Chapter 135. Gas Gangrene and Other Clostridial Infections (Part 2) Clinical Manifestations Intestinal Disorders Food Poisoning C. perfringens, primarily type A, is the second or third most common cause of food poisoning in the United States (Chap. 122). The responsible toxin is thought to be a cytotoxin produced by >75% of strains isolated from cases of food- borne disease. The cytotoxin binds to a receptor on the small-bowel brush border and induces a calcium ion–dependent alteration in permeability. The associated loss of ions alters intracellular metabolism, resulting in cell death. Outbreaks generally have resulted from problems in the cooling and storage of food cooked in bulk. The food sources primarily involved are meat, meat products, and poultry. Generally, the implicated meats have been cooked, allowed to cool, and then recooked the following day, often in a stew or hash. Strains of C. perfringens that contaminate meat manage to survive initial cooking. During reheating, the organisms sporulate and germinate. The disease is associated with an attack rate that is often as high as 70%. Symptoms of food poisoning from type A strains develop 8–24 h after ingestion of foods heavily contaminated with the organism. The primary symptoms include epigastric pain, nausea, and watery diarrhea usually lasting 12–24 h. Fever and vomiting are uncommon. Molecular methods including ribotyping and pulsed-field gel electrophoresis have been used to detect fecal cytotoxin in outbreaks of food poisoning caused by C. perfringens. C. perfringens has also been implicated in a more severe form of diarrhea than that of classic food poisoning. This more severe disease tends to occur in the elderly and has been associated with antibiotic use in hospitalized populations. In this form of disease, diarrhea is generally more profuse, of longer duration, and accompanied by abdominal pain. Blood and mucus have been detected in the feces of the affected patients. In one hospital-based study of a cluster of cases, widespread environmental contamination with C. perfringens spores was documented. Enteritis Necroticans Necrotizing enteritis (enteritis necroticans, or pigbel) is caused by β toxin produced by type C strains of C. perfringens following ingestion of a high-protein meal in conjunction with trypsin inhibitors (e.g., in sweet potatoes) by a susceptible host who has limited intestinal proteolytic activity. This disease has been reported among children and adults in New Guinea. A similar disease, darmbrand, was epidemic in Germany after World War II. Clinical features of pigbel include acute abdominal pain, bloody diarrhea, vomiting, shock, and peritonitis; 40% of patients die. Pathologic studies reveal an acute ulcerative process of the bowel restricted to the small intestine. The mucosa is lifted off the submucosa, with the formation of large denuded areas. Pseudomembranes composed of sloughed epithelium are common, and gas may dissect into the submucosa. The source of the organisms may be the patient's own intestinal flora; cultures of ingested pork have failed to yield the organism. Antibodies to the β toxin of C. perfringens have been of considerable benefit in changing the course of established disease. In a large-scale trial, children immunized with C. perfringens β toxoid were protected. Neutropenic Enterocolitis (Typhlitis) See Chaps. 82 and 157. Suppurative Deep-Tissue Infections Clostridia are frequently recovered from various suppurative conditions in conjunction with other anaerobic and aerobic bacteria but can also be the only organisms isolated. These suppurative conditions, which exist with severe local inflammation but usually without the characteristic systemic signs induced by clostridial toxins, include intraabdominal sepsis, empyema, pelvic abscess, subcutaneous abscess, frostbite with gas gangrene, infection of a stump in an amputee, brain abscess, prostatic abscess, perianal abscess, conjunctivitis, infection of a renal cell carcinoma, and infection of an aortic graft. Clostridia are isolated from approximately two-thirds of patients with intraabdominal infections resulting from intestinal perforation. C. ramosum, C. perfringens, and C. bifermentans are the most commonly isolated species. The presence of clostridial species does not affect the clinical presentation or outcome of these infections (Chap. 157). An association has been made between malignancy and the isolation of C. septicum in the absence of a grossly contaminated deep traumatic wound; in this situation, C. septicum may cause spontaneous nontraumatic myonecrosis (Fig. 135-1). A major site for such a malignancy is the gastrointestinal tract, particularly the colon. An association with leukemia or with other solid tumors has also been noted, and one case of fatal myonecrosis has been reported in a patient with ovarian cancer. Some of these patients present with C. septicum bacteremia; these cases have a fulminant clinical course (discussed below). Others develop localized suppurative infection in the abdomen or the abdominal wall without bacteremia. Presumably, this infection arises from a silent perforation that leads to intraabdominal abscess formation. Figure 135-1 . Chapter 135. Gas Gangrene and Other Clostridial Infections (Part 2) Clinical Manifestations Intestinal Disorders Food Poisoning. primary symptoms include epigastric pain, nausea, and watery diarrhea usually lasting 12–24 h. Fever and vomiting are uncommon. Molecular methods including ribotyping and pulsed-field gel electrophoresis. (Typhlitis) See Chaps. 82 and 157. Suppurative Deep-Tissue Infections Clostridia are frequently recovered from various suppurative conditions in conjunction with other anaerobic and aerobic bacteria