Disease
Shigella species cause enterocolitis. Enterocolitis caused by Shigella is often called shigellosis or bacillary dysentery. The term dysentery refers to bloody diarrhea.
Important Properties
Shigellae are non–lactose-fermenting, gram-negative rods that can be distinguished from salmonellae by three criteria: they produce no gas from the fermentation of glucose, they do not produce H2S, and they are nonmotile. All shigellae have O antigens (polysaccharide) in their cell walls, and these antigens are used to divide the genus into four groups: A, B, C, and D.
Pathogenesis & Epidemiology
Shigellae are the most effective pathogens among the enteric bacteria. They have a very low ID50. Ingestion of as few as 100 organisms causes disease, whereas at least 105 V. cholerae or Salmonella organisms are required to produce symptoms. Various properties of shigellae and salmonellae are compared in Table 1.
Table1. Comparison of Important Features of Salmonella and Shigella
Shigellosis is only a human disease (i.e., there is no animal reservoir). The organism is transmitted by the fecal–oral route. The four Fs—fingers, flies, food, and feces—are the principal factors in transmission. Foodborne outbreaks outnumber waterborne outbreaks by 2 to 1. Outbreaks occur in daycare nurseries and in mental hospitals, where fecal–oral transmission is likely to occur. Children younger than 10 years account for approximately half of Shigella-positive stool cultures. There is no prolonged carrier state with Shigella infections, unlike that seen with S. typhi infections.
Shigellae cause disease almost exclusively in the gastrointestinal tract. They produce bloody diarrhea (dysentery) by invading the cells of the mucosa of the distal ileum and colon. Local inflammation accompanied by ulceration occurs, but the organisms rarely penetrate through the wall or enter the blood stream, unlike salmonellae. Although some strains produce an enterotoxin (called Shiga toxin), invasion is the critical factor in pathogenesis. The evidence for this is that mutants that fail to produce enterotoxin but are invasive can still cause disease, whereas noninvasive mutants are nonpathogenic.
Shiga toxins are encoded by lysogenic bacteriophages. Shiga toxins very similar to those produced by Shigella are produced by EHEC O157:H7 strains that cause enterocolitis and HUS.
Clinical Findings
After an incubation period of 1 to 4 days, symptoms begin with fever and abdominal cramps, followed by diarrhea, which may be watery at first but later contains blood and mucus. The dis ease varies from mild to severe depending on two major factors: the species of Shigella and the age of the patient, with young children and elderly people being the most severely affected. Shigella dysenteriae, which causes the most severe disease, is usually seen in the United States only in travelers returning from abroad. Shigella sonnei, which causes mild disease, is isolated from approximately 75% of all individuals with shigellosis in the United States. The diarrhea frequently resolves in 2 or 3 days; in severe cases, antibiotics can shorten the course. Serum agglutinins appear after recovery but are not protective because the organism does not enter the blood. The role of intestinal IgA in protection is uncertain.
Laboratory Diagnosis
Shigellae form non–lactose-fermenting (colorless) colonies on MacConkey’s or EMB agar. On TSI agar, they cause an alkaline slant and an acid butt, with no gas and no H2S. Confirmation of the organism as Shigella and determination of its group are done by slide agglutination.
One important adjunct to laboratory diagnosis is a methylene blue stain of a fecal sample to determine whether neutrophils are present. If they are found, an invasive organism such as Shigella, Salmonella, or Campylobacter is involved rather than a toxin-producing organism such as V. cholerae, enterotoxigenic E. coli (ETEC), or Clostridium perfringens. (Certain viruses also cause diarrhea without neutrophils in the stool.)
Treatment
The main treatment for shigellosis is fluid and electrolyte replacement. In mild cases, no antibiotics are indicated. In severe cases, a fluoroquinolone (e.g., ciprofloxacin) is the drug of choice, but strains resistant to fluoroquinolones have emerged and antibiotic sensitivity tests must be performed. Trimethoprim-sulfamethoxazole is an alternative choice. Anti peristaltic drugs are contraindicated in shigellosis, because they prolong the fever, diarrhea, and excretion of the organism.
Multidrug-resistant strains of S. sonnei have caused out breaks of shigellosis in the United States. These strains are resistant to ampicillin, ceftriaxone, and trimethoprim-sulfa.
Prevention
Prevention of shigellosis is dependent on interruption of fecal–oral transmission by proper sewage disposal, chlorination of water, and personal hygiene (handwashing by food handlers). There is no vaccine, and prophylactic antibiotics are not recommended.
