Shigellae
ObjectivesDescribe general structure, biochemical and diagnostic criteria of Shigellae
Know the role of antigenic structures and toxins
Illustrate pathogenesis and clinical findings of Bacillary dysentery
List lab diagnosis of bacillary dysentery.
Shigella species are the causative agents of bacillary dysentery (enterocolitis of humans)
Gram negative rods, non–motile, non–sporing and non-capsulatedAerobic and facultative anaerobes and can not grow on simple media
All are non lactose fermentor except for Sh.sonnei (late lactose fermenter), but ferment other sugars producing acid only.
They are urease negative, gelatin not liquefied and H2S 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:
Group A (Sh.dysenteriae) 12 serotypes
Group B (Sh.flexneri) 1-6 serotypes
Group C (Sh.boydii) 18 different serotypes
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:
Endotoxin: Toxic polysaccharide released during autolysis causing irritation of bowel wall.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.
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
IP 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 fermentor (NLF) but no H2S 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.
Summary
Shigella species are the causative agents of bacillary dysenteryGram negative rods, non–motile, non–sporing, non-capsulated and H2S not produced.
It has somatic O Ag (LPS) and produce Endotoxin and Exotoxin(Shiga bacillus).
Symptoms are related to effect of exotoxin and localized invasion of the intestinal mucosa