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13 Cards in this Set

  • Front
  • Back
Shigella spp based serologically on what?

What antigen do they not have?

Four spp and severity of infections
serologically based on O antigen (LPS)

don't have H antigen (no flagella)

S. dysenteriae- most severe infections
S. flexneri- infections in developing countries
S. boydii- not commonly isolated
S. sonnei- most infections in developing countries
Shigella physiology and structure
gram? shape?
oxygen use?
fermentation?
resistant to what in humans?
oxidase rxn?
outer membrane effect on org?

similarity to e. coli
gram neg bacilli
facultative anaerobe
fermenter
highly resistant to stomach acids
oxidase neg
outer membrane makes org susceptible to drying

shigella spp are pathogenic clones of e. coli, and hard to distinguish from it
Shigella plasmid
fcn
can transfer to what sp?
what genes encoded? how are the genes regulted?
plasmid encodes virulence
can be transferred to E. coli K12 (causes shigella phenotype)
Has genes for adherence, invasion, replication, and cell-to-cell spread
Regulated by chromosomal genes
Type III secretion genes on plasmid
function?
Invasion plasmid antigens (IpaA,B,C,D)
these are secreted into macs and epithelial cells and induce membrane ruffling on the target cell, leading to engulfment of bacteria
Other genes encoded on plasmid
Mxi- membrane expression of invasion plasmid genes
Ics- intracellular spread
Spa- surface presentation of antigens
Ipg- invasion plasmid gene
Other shigella virulence factors
permeability barrier (outer membrane)
endotoxin
Shiga toxin
Shiga toxin
produced by what spp?
function?
how does it work?
decreases absorption of what?
contribues to what symptom of shigella infection?
produced by S. dysenteriae type 1
Cytotoxic exotoxin that kills epithelial and endothelial cells
inhibits protein synthesis by cleaving 60S ribo subunit
decreases sodium absorption= excess fluid in lumen
conributes to bloody diarrhea by damaging mucosal endothelial cells
Shigella invasion
initially invade thru which cells?
then enter what cells?
once there, what cytokines do they induce? how?
this generates an influx of what?
what does this influx cause?
this then allows shigella to invade what cells?
then what do the bact do?
what results from the infection?
initially enter mucosa via M cells
then they can enter macrophages
Type III secretion system secretes proteins (Ipas), causes mac apoptosis, inducing cytokines IL-1 and IL-8
This generates an influx of PMNs
the PMNs cause separation of tight junctions between epithelial cells, allowing the orgs to penetrate and invade the basal surface of epithelial cells
Internalized bact can escape from phagosomes and spread to neighboring cells using host actin to make COMET TAILS

infection causes cell death, resulting in focal ulcers and exudation of inflammatory cells into lumen, along w/RBCs to produce dysentery stool
Shigellosis
infectious dose
onset
symptoms
low infectious dose (100-200 orgs) means rapid spread possible
onset 16-72 hours after ingestion
initial profuse, watery diarrhea is caused by enterotoxin
cardinal features: lower abdom. cramps, tenesmus, abdundant blood, pus, and mucus in stools (stool volume usually small)
Shigellosis
site of infection
invasion?
ileum and large intestine
invasion present- microabsesses in wall lead to ulcers, bleeding, and formation of pseudomembrane on ulcer
Shigella
cases annually worldwide
host
transmission
mostly in what age group?
150 million cases annually worldwide
humans are primary host
person-to-person transmission, fecally contaminated food/water, raw veggies, fruits, poor hygiene

70% of infections are in kids under 15
At risk populations
young kids in daycare/nursery and custodial institutions
siblings/parents of these kids
male homosexuals
travelers to underdeveloped countries
Shigella diagnosis

treatment
stool specimen isolation
ID of serotype

treatment- Abx shorten disease and bacterial shedding to limit transmission
can initiate w/fluoroquinolones or trimeth/sulfa, but should do drug susceptibility testing
avoid antidiarrheals!!!