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Shigella Infection (Shigellosis) Antibodies, Proteins & ELISA Kits

Shigella Antibodies, Proteins & ELISA Kits | Assay Genie
Infectious Disease · Shigella species

Shigella antibodies, proteins & ELISA kits

Shigellosis is a highly infectious cause of bacillary dysentery caused by Shigella species; S. dysenteriae produces Shiga toxin, and the O-antigen of LPS defines serotypes.

ShigellaShiga toxin / LPSDysentery
Shigella
Gram-negative
Shiga toxin
Key virulence factor
Faecal-oral
Low dose
Dysentery
Bloody diarrhoea
Overview

What is Shigella?

Shigellosis is a highly infectious cause of bacillary dysentery caused by Shigella species; S. dysenteriae produces Shiga toxin, and the O-antigen of LPS defines serotypes.

Transmission is faecal-oral and requires only a low infectious dose. Antibody and antigen assays support diagnosis, serotyping research and vaccine development.

Transmission & symptoms

Shigella causes bacillary dysentery and is highly transmissible by the faecal-oral route, needing only a very low infectious dose. It invades the colonic epithelium, causing bloody, mucoid diarrhoea; S. dysenteriae type 1 also produces Shiga toxin.

Diagnosis & serology

Diagnosis uses stool culture and PCR; serotyping is based on the O-antigen of lipopolysaccharide. Antibody and antigen assays support surveillance and vaccine research.

Research applications

Research tools cover host innate responses to invasion (IL-8, caspase-1/inflammasome, NOD1, defensins) and O-antigen/Shiga-toxin immunity relevant to vaccine development.

FAQs

Shigella — frequently asked questions

How is shigellosis diagnosed?
By stool culture and PCR, with serotyping based on the lipopolysaccharide O-antigen; serology supports epidemiological research.
Why is Shigella so infectious?
It survives stomach acid well and needs only a very low infectious dose, so it spreads readily person-to-person and through contaminated food/water.
What host responses does Shigella trigger?
Epithelial invasion activates inflammasome/caspase-1, IL-8-driven neutrophil recruitment and NOD1 signalling, causing the intense colonic inflammation of dysentery.

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