Dent 201 MB Shegillae Week 9.

Microbiolog
y Dr. Beriwan A. Ali

The SHIGELLAE
Lecturer PhD. Manchester University, England, UK.

Medical Microbiologist MSc. Salahaddin University, Erbil, Iraq.
Erbil Medical Institute BSc. Salahaddin University, Erbil, Iraq.
Erbil Polytechnic University
Kirkuk Road
Erbil-Iraq
Lecturer
TISHK Int.University
100 Meters Road
Erbil-Iraq
GBD Collaborator
Institute of Health Metrics and Evaluation
University of Washington
Seattle, Washington
USA
• Genus Shigella belongs to Enterobacteriaceae
family
• Shigella has traditionally been grouped with

Salmonella and Yersinia because these 3 genera are
invasive organisms that do not ferment lactose.
• However, recent taxonomic studies that have focused

on DNA homology have shown that Shigella is closely
related to Escherichia, and some researchers believe
that it is a subspecies of Escherichia coli.
General features
Four species (groups) of Shigella sp. have been identified:
• Shigella dysenteriae (group A), (12 serotypes).

• Shigella flexneri (group B), (6 serotypes).
• Shigella boydii (group C), (18 serotypes).
• Shigella sonnei (group D), (1 serotype).
• Members of the genus Shigella are the principal
agents of bacillary dysentery.
• This disease differs from profuse watery diarrhea, as

is commonly seen in choleraic diarrhea or in
enterotoxigenic Escherichia coli diarrhea, in that the
dysenteric stool is scant and contains blood,
mucus, and inflammatory cells.
Gram negative
Epidemiolog
y
• Shigella is one of the most infectious bacteria and ingestion
of as few as 100-200 organisms will cause disease.
• Most individuals are infected with shigellae when they

ingest food or water contaminated with human fecal
material.
• Shigellae can survive up to 30 days in milk, eggs , cheese or

shrimps.
• Spread is always from a human resource and generally involves
one of the :
• food,
• fingers,
• feces,
• flies or
• Fomites (clothing, sheets, etc).
• This contrasts with salmonellae, which
are often spread to humans from
infected animals
• Shigellosis is primarily a pediatric disease.
• 70% of all infections occur in children younger than 15 years.
• Dysentery outbreaks are usually associated with closed

populations, such as:
o families,
o cruise ships,
o mental hospitals,
o children in day-care facilities, and
o prisoners
Bacterial products involved in virulence
• Shigella sp. cause disease by invading, replicating in cells linning the colonic
mucosa, and cell to cell spread.
• The ability of shigellae to invade host cells depends on the presence of a 220 –kb
plasmid that encodes for a set of 4 proteins known as invasion plasmids antigens
(IpaA, IpaB, IpaC, IpaD).
• One of these antigens, IpaD, is believed to be an adhesion that allows the

bacterium to be phagocytosed.
• The host cell receptor for IpaD is not known, but it is expressed only on the
basolateral pole of enterocytes
PATHOGENESIS
• Once the Shigella sp. is inside the host phagosome, a cell associated hemolysin
lyse the phagosome, and the bacterium multiplies within the cell cytoplasm.
• Within 2 hours of entry, the Shigella sp. is coated with gelatinized actin.
• This coat is soon converted to a “tail” of polymerized actin that streams away
from the bacterium.
• Actin polymerization is caused by a 120 –kD outer membrane protein.
• This polymerization allows the bacteria to move directly from

cell to cell.
• Shigella dysenteriae produces Shiga neurotoxin.
• This toxin is identical to verotoxin –1 produced by enterohemorrhagic strains of E. coli

and it has one A subunit and five B subunits.
• The B subunits bind to a host cell glycolipid (Gb3) and facilitate transfer of the A subunit
into the cell. The A subunit disrupts protein synthesis.
• The primary manifestation of toxin activity is damage to the intestinal epithelium.
• In some cases, Shiga toxin can mediate damage to the glomerular endothelial cells,
resulting in renal failure.
• Shiga toxin production is not need to kill host colonic epithelial cells, in fact
invasion seems to be the critical event in cell death and kills host cells faster
than does Shiga toxin.
• Nevertheless, shigellae that produce Shiga toxin cause more severe disease,
possibly because the toxin damages the capillaries of the lamina propria of
the colonic villi, causing ischemia and hemorrhagic colitis
The Shigella sp. infection
cycle
• Shigellae transiently infect the small intestine during the first
few days of disease, and dysentery occurs when the colon is
infected.
• Invasion of the colon is probably initiated through colonic

