Shigella 

Shigella is the causative pathogen in bacterial dysentery. The genus comprises the species S. dysenteriae, S. flexneri, S. boydii, and S. sonnei. Shigellae are nonmotile. The three primary species can be classified in serovars based on the fine structure of their O antigens. Shigellae are characterized by invasive properties. They can penetrate the colonic mucosa to cause local necrotic infections. Humans are the sole source of infection since shigellae are pathologically active in humans only. The pathogens are transmitted directly, more frequently indirectly, via food and drinking water. Antibiotics can be used therapeutically.   

Classification. The genus Shigella includes four species: S. dysenteriae, S. flex-neri, S. boydii, and S. sonnei. The first three are subdivided into 10, six, and 15 serovars, respectively, based on their antigen structures. Shigellae are nonmotile and therefore have no flagellar (H) antigens.

Pathogenesis. Shigellae are only pathogenic in humans. The pathogens are ingested orally. Only a few hundred bacteria suffice for an infective dose. Shigellae enter the terminal ileum and colon, where they are taken up by the M cells in the intestinal mucosa, which in turn are in close vicinity to the macrophages. Following phagocytosis by the macrophages, the shigellae lyse the phagosome and actively induce macrophage apoptosis. The shigellae released from the dead macrophages are then taken up by enterocytes via the basolateral side of the mucosa (i.e., retrograde transport). The invasion is facilitated by outer membrane polypeptides, the invasins, which are coded by inv genes localized on 180-240 kb plasmids. Adjacent enterocytes are invaded by means of lateral transfer from infected cells. In the enterocytes, the shigellae reproduce, finally destroying the cells. Shigella dysenteriae produces shigatoxin, the prototype for the family of shigalike toxins (or verocytotox- ins), which also occur in several other Enterobacteriaceae. The toxin inhibits protein synthesis in eukaryotic cells by splitting the 23S rRNA at a certain locus. Shigatoxin contributes to the colonic epithelial damage, the small in-testine diarrhea with watery stools at the onset of shigellosis and (less frequent) the hemolytic-uremic syndrome (HUS).

Clinical picture. Following an incubation period of two to five days, the disease manifests with profuse watery diarrhea (= small intestine diarrhea). Later, stools may contain mucus, pus, and blood. Intestinal cramps, painful stool elimination (tenesmus), and fever are observed in the further course of the infection. Complications include massive intestinal bleeding and perforation peritonitis. These severe effects are caused mainly by S. dysenteriae, whereas S. sonnei infections usually involve only diarrhea.

Diagnosis requires identification of the pathogen in a culture. Combined se-lective/indicator mediums must be used for the primary culture. Suspected colonies are identified by using indicator media to detect certain metabolic characteristics . The serovar is determined with specific antisera in the slide agglutination test.

Therapy. Anti-infective agents are the first line of treatment (aminopenicillins, 4-quinolones, cephalosporins). Losses of water and electrolytes may have to be replaced.

Epidemiology and prevention. Bacterial dysentery occurs worldwide, although it is usually seen only sporadically in developed countries. In developing countries, its occurrence is more likely to be endemic and even epidemic. The source of infection is always humans, in most cases infected persons whose stools contain pathogens for up to six weeks after the disease has abated. Transmission is by direct contact (smear infection) or indirect uptake via food, surface water, or flies. Control of dysentery includes exposure prophylaxis measures geared to prevent susceptible persons from coming into contact with the pathogen.