Microbiology: Lower GI Flashcards
What are some general types of lower GI infections caused by enteric Gram-negative Rods?
- 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)
What is dysentery?
Small volume stools with blood and pus
What are characteristics of Enterobacteriaceae? What are some examples?
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
How does lactose fermentation differ in Eneterobacteriaceae?
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
What is the shigella classification system?
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
How can a patient present with Shigella disease?
Asymptomatic
Watery Diarrhea
Bacillary (colonic) dysentery
Abdominal pain
Tenesmus
Fever
Low volume stools:
bloody, mucoid
fecal leukocytes
What are possible complications of Shigella disease?
Reiter’s syndrome - reactive arthritis
Hemmolytic uremic syndrome (HUS)
(for Shiga toxin producing strains)
Hemolytic anemia
Acute Kidney Failure
Low Platelet count
What is the pathogenesis of Shigellosis?
- Enters through the M cells in the intestine
- 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
- 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)
What are the four Fs of Shigella transmission?
Feces, Fingers, Fomites, Flies
Often Found in:
Institutions (prisons, asylums)
Day care centers
POW camps, refugee camps
Latrines
Cruise Ships
Public pools
What are characteristics of Shigella sp?
Gram neg rod
Nonlactose fermenter
Nonmotile
Highly infectious! ( ID = 10 organisms)
Human specific
How is Shigella sp. diagnosed?
Cell Culture
Serotyping
Methylene blue staining of stool prep
Lactoferrin test (quantitative)
What is the clinical presentation of nontyphoidal Salmonelloses Enterocolitis?
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
What is the clinical presentation of nontyphoidal salmonelloses systemic bacteremia?
- 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
What is the pathogenesis of nontyphpoidal salmonella (enterocolitis)?
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
What is the pathogenesis of Sustained bacteremia with non-typhoidal salmonella?
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
What are the most common sources of Nontyphoidal Salmonellae?
Most Common:
Eggs
Unpasteurized milk
Meat (beef, poultry)
Less Common:
Vegetables
Pet turtles and reptiles
Baby ducks and chickens @ Easter
What is the clinical presentation of Salmonelloses with enteric (typhoid) fever?
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
What is the pathogenesis of Typhoid fever?
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
What are virulence factors of Salmonella enterica, serovar Tyhpi (i.e. S. typhi)?
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
When are Salmonella Infections treated?
Debilitated hosts
Sustained bacteremia
Extra-intestinal infection
Enteric Fever
(NOT enterocolitis)
How can yersinia pseudotuberculosis present in a patient?
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
What are characteristics of yersinia and how is it spread?
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**
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
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
What is the pathogenesis of ETEC?
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
What are the virulence factors of ETEC?
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
What are characteristics of EIEC?
Enteroinvasive E.coli:
Gram neg rod
lactose fermenter
Disease is identical to Shigellosis (ranges from watery to dysentery)
Has large shigella virulence plasmid
What is protective against EPEC infection?
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
What are characteristics of EPEC infection?
- *Effacement of brushborder:**
- EPEC makes “attaching effacing” (A/E) lesions in small intestine
Infection has 2 stages:
- Initial adherence to BB
- Late adherence, formation of A/E lesions
What is the spectrum of EHEC/STEC disease?
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
What is the prototype EHEC?
E. coli O157:H7
(it is a subset of STEC)
What is the mechanism of Shiga toxin (from E. coli)?
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
What is counter indicative of antibody use in E. coli infection?
Hemorrhagic colitis
–> treatment with Abx may cause cells to release all Shiga toxin into blood stream, leading to
Hemolytic Uremic Syndrome
What are characteristics of EAEC?
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
How are MacConkey and sorbitol MacConkey plates used to identify Diarrheagenic E. coli?
MacConkey lactose fermentation is only useful for EIEC
SMAC plate is used to identify EHEC (i.e. O157:H7)
-> Sorbitol negative
