Gram-negative rods four main groups: Sh. dysenteriae, flexneri, boydii and sonnei. Sh. Dysenteriae- most severe disease Culture- non-lactose fermenters (MacConkey & EMB), non-motile, non-H2S producers(TSI slant agar) Epidemiology Fecal- oral spread (5Fs) Although shigellae are found world-wide, transmission is strongly associated with poor hygiene. More prevalent in the developing world, where the main burden falls on children( under 5) Only small numbers need to be ingested to cause illness < 200 (i.e. very acid stable) Pathogenesis 1. 2. Invasive: Invade M cells, get into the cytoplasm,replicate & then polymerize actin jet trails & go laterally into adjacent cells without the need to go back into the ECF. Thus RBCs & PMNs in stool Endotoxin: (Shiga toxin). Produced by Sh. Dysenteriae type 1. Has 3 acivities : Neurotoxic, cytotoxic & enterotoxic. A-B toxin. Inhibits protein synthesis by clipping the 60S ribosomal subunit. Recall which other toxin has a similar mode of action? Clinical features • • • • • 1-4 day incubation preiod Disease severity varies: 1. Sh. sonnei infections- mild & may escape detection 2. Sh. flexneri infections- more severe 3. Sh. Dysenteriae-most severe form of dysentery may be fulminating and cause death within 48 hours Diarrhoea-mucus,bloody with PMNs Colicky abdominal pain Tenesmus Fever
