Shigellae
Shigella species are the causative agents of
bacillary dysentery
(enterocolitis of humans)
General characteristics of Shigellae
- Gram negative rods, non–motile, non–sporing and non-
capsulated
- Aerobic and facultative anaerobes and can not grow on
simple media
- All are non lactose fermenter except for Sh.sonnei (late
lactose fermenter), but ferment other sugars producing
acid only.
- They are urease negative, gelatin not liquefied and H
2
S not
produced.
- I M Vi C
- Manitol reactions are important because they distinguish
group A strains (do not ferment manitol) from groups (B,
C & D) which ferment manitol.
- Ornithin
decarboxylase
test
also
important
in
differentiation between Shigella subtypes (all are negative
only for subgroup D).
Subgroups of Shigella
>40 serotypes
classified according to their biochemical &
serological criteria:
1.
Group A (Sh.dysenteriae)
12 serotypes
2.
Group B (Sh.flexneri)
1-6 serotypes
3.
Group C (Sh.boydii)
18 different serotypes
4.
Group D (Sh.sonnei)
antigenically homogeneous but
present in 2 forms
Antigenic structure
The somatic O Ag of Shigella (LPS) and their serologic
specificity depends on cell wall polysaccharide.
Toxins:
A. Endotoxin: Toxic polysaccharide released during autolysis
causing irritation of bowel wall.
B. Exotoxin: An antigenic protein released by Sh.dysenteriae
type 1 (Shiga bacillus). Like E.coli verotoxin, act on gut
diarrhea and on CNS (Neurotoxin)
meningism &
coma.
Pathogenesis & pathology
Shigellae cause disease exclusively in GIT, it is highly
communicable disease, transmitted by feco-oral rout with low
dose (100 organisms). Although some strains produce
enterotoxin but invasion is the critical factor in pathogenesis.
Blood stream invasion is rare.
The pathologic process of bloody diarrhea (dysentery)
Invasion of mucosal epithelial cells of large intestine and
terminal ileum by induce phagocytosis
micro-organisms
multiply within the cytoplasm and pass to adjacent cells
microabscesses of the wall
necrosis, superficial ulceration,
bleeding and pseudomembrane formation (fibrin, leukocytes,
cell depris, necrotic tissues and bacteria)
then subsides by
granulation and formation of scar tissues.
Clinical findings
Incubation period of 1-4 days
symptoms begin with fever and
abdominal camps
watery diarrhea caused by action of
exotoxin on small intestine then diarrhea will be less liquid
containing blood and mucus.
Severity of disease depend on 2 factors:
-Species of shigella
→ Sh.dysenteriae is the most sever
Sh.sonnei is the milder
-age of patient (children and elderly people being the most
severly affected)
The diarrhea resolves within 2-3 days but in sever cases
antibiotics can shorten the course of attack.
-Anti bodies appear after recovery but not protective. Some
remains as carriers shedding the bacilli with their stool.
Laboratory Diagnosis
1-Specimens, stool or rectal swab
culture.
2-Cultured on same media used for isolation of Salmonella
non lactose fermenter (NLF) but no H
2
S production and then
identified by biochemical tests and agglutination produced by
mixing with specific antisera.
3-Serum specimen may be done for detection of agglutinins, but
not diagnostic.
Treatment
1-Fluid and electrolyte replacement.
2-Antibiotic in sever cases, usually after sensitivity test because
resistance may develop by plasmid.
3-Anti-peristaltic drugs are contraindicated in shigellosis
they
prolong excretion of micro-organisms.