A

Gram neg rod

Nonlactose fermenter

Nonmotile

Highly infectious! ( ID = 10 organisms)

Human specific

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11
Q

How is Shigella sp. diagnosed?

A

Cell Culture

Serotyping

Methylene blue staining of stool prep

Lactoferrin test (quantitative)

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12
Q

What is the clinical presentation of nontyphoidal Salmonelloses Enterocolitis?

A

8-48hr incubation

Abrupt onset

Low fever

2-5 days of disease duration

Symptoms:
Nausea
Vomiting
Diarrhea at onset

Negative Blood Cultures

Positive Stool Cultures

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13
Q

What is the clinical presentation of nontyphoidal salmonelloses systemic bacteremia?

A
  • Most common in immunecompromised

Variable incubation

Abrupt onset

Rapid rise, then spiking “septic” temp.

variable duration

Often no GI symptoms

Positive Blood Cultures during fever

Infrequently positive Stool Cultures

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14
Q

What is the pathogenesis of nontyphpoidal salmonella (enterocolitis)?

A

Ingestion of contaminated food or water (animals are major reservoir)

–> Colonization of small intestine (produce enterotoxin)

–> Invasion of epithelium

–> Multiplication of bacteria within endosomal vacuole (no tissue death)

–> Iflammation and PMN recruitment

–> small # of bacteria enter submucosa

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15
Q

What is the pathogenesis of Sustained bacteremia with non-typhoidal salmonella?

A

Occurs in immunecompromised hosts:

Ingestion of contaminated food or water (animal reservoir)

–> Colonization of intestine

–> Invasion of epithelium, multiplication of bacteria in endosomal vacuole (no tissue death)

–> Invasion of blood stream

–> Focal lesions in:
lungs, bones, heart, meninges

–> can lead to septic shock and death

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16
Q

What are the most common sources of Nontyphoidal Salmonellae?

A

Most Common:
Eggs
Unpasteurized milk
Meat (beef, poultry)

Less Common:
Vegetables
Pet turtles and reptiles
Baby ducks and chickens @ Easter

17
Q

What is the clinical presentation of Salmonelloses with enteric (typhoid) fever?

A

7-20 day incubation period

Insidious onset

Fever is gradual, then high plateau with “typhoidal” state

Disease duration is several weeks

GI symptoms:
Constipation followed by blood diarrhea

Positve blood cultures in first 2 weeks

Positive stool cultures after first 2 weeks

18
Q

What is the pathogenesis of Typhoid fever?

A

Ingestion of contaminated food or water (Humans are only reservoir)

–> Colonization of small intestine

–> Invasoin of Peyer’s Patches (through M cells)

–> Invasion into blood stream (through Macrophages)

–> Focal lesions in:
Spleen, liver, bones, lung,
intestine, heart, meninges

19
Q

What are virulence factors of Salmonella enterica, serovar Tyhpi (i.e. S. typhi)?

A

Survival in macrophages

Invasion of epithelial cells

  • *Capsule (Vi antigen)**
  • not found in non-typhoidal serotypes
  • composed of N-acetylgalactosaminuronic acid
  • inhibits complement-mediated killing
  • Component of one of the three vaccines against S.typhi
  • *Persistence in body sites (i.e. gall bladder)**
  • -> Carrier state typically have high titered Abs against Vi antigen
20
Q

When are Salmonella Infections treated?

A

Debilitated hosts

Sustained bacteremia

Extra-intestinal infection

Enteric Fever

(NOT enterocolitis)

21
Q

How can yersinia pseudotuberculosis present in a patient?

A

Entercolitis
Fever, abdominal pain,
inflammatory diarrhea
–> Reiter’s Syndrome
(post-infectious complication

Mesenteric Lymphadenitis
can mimic appendicitis

Extraintestinal infections (less common)
Septicemia
endocarditis
pyomyositis
pharyngitis

22
Q

What are characteristics of yersinia and how is it spread?

