Shigella

Bacillary dysentery Irfana Azad

Sem:-M.sc 3rd sem
Shigellosis
Enroll no:20072119008
CORD,Microbiology.
University of Kashmir
 Contents
01 Shigella 04 LaboratoryDiagnosis
Morphology,
culture characteristics, Specimen collection,selective
Classification,etc media,transport media,microscopic
observations;etc
02 Transmission..
Pathogenesis
virlunce factors:-virulence plasmid,exotoxin,
endotoxin,etc ;pathogenesis.
05 Treatment
03 Symptoms
Abdominal Cramps,vomiting,fever
Clinical symptoms :
06 Prevention
Bloodstained,mucopurulent stools
Shigella
• The genus Shigella belongs to Enterobacteriaceae
family.

• Named after Japanese scientist Kiyoshi Shiga,

• Isolated the first member of this genus,Shigella

dysenteriae serotype 1( the Shiga bacillus) in 1896
from epidemic dysentery in Japan
●Morphology
• Shigella are short, Gram negative
rods (0.5µm× 1–3 µm in size)

● They are non – motile,

non – sporing and
non – capsulated .
Fig:Gram Staining of
Shigella
● Fimbriae are only present in
Shigella flexneri.
Antigenic structure
of shigella:
• Posses Somatic “O“ antigens.

• Flagellar(H) antigen is absent.

• Some strains posses capsular

“K“ antigens.

• Fimbrail antigens present in

some strains especially
Shigella flexneri.
 Cultural characteristics:-
• Aerobes and facultative anaerobes. Optimum temperature is 37°C and optimum pH – 7.4.

• Non-lactose fermenters except Shigella sonnei.

• All shigella are mannitol fermenters except S.dysenteriae.

Media Colony Morphology

Xylose lysine deoxycholate Colonies are red__ no black centre

Agar(XLD) like salmonella

Deoxycholate citrate agar(DCA) Pale colonies,1-1.5mm

diameter,more translucent.
Salmonella shigella Agar Colorless colonies

Maconkey Agar Colorless colonies

• Transport medium: Carry Blair
medium;Sach’s buffered glycerol
saline
• Enrichment media:Salenite F broth

Classification
Shigella are classified into 4
species(subgroups) and each species
further differentiated into serotype:-
• Shigella dysenteriae (group A), (16
serotypes);

• Shigella flexneri (group B), (6

serotypes);

• Shigella boydii (group C), (19

serotypes);

• Shigella sonnei (group D). (1

serotype).
 Virulence factors of shigella
1:-Large virulence plasmid
214kb size
2:Pathogenecity
31kb region(ipa-mxi –spa region) posses 50 to 60 virulence- ■
.associated genes
islands(PAIs):-
This region encodes a type-III secretion system(T3SS) and ■ ■ Cluster of Genes
many effector proteins like invasion plasmid antigens present on plasmid
and IcsA )IpaA,IpaB,IpaC,IpaD ( and chromosome.
.)Intracellular spread protein A (
■ Encode virulence
Among Ipa, IpaB is an essential virulence ■ factors.
factor 》》 Control of T3SS secretion, phagsome escape and
.macrophage apoptosis

.IpaC 》 Role in actin polymerization■

IpaD 》 Activation of T3SS ■
IcsA 》》 secrete at the pole of Shigella daughter cells,elicits ■
polymerization of filamentous actin
 3:-Toxins
a) Shigella enterotoxin 1 b) Shigella enterotoxin 2
(ShET-1):- (ShET-2):-
encoded by Genes on the ● • Plasmid encoded.
.chromosome • Present in all four species of shigella.
.found in S.flexneri ●

ShET-1 and ShET-2 cause severe watery diarrhea(prodrome stage).

C) Shiga toxin(Stx):-
▪︎Only produced by Shigella dysenteriae.

▪︎ AB5 toxin-one A subunit and 5 B subunits.

B subunit bind to GB3 (Globotriaosyceramide) receptor[GB3 receptor is present on
endothelial cells of the intestine, kidney
and the brain and thus these organs are susceptible to the toxicity of Shiga toxin.)

A subunit cleaves into A1-fragment and A2-fragment by furin.

