3. Shigella

Shigella vaccine

Some clinical trials but no

Shigella sonnei

the most common species in the US and other high-
income countries, generally causes milder disease

Shigella flexneri

widespread in low- and middle-income countries

Shigella boydii

very rare in the US, most cases occur in India

Shigella dysenteriae

very rare in the US, most cases occur in Africa,
can lead to death

Shigella transmission

usually through
the fecal-oral route, meaning that
Shigella is transmitted by eating
small amounts of feces

Hemolytic uremic syndrome

a serious condition that can occur after Shigella infection, characterized by anemia, low platelet count, and acute kidney failure.

The genomes of Shigella and Enteroinvasive E. coli (EIEC

VERY SIMILAR
have a 230 kb virulence plasmid with the mxi-spa
locus which encodes a T3SS

similarity observed across
the Shigella species is the result of

convergent evolution

Shigella pathogenicity
islands (SHI PAIs)

carry virulence factors

Mxi-Spa T3SS

plasmid-
encoded, and also found in EIEC to secrete effectors into host cell

How does shigella invade from the intestinal lumen 

invade via M cells (microfold cells) and use transcytosis to cross the epithelium

M cells

specialized intestinal epithelial cells that sample the intestinal microbiota

How does Shigella enter host cells

uses a trigger mechanism to induce membrane ruffling like Salmonella

Shigella Mxi-Spa T3SS- role in invasion

injects the IpaABC effectors which activate Rho GTPases to allow actin cytoskeleton remodeling for membrane ruffling

Shigella-containing vacuole

a vacuole formed after Shigella invasion, which facilitates bacterial survival and replication within the host cell.

M cell pocket

A specialized region in the intestinal mucosa where M cells capture and transport antigens to immune cells, facilitating the entry of Shigella into the host.

IL-8

produced by neighboring
epithelial cells (12) recruits PMNs,
which travel from the basolateral to
the apical colonic epithelium,
destabilizing the junctions between
the epithelial cells and allowing
further invasion of Shigella

How can Shigella spread from cell-cell

actin modification

Cell-to-cell spread is seen in

Shigella, Rickettsia, and Listeria

The IscA and IscB effectors of the T3SS of Shigella

play a large role
in cell-to-cell spread

IscA

induces actin polymerization to help facilitate cell-cell spread

Shigella immune response

IL-8 weakens junctions to promote spread, BUT also facilitates full clearance

Shiga toxin

depurinates (removes a purine, adenine) from ribosomal
RNA and inhibits protein synthesis

ShET1 and ShET2

are not homologous, but both are exotoxins that
cause fluid secretion and watery diarrhea

S. dysenteriae produces

Shiga AB5 toxin to inhibit protein synthesis

Shiga toxin- B subunit

binds to a host glycolipid (GB3 in
figure) that is found mainly on kidney epithelial
cells (HUS)

Shiga toxin- A subunit 

released into the
cytosol where it removes an adenine from
ribosomal RNA and blocks protein synthesis

4 Shigella species are differentiated based on
biochemical tests and their

LPS O antigen

Shigella vaccine candidate

engineered Shigella to
produce the 4 most common LPS
serogroups and to excessively form
OMVs, which will deliver the 4 component O antigen vaccine