Bacterias

The Shigellae
The natural habitat of shigellae is limited to the intestinal tracts of humans and other primates, where they produce bacillary dysentery.
Morphology & Identification
Typical Organisms
Shigellae are slender gram-negative rods; coccobacillary forms occur in young cultures.
Culture
Shigellae are facultative anaerobes but grow best aerobically. Convex, circular, transparentcolonies with intact edges reach a diameter of about 2 mm in 24 hours.
Growth Characteristics
All shigellae ferment glucose. With the exception of Shigella sonnei, they do not ferment lactose. The inability to ferment lactose distinguishes shigellae on differential media. Shigellae form acid from carbohydrates but rarely produce gas. They may also be divided into those that ferment mannitol andthose that do not (Table 15–4).
Table 15–4 Pathogenic Species of Shigella |
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Present Designation  | Group and Type  | Mannitol  | Ornithine Decarboxylase  |
Shigella dysenteriae  | A | – | – |
Shigella flexneri  | B | + | – |
Shigella boydii  | C | + | – |
Shigella sonnei  | D | + | + |
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Antigenic Structure
Shigellae have a complex antigenic pattern. There is greatoverlapping in the serologic behavior of different species, and most of them share O antigens with other enteric bacilli.
The somatic O antigens of shigellae are lipopolysaccharides. Their serologic specificity depends on the polysaccharide. There are more than 40 serotypes. The classification of shigellae relies on biochemical and antigenic characteristics. The pathogenic species are shown in Table15–4.
Pathogenesis & Pathology
Shigella infections are almost always limited to the gastrointestinal tract; bloodstream invasion is quite rare. Shigellae are highly communicable; the infective dose is on the order of 103 organisms (whereas it usually is 105–108 for salmonellae and vibrios). The essential pathologic process is invasion of the mucosal epithelial cells (eg, M cells) by inducedphagocytosis, escape from the phagocytic vacuole, multiplication and spread within the epithelial cell cytoplasm, and passage to adjacent cells. Microabscesses in the wall of the large intestine and terminal ileum lead to necrosis of the mucous membrane, superficial ulceration, bleeding, and formation of a "pseudomembrane" on the ulcerated area. This consists of fibrin, leukocytes, cell debris, anecrotic mucous membrane, and bacteria. As the process subsides, granulation tissue fills the ulcers and scar tissue forms.
Toxins
Endotoxin
Upon autolysis, all shigellae release their toxic lipopolysaccharide. This endotoxin probably contributes to the irritation of the bowel wall.
Shigella Dysenteriae Exotoxin
S dysenteriae type 1 (Shiga bacillus) produces a heat-labile exotoxin that affectsboth the gut and the central nervous system. The exotoxin is a protein that is antigenic (stimulating production of antitoxin) and lethal for experimental animals. Acting as an enterotoxin, it produces diarrhea as does the E coli Shiga-like toxin, perhaps by the same mechanism. In humans, the exotoxin also inhibits sugar and amino acid absorption in the small intestine. Acting as a "neurotoxin,"this material may contribute to the extreme severity and fatal nature of S dysenteriae infections and to the central nervous system reactions observed in them (ie, meningismus, coma). Patients with Shigella flexneri or Shigella sonnei infections develop antitoxin that neutralizes S dysenteriae exotoxin in vitro. The toxic activity is distinct from the invasive property of shigellae in dysentery.The two may act in sequence, the toxin producing an early nonbloody, voluminous diarrhea and the invasion of the large intestine resulting in later dysentery with blood and pus in stools.
Clinical Findings
After a short incubation period (1–2 days), there is a sudden onset of abdominal pain, fever, and watery diarrhea. The diarrhea has been attributed to an exotoxin acting in the small...