A1-fragment has enzymatic activity,inhibits protein synthesis.
 Pathogenesis
Transmission
• Transmitted by the faecal-oral route-primarily via
Shigellosis food,fingers,feces,flies and fomites (the five “F'S")

Or Bacillary dysentry

Infection dose
● 10-100 bacilli cells
● Acid tolerant
Pathogenesis contd..
• Infects intestinal cells
Shigellae are Intracellular parasites
that multiply within the cells of
colonic epithelium..
 The invasion process of Shigella is divided into 6 steps:-

1:-The path through Microfold cells:when Shigella

reaches the large intestine,they are transcytosed
through the M (Microfold) cells into the subepithelial
space(membrane ruffling)

2:-The escape from immune cells:-In subepithelial space,

they are engulfed by the resident macrophages .
Inside the macrophage,the Shigella lyse the phagosome
and induce apoptosis.Shigella use T3SS to secrete IpaB
in order to escape from phagosome and induce
macrophage apoptosis.

Apoptotic or infected macrophage release cytokines,Interleukin:-IL-1B and IL-18 and these initiate
inflammatory and immune responses such as infiltration of PMN(neutrophils) for mediating bacterial
clearance.Transmigration of infiltrating PMNs through tight junctions of local epithelial cells into the
intestinal lumen facilitates invasion of Shigella from lumen into subepithelial space.
 3:-Epithelial cell invasion:- The
surviving bacteria then invade colonic
epithelial cells basolaterally by
assembling T3SS, which secretes
effector proteins into the epithelial cells
to induce bacterial endocytosis.

4:-Intracellular multiplication:- The

endocytosed bacteria then lyse the endocytic
vacuoles by IpaB protein and replicate in the
cytoplasm of epithelial cell.

5:-Intra and intercellular spread:- Actin

polymerization occurs at the poles of daughter
cells and forms actin tail that help the bacteria to
move within the enterocyte cytoplasm and help
in cell to cell spread.Actin based motility.
In Intracellular spread, actin tails propel the
Shigella into protrusions impinging on adjacent
enterocytes.
…..The protrusion is then endocytosed by
the adjacent cell using the T3SS system.
The bacteria then lyse the
two-membrane vacuole and multiply in the
cytoplasm and continuing the spread of
infection.
 6:- The destruction of host cells:- As a result of infection, colonic cells are
damaged and exhibit impaired absorption of water and nutrients, leading to
watery diarrhea accompanied by blood and mucus in stools.

Clinical symptoms:-
5 phases
1. Incubation period:-1-4days
2. Initial phase:- watery diarrhea with fever, malaise and vomiting.
3. Dysentery phase:- bloody mucopurulent stools,increased tenesmus and
abdominal cramps
4. Phase of complication:- commonly seen in children < 5 years age.
Intestinal complications:- toxic megacolon; perforations
Metabolic complications:- hypoglycemia;hyponatremia and dehydration.
Ekiri syndrome or toxic encephalopathy:- Metabolic complications+
neurological complications like abnormal posturing,delirium(confusion)
5. Postinfection phase:- patients expressing HLA-B27, develop an autoimmune
reaction months after infection……reactive arthritis; conjunctivitis and urethritis.
(Reiter syndrome)
 163.4 million
cases per year worldwide due to shigellosis

5 to 11 lakh
deaths worldwide due to bacillary dysentery or shigellosis
 Laboratory Diagnosis

Fresh Stool sample Culture analysis

Direct smear Shows large number of pus cells, XLD; DCA ; MacConkey agar
erythrocytes and macrophages
Gram staining
 Treatment
■ Ciprofloxacin is the drug of choice.

■ Alternative drugs which are effective are

ceftriaxone,azithromycin,pivmecillinam

■ Duration of treatment is about 3days

except Shigella dysenteriae 1 infection-
5days.

■ ORS(Oral rehydration solution ) for

correction of dehydration.
 Prevention
■ Stool decontamination
with sodium
Clean hands hypochlorite
Use safe water
After handling of children’s
feces,before handling of food.

Clean surfaces Close the trash

Use latrines
References
● Apurba S.Sastry(2021;third edition); Sandhya
Bhat.Essentials of medical microbiology.
● Prescott Microbiology.
● Molecular Pathogenesis of Shigella spp.: Controlling Host
Cell Signaling, Invasion, and Death by Type III Secretion
Gunnar N. Schroeder and Hubert Hilbi
https://dx.doi.org/10.1128%2FCMR.00032-07
 Thanks!
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