The Shigellae: Morphology and Identification, Antigenic Structure, Pathogenesis and Pathology, Toxins, Clinical Findings, Diagnostic Laboratory Tests, Flashcards
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Morphology and identification of Shigella
Shigella are Gram-negative, nonmotile, non–lactose-fermenting rods that do not produce H2S. They belong to the Enterobacteriaceae family. They are facultative anaerobes. On MacConkey agar, colonies are pale due to lack of lactose fermentation. On XLD agar, they appear red without black centers (unlike Salmonella). Identification involves culture, biochemical tests, and serologic typing.
Antigenic structure of Shigella
Shigella are classified into four species based on O antigens: Group A (S. dysenteriae), B (S. flexneri), C (S. boydii), and D (S. sonnei). O antigens determine serogroups and are used for epidemiologic purposes. Shigella lack H antigens (nonmotile) and K antigens.
Pathogenesis and pathology of Shigella
Shigella are highly invasive pathogens that cause disease by invading the colonic mucosa. The infectious dose is very low (~10–100 organisms). They pass through M cells, are phagocytosed by macrophages, and then escape into the cytoplasm. They induce apoptosis of macrophages and spread cell to cell using actin-based motility. The primary pathology is inflammation and ulceration of the colonic mucosa, especially in the distal colon and rectum.
Toxins of Shigella
Shigella dysenteriae type 1 produces Shiga toxin, which inhibits protein synthesis by inactivating the 60S ribosomal subunit. It causes endothelial damage and may lead to hemolytic-uremic syndrome (HUS). The enterotoxin component also contributes to watery diarrhea early in infection. Other Shigella species may produce lesser amounts of similar toxins, but invasion is the main virulence mechanism.
Clinical findings of Shigella infections
After a short incubation (1–4 days), symptoms include fever, abdominal cramps, and watery diarrhea that may progress to bloody diarrhea with mucus (dysentery). Tenesmus (painful straining) is common. Illness lasts 4–7 days. Complications include HUS, reactive arthritis (especially with S. flexneri), and seizures in children.
Diagnostic laboratory tests for Shigella
Diagnosis is confirmed by stool culture on selective media like MacConkey or XLD agar. Suspicious colonies are tested biochemically and with serologic typing using antisera against O antigens. PCR may be used to detect Shigella DNA. Fecal leukocytes and blood are often present in microscopy. Shiga toxin can be detected by ELISA or PCR in severe cases.
Treatment of Shigella infections
Mild cases are self-limited and may not require antibiotics. For moderate to severe cases or to reduce transmission, antibiotics such as ciprofloxacin, azithromycin, or ceftriaxone are used. Resistance is common, so susceptibility testing is important. Antimotility agents are contraindicated. Rehydration is essential to manage fluid loss.
Epidemiology of Shigella
Shigella is a major cause of bacillary dysentery worldwide, especially in children under 5 in developing countries. Transmission is fecal–oral, via contaminated food, water, or direct person-to-person contact. It is highly contagious due to the low infectious dose. S. sonnei predominates in industrialized nations; S. flexneri is more common in developing areas.
Prevention and control of Shigella
Prevention includes improved sanitation, hand hygiene, and safe food and water practices. There is no licensed vaccine, though several candidates are under development. In outbreaks, prompt treatment and isolation help control spread. Public health education and access to clean water are crucial.
