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CLASSIFICATION

There are currently four accepted species, Sh. dysenteriae, Sh. flexneri, Sh. boydii and Sh. sonnei. Shigella organsms are typical members of the Enterobacteriaceae. They non-motile facultatively anaerobic Gram-negative bacilli. They are characterised by an inability to grow on synthetic media and generally weak fermentative ability against many carbohydrate substrates. They are very closely related to the Escherichia and many taxonomists suggest grouping them in that genus. The chromosomal DNA of the shigellae have a GC content of 50-52mol%.

BIOCHEMISTRY

Their production of indole is variable, they ferment glucose by the mixed acid fermentation but do not produce gas. They do not produce H2S, phenylalaninedeaminase or urease, do not utilize citrate as sole carbon source. They are not motile, ferment a few carbohydrates and only some strains decarboxylate ornithine, none decarboxylate arginine or lysine.

The genome is very similar to that of E. coli. It consists of a single circular DNA molecule of about 4 x 106 base pairs with a molecular weight of 4 x 109 and a total length of about 1.4mm. Most strains carry an invasion-associated plasmid (120-140 MDa), similar to the one carried by enteroinvasive E. coli (EIEC).

The Shigella species (Subgoups) can be subdivided according to their somatic (cell-wall) or O antigens. Sh. dysenteriae contains 12 serotypes, Sh. flexneri eight serotypes, Sh. boydii eighteen serotypes and Sh. sonei one serotype. All serotypes except Sh. sonnei are related or even identical to some of the E. coli O antigens. There are also capsular and fimbrial antigens.

Enterotoxins: Shigellae do not produce enterotoxins. Verotoxins or Shiga toxin: The term Verotoxin is based on the reactions of this toxin on Vero cells. Some strains of Shigella dysenteriae serotype 1 (Old name: Sh. shiga) produce a toxin active on Vero cells. This is known as Shiga-toxin. It is closely related to Shiga-like toxin I (SLT I, VT1) produced by some strains of enterohaemorrhagic E. coli (EHEC). Other Toxins: No other toxins are produced. Haemolysins: Shigella strains are not haemolytic. Adhesins & Fimbriae: As a prerequisite of Shigella virulence, the bacteria have to penetrate into the intestinal epithelial cells and proliferate there. This is penetration is mediated by a Shigella-induced phagocytic event. The products of the genes encoded in the large virulence plasmid as well as some chromosomal genes are involved in this step.

NORMAL FLORA

The members of the Shigella genus are pathogens and not part of the normal flora of humans or animals.

Enteric Infections: The members of the Shigella genus cause human bacillary dysentery. They may also cause similar infections in primates but not in other animals. Extraintestinal Infections: Apart from occasional septicaemia Shigellae rarely cause extraintestinal infections. Animal Infections: Only primates appear able to get bacillary dysentery and then apparently only in association with humans, not in the wild.

Shigella strains can be grown very easily on most microbiological media. Generally the infecting dose is very small so often only small numbers of organisms may be present in a sample. There are no specific enrichment media for Shigella. Faecal specimens should be examined as quickly as possible and it is advisable to use both non-selective and selective (bile salt containing) media to attempt to isolate the Shigelae. Being non-lactose fermenting they can easily be picked from the E. coli which are usually also present.

Shigalae may survive in faecally contaminated materials but not very long. While a faecal-oral route of infection is postulated, it is generally considered most likely to be mediated from person-to-person, rather than through the environment.

There are no specific industrial uses of Shigellae.

While persons recovering from overt or inapparent bacillary dysentery appear to have acquired immunity to Shigella infections, this seems rather short-lived. No protection is afforded by circulating antibodies.

Enterobacteriaceae

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