lymphoid follicles that are rich in M (microfold) cells and are
analogous to Peyer`s patches found in small intestine.
A proposed model for invasion of epithelial cells of the colon.
1) The Shigella sp. first cross the mucosa by passing through specialized cells called M
cells.
The M cell passes the Shigella sp. on to a macrophage from which it subsequently
escapes - possibly by inducing apoptosis, a programmed cell suicide.
2) The Shigella then uses its invasions to enter the mucosal epithelial cells from
underneath.
The invasions cause actin polymer rearrangements in the cell's cytoskeleton resulting in
the bacterium being engulfed and placed in an endocytic vesicle in a manner similar to
phagocytic cells.
Once inside, the Shigella sp. escape from the vacuole into the cytoplasm and multiply.
3) The Shigella sp. are able to move through the host cell and spread to adjacent
host cells by a unique process called actin-based motility.
In this process, actin filaments polymerize at one end of the bacterium,

producing comet-like tails that propel the Shigella sp. through the cytoplasm of
the host cell.
4) When they reach the boundary of that cell, the actin filaments push the
Shigella sp. across that membrane and into the adjacent cell.
• Some shigellae subsequently invade the connective tissue (the
lamina propria), elicit an inflammatory response, and cause
ulceration at the invasion site.
• The inflammatory response involves PMNs and fibrin

pseudomembrane typically forms over the ulcer.
• Shiga toxin may exacerbate the inflammation by causing ischemia

and hemorrhage.
• Shiga toxin that enters the circulation may also cause hemolytic-
uremic syndrome.
• Unlike salmonellae, shigellae are restricted to the mucosa and

submucosa and rarely cause bacteriemia or sepsis.
CLINICAL
DISEASE
• Two to three days after exposure to shigellae, the symptoms of shigellosis
begin.
• There is a sudden onset of
• fever,
• abdominal cramping and tenderness, and
• diarrhea.
• During the first 2-3 days, fluid loss may be extensive and may endanger the lives of children
and others that tolerate fluid and electrolyte loss poorly.
• However, the cardinal feature of shigellosis is lower abdominal cramps and tenesmus, with
abundant pus and blood in the stool.
• The onset of tenesmus (straining at stool) is usually accompanied by decrease in the number and
• Sigmoidoscopy reveals that the mucosa is hyperemic and hemorrhagic and
demonstrates the presence of ulceration covered with fibrin pseudo
membrane.
• The finding of mucus, PMNs, and blood in the stool is hallmark of dysentery
and indicates that the bowel wall has been invaded.
• To identify the causative agent, stool samples can be cultured.
• The best sample for culture, however, consists of a rectal swab of an

ulcer and is obtained during sigmoidoscopy.
• Dysentery due to Shigella must be differentiated from dysentery like

diseases caused by:
o Enteroinvasive E. coli,
o Campylobacter jejuni,
o and the parasite Entamoeba histolytica.
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Microbiolog

y Dr. Beriwan A. Ali

Lecturer PhD. Manchester University, England, UK.

• Shigella has traditionally been grouped with

• However, recent taxonomic studies that have focused

• Shigella dysenteriae (group A), (12 serotypes).

• This disease differs from profuse watery diarrhea, as

• Most individuals are infected with shigellae when they

• Shigellae can survive up to 30 days in milk, eggs , cheese or

• 70% of all infections occur in children younger than 15 years.

• Dysentery outbreaks are usually associated with closed

• One of these antigens, IpaD, is believed to be an adhesion that allows the

• Actin polymerization is caused by a 120 –kD outer membrane protein.

• This polymerization allows the bacteria to move directly from

• This toxin is identical to verotoxin –1 produced by enterohemorrhagic strains of E. coli

• The primary manifestation of toxin activity is damage to the intestinal epithelium.

• Invasion of the colon is probably initiated through colonic

In this process, actin filaments polymerize at one end of the bacterium,

• The inflammatory response involves PMNs and fibrin

• Shiga toxin may exacerbate the inflammation by causing ischemia

• Unlike salmonellae, shigellae are restricted to the mucosa and

• The best sample for culture, however, consists of a rectal swab of an

• Dysentery due to Shigella must be differentiated from dysentery like

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