C perfringens part 2

C perfringens part 2
Some strains of C perfringens produce a powerful enterotoxin, especially when grown in meat dishes. When more than 108 vegetative cells are ingested and sporulate in the gut, enterotoxin is formed. The enterotoxin is a protein (MW 35,000) that may be a nonessential component of the spore coat; it is distinct from other clostridial toxins. It induces intense diarrhea in 6–18 hours. The action of C perfringens enterotoxin involves marked hypersecretion in the jejunum and ileum, with loss of fluids and electrolytes in diarrhea. Much less frequent symptoms include nausea, vomiting, and fever.
Pathogenesis
In invasive clostridial infections, spores reach tissue either by contamination of traumatized areas (soil, feces) or from the intestinal tract. The spores germinate at low oxidation-reduction potential; vegetative cells multiply, ferment carbohydrates present in tissue, and produce gas. The distention of tissue and interference with blood supply, together with the secretion of necrotizing toxin and hyaluronidase, favor the spread of infection. Tissue necrosis extends, providing an opportunity for increased bacterial growth, hemolytic anemia, and, ultimately, severe toxemia and death. In gas gangrene (clostridial myonecrosis), a mixed infection is the rule. In addition to the toxigenic clostridia, proteolytic clostridia and various cocci and gram-negative organisms are also usually present.
Clinical Findings
From a contaminated wound (eg, a compound fracture, postpartum uterus), the infection spreads in 1–3 days to produce crepitation in the subcutaneous tissue and muscle, foul-smelling discharge, rapidly progressing necrosis, fever, hemolysis, toxemia, shock, and death. Treatment is with early surgery (amputation) and antibiotic administration. C perfringens food poisoning usually follows the ingestion of large numbers of clostridia that have grown in warmed meat dishes. The toxin forms when the organisms sporulate in the gut, with the onset of diarrhea—usually without vomiting or fever—in 6–18 hours. The illness lasts only 1–2 days.
Diagnostic Laboratory Tests
Specimens consist of material from wounds, pus, and tissue. The presence of large gram-positive rods in Gram-stained smears suggests gas gangrene clostridia.
Material is inoculated into chopped meat-glucose medium and thioglycolate medium and onto blood agar plates incubated anaerobically. The growth from one of the media is transferred into milk. A clot torn by gas in 24 hours is suggestive of C perfringens. The biochemical reactions (various sugars in thioglycolate, action on milk), hemolysis, and colony form. Lecithinase activity is evaluated by the precipitate formed around colonies on egg yolk media. Final identification rests on toxin production and neutralization by specific antitoxin. C perfringens rarely produces spores when cultured on agar in the laboratory.
Treatment
The most important aspect of treatment is prompt and extensive surgical debridement of the involved area and excision of all devitalized tissue, in which the organisms are prone to grow. Administration of antimicrobial drugs, particularly penicillin, is begun at the same time. Hyperbaric oxygen may be of help in the medical management of clostridial tissue infections. It is said to "detoxify" patients rapidly.
Clostridium difficile & Diarrheal Disease
Pseudomembranous Colitis
Pseudomembranous colitis is diagnosed by detection of one or both C difficile toxins in stool and by endoscopic observation of pseudomembranes or microabscesses in patients who have diarrhea and have been given antibiotics. Plaques and microabscesses may be localized to one area of the bowel. The diarrhea may be watery or bloody, and the patient frequently has associated abdominal cramps, leukocytosis, and fever. Although many antibiotics have been associated with pseudomembranous colitis, the most common are ampicillin and clindamycin. The disease is treated by discontinuing administration of the offending antibiotic and orally giving either metronidazole or vancomycin.
Administration of antibiotics results in proliferation of drug-resistant C difficile that produces two toxins. Toxin A, a potent enterotoxin that also has some cytotoxic activity, binds to the brush border membranes of the gut at receptor sites. Toxin B is a potent cytotoxin. Both toxins are found in the stools of patients with pseudomembranous colitis. Not all strains of C difficile produce the toxins.