Shigella species cause shigellosis (bacillary dysentery), a human intestinal disease that occurs most commonly among young children. Shigellae are nonmotile, unencapsulated, and Lac^–. Most strains do not produce gas in a mixed-acid fermentation of glucose.

A. Epidemiology

 Shigella are typically spread from person to person, with contaminated stools serving as a major source of organisms. Humans are the only natural host for Shigella species. Flies and contaminated food or water can also transmit the disease. Shigellosis has a low infectious dose: Approximately 10–100 viable organisms are sufficient to cause disease. Therefore, secondary cases within a house hold are common, particularly under conditions of crowding or poor sanitation. The 40 serotypes of Shigella are organized into four groups (A, B, C, and D) based on the serologic relatedness of their polysaccharide O antigens. Group D (Shigella sonnei) is the serogroup found most commonly in the United States. Shigella flexneri is the second most common species isolated in the United States and has been associated with outbreaks among sexually active men who have sex with men. Shigella dysenteriae causes the most serious infections, including HUS similar to that caused by EHEC. S. dysenteriae type 1 produces Shiga toxin, which is structurally and genetically very similar to Shiga-like toxins 1 and 2 produced by E. coli virotypes. All Shiga and Shiga-like toxins are capable of resulting in HUS in susceptible individuals.

B. Pathogenesis and clinical significance

 Shigellae invade and destroy the mucosa of the large intestine. Infection rarely penetrates to deeper layers of the intestine and does not lead to bacteremia (Figure1). The Shigellae invade the colonic epithelium by expression of plasmid-encoded virulence genes that encode a type III secretion system. Injection of effector proteins results in bacterial engulfment. The same plasmid encodes proteins that allow the Shigellae to polymerize actin at one pole, thereby propelling the bacterium though the cytoplasm and into adjacent cells. This virulence plasmid is also possessed by EIEC. An exotoxin (Shiga toxin) with enterotoxic and cytotoxic properties has been isolated from S. dysenteriae type 1, and its toxicity results in the development of hemorrhagic colitis and HUS. Shigellae cause classic bacillary dysentery, characterized by diarrhea with blood, mucus (“currant jelly” stools), and painful abdominal cramping. The disease is generally most severe in the very young; older adults; and among malnourished individuals, in whom shigellosis may lead to severe dehydration and, sometimes, death. Among uncompromised populations, untreated dysentery commonly resolves in a week but may persist longer.

Fig1. Mechanism of Shigella infection causing diarrhea.

C. Laboratory identification

 During acute illness, organisms can be cultured from stools using differential, selective Hektoen agar or other media specific for intestinal pathogens.

 D. Treatment and prevention

Antibiotics (for example, ciprofloxacin or azithromycin) can reduce the duration of illness and the period of shedding organisms but usage is controversial because of widespread antibiotic resistance (Figure 2). Protection of the water and food supply and personal hygiene are crucial for preventing Shigella infections. Candidate vac cines in advanced development stages include a conjugate vaccine composed of O-antigen polysaccharides from Shigellae and a live attenuated vaccine.