A

Gram negative rod

Zoonotic transmission:
–> contaminated produce and undercooked chitterlings

  • *Lab Dx:
  • nonlactose fermenter (Y. pseudotuberculosis)
  • lactose fermenter (Y. enterocolitica)
  • -> both grow well at RT and 4deg**
23
Q

What diseases are caused by:

Entertoxigenic E. coli

Enteroinvasive E. coli

Enteropathogenic E. coli

Enterohemorrhagic E. coli (aka Shiga Toxin-producing E. coli)

Enteroaggregative E. coli

Diarrheagenic E. coli

A

ETEC:
Traveler’s Diarrhea
Children’s Diarrhea

EIEC:
Bacillary Dysentery

EPEC:
Infant Diarrhea

EHEC/STEC:
Hemorrhagic colitis
Hemolytic uremic syndrome

EAggEC/EAEC:
Infant diarrhea
Adult diarrhea

DAEC:
Pediatric Diarrhea

24
Q

What is the pathogenesis of ETEC?

A

Enterotoxigenic E. coli:

Ingestion of water or food contaminated w/human feces

–> Colonization of small intestine mediated by colonization of fimbriae

--\> Elaborations of enterotoxins:
 Heat labile(LT) and Heat stable(ST)

–> Causes:
Water Diarrhea
No fecal PMNs
No Blood

25
Q

What are the virulence factors of ETEC?

A

LT: Labile toxin:
Causes constitutive production of cAMP
–> No uptake of Na+ and Cl+ in enterocytes, causing watery diarrhea

ST: Stable toxin:
Causes constitutive production of cGMP
–> No release of K+, Na+, or HCO3- from enterocytes

26
Q

What are characteristics of EIEC?

A

Enteroinvasive E.coli:

Gram neg rod
lactose fermenter

Disease is identical to Shigellosis (ranges from watery to dysentery)

Has large shigella virulence plasmid

27
Q

What is protective against EPEC infection?

A

Breast feeding and age

–> Enteropathogenic E. coli is major cause of diarrhea (acute and chronic) in children <2yrs

–> age restricted, but not due to acquisition of immunity

28
Q

What are characteristics of EPEC infection?

A
  • *Effacement of brushborder:**
  • EPEC makes “attaching effacing” (A/E) lesions in small intestine

Infection has 2 stages:

  1. Initial adherence to BB
  2. Late adherence, formation of A/E lesions
29
Q

What is the spectrum of EHEC/STEC disease?

A

Asymptomatic infection

Mild diarrhea

Hemorrhagic Colitis
(“Big Mac Attack”)
abdominal pain
no fever
bloody diarrhea
presence of fecal PMNs is variable

Hemolytic Uremic Syndrome
(shiga toxin in blood stream)
Microangiopathic hemolytic anemia
thrombocytopenia
glomerular thrombosis

30
Q

What is the prototype EHEC?

A

E. coli O157:H7

(it is a subset of STEC)

31
Q

What is the mechanism of Shiga toxin (from E. coli)?

A

Once colonized:
Toxin travels from intestine to kidneys (target)

–> Binds to Gb3 receptor on glomeruli

–> Inhibits protein synthesis

–> Destruction of glomerular endothelial cells occurs

–> decreased glomerular filtration

–> Acute Renal Failure

32
Q

What is counter indicative of antibody use in E. coli infection?

A

Hemorrhagic colitis

–> treatment with Abx may cause cells to release all Shiga toxin into blood stream, leading to
Hemolytic Uremic Syndrome

33
Q

What are characteristics of EAEC?

A

Enteroaggregative E. coli:

Gram neg rod
lactose fermenter

Causes inflammatory diarrhea with occasional blood or mucus

  • *Virulence factors:**
  • hydrophobic colonization pili cause bacterial aggregation and dense intestinal colonization
  • plasmid encoded enterotoxins

Stacked Brick appearance on tissue culture

34
Q

How are MacConkey and sorbitol MacConkey plates used to identify Diarrheagenic E. coli?

A

MacConkey lactose fermentation is only useful for EIEC

SMAC plate is used to identify EHEC (i.e. O157:H7)
-> Sorbitol negative

Module 5: GI (19 decks)

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