66-year-old woman with fever and hemolysis.
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There is a broad spectrum of presentations and severity of necrotizing enterocolitis. Because it may have several different causes, ncerotizing enterocolitis may be a syndrome rather than a specific disease. The triad of formula feeding, intestinal ischemia, and bacterial growth may be part of the pathogenesis of necrotizing enterocolitis. Bacteria are of central importance for the production of pneumatosis, a prerequisite of which is formula feeding. Bacteria may also contribute to the intestinal injury seen after ischemia. However, the disease in the low risk patient seen during an epidemic associated with a single organism is probably caused by a primary gastrointestinal infection. On the other hand, in the stressed newborn infant with mucosal injury the presence of the appropriate bacteria may be all that is needed to initiate the chain of events leading to necrotizing enterocolitis. Figure 2 illustrates the importance of bacteria in all the causes proposed to be involved in the pathogenesis of necrotizing enterocolitis. Whether bacteria are primary or secondary agents, necrotizing enterocolitis should always be approached therapeutically as an infectious disease.
There have been several case reports of foal diarrhoea associated with Clostridium perfringens. However, there has been no epidemiological assessment of the strength of the association of these bacteria with foal diarrhoea or of their relative importance. To prepare methods for such a study, the success of different cultural techniques for the isolation of C perfringens was examined with respect to the various physiological states of the bacteria. The germination and growth of C perfringens NCTC 8239 endospores of differing maturity were favoured by different pre-treatments which failed to recover vegetative cells or endospores of C perfringens NCTC 8237. Faecal samples from 271 foals were used to test the hypothesis that the recovery of C perfringens, probably present in different states ranging between vegetative cell and germinating endospore, would be improved by using several methods in parallel. Five methods (two pre-enrichment and three direct), using different pre-treatments with heat, ethanol and EDTA, or no pre-treatment, together isolated C perfringens from 64 per cent of the samples; the most sensitive method (which isolated the most C perfringens) detected only 74 per cent of these positive samples. All the methods detected C perfringens in at least one sample from which it was not isolated by any other method. It was concluded that several methods used in combination on each sample would be required to evaluate fully any epidemiological association between C perfringens and foal diarrhoea.
BACKGROUND: Gas-containing brain abscesses are very rare, and the majority are caused by Clostridium perfringens. We report a case of gas-containing brain abscess that required urgent surgery after a craniotomy for a brain tumor. METHODS AND RESULTS: The patient was a 53-year-old male who presented with a cerebral neoplasm. A temporal lobectomy was performed and the diagnosis of low grade glioma was confirmed. Although the surgery was uneventful the postoperative course was complicated; the patient became agitated and febrile and deteriorated to a deep coma. A computed tomography scan demonstrated gas in the temporal fossa at the lobectomy site, producing mass effect. Urgent surgical debridement and drainage was performed and C. perfringens and mixed flora were found. Antibiotics were started and the patient's condition markedly improved. He was awake and alert, followed commands adequately and was extubated; however, after a week he suffered massive gastrointestinal bleeding and died. CONCLUSIONS: Early recognition of a gas-containing brain abscess is of great interest to immediately start the appropriate treatment. Urgent surgical debridement and broad spectrum chemotherapy are major components in the management of this entity.
The reactogenicity and immunogenicity of various strengths of plain and adsorbed Cl. welchii type C toxoid have been evaluated in laboratory tests and in man in Papua New Guinea. The greater antigenicity and acceptable clinical reactivity of a vaccine containing 50 total combining power units per 0.5 mm of adsorbed toxoid resulted in its selection for further field studies.
The results obtained with four laboratory tests on four candidate formulations of Clostridium welchii type C vaccine for use in man have been compared with clinical responses to the same vaccines. Quantal response assays in mice appeared to reflect the ranking of the four vaccines in human subjects better than did the guinea pig tests. They also enabled the potency of the vaccine preparations to be related to an existing International Reference Preparation. Mouse assays in which the animals received two spaced doses of vaccine prior to challenge yielded marginally more satisfactory results in terms of precision and reflection of human responses than did assays involving a single dose of vaccine.
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It is suggested that enteritis necroticans occurs in the people of the Highlands of Papua New Guinea because they have low levels of digestive proteases in the intestinal lumen. These low protease levels are the result of a low-protein diet and the presence of heat-stable trypsin inhibitors in sweet potatato, the dietary staple. Low proteolytic activity allows the B toxin of Clostridium welchii type C, which is extremely susceptible to proteolysis, to initiate the disease.
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5 infants with no growth of bacteria on cultures of blood and peritoneal fluid recovered from necrotising enterocolitis after medical treatment alone. 12 infants with positive cultures required surgery. 5 of these 12, who did not harbour clostridia, had a mild clinical course and all 5 survived segmental bowel resection. The 7 infants who harboured clostridia had a more severe clinical course and 4 died. In 3 of 4 infants with Clostridium perfringens, the necrotising enterocolitis was fulminant, characterised by severe pneumatosis intestinalis, extensive gangrene, early intestinal perforation, and a fatal outcome.
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Necrotising enteritis (pig-bel) caused by Clostridium welchii type C is a major cause of illness and death in the Highlands of Papua New Guinea. In a controlled trial of active immunisation with a clostridial toxoid prepared from type-C cultures the incidence of pig-bel in over 2500 immunised children within 24 months of immunisation was less than an eighth of that in a control group. Necrotising enteritis in Papua New Guinea is now a preventable disease.
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Free Clostridium perfringens enterotoxin was detected in the stools of 11 patients with diarrhoea. All had high faecal counts of enterotoxigenic strains of C perfringens, mostly of serotypes not commonly associated with food poisoning. 10 of these 11 patients had severe or prolonged diarrhoea which had developed after antibiotic treatment. Enterotoxigenic C perfringens appears to be one of the causes of antibiotic-associated diarrhoea.
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