Anaerobic infections.
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The patient with diarrhea is generally looking for prompt relief, not a prolonged diagnostic workup. In many cases effective treatment can be initiated after careful review of the clinical symptoms and of the patient's recent travel or other activities. Stool examination, sigmoidoscopy, or other studies may be necessary for definitive diagnosis or in refractory cases. Drugs are useful to combat many of the causative organisms, but in mild, self-limited infections, supportive therapy may suffice. Indeed, antimotility agents are contraindicated in some types of infectious diarrhea.
Following trauma, wound contamination with aerobic and/or anaerobic bacteria should always be suspected. Treatment with antibacterial antibiotics should begin immediately in the emergency room, particularly for those patients with fractures. Patients with serious trauma are best treated by a team of specialists including general surgeons, orthopedists, infectious disease specialists, and intensive care specialists. The author recommends transport of seriously injured patients to major hospitals specializing in the care of trauma. Particularly when gas gangrene secondary to clostridial infection is suspected, the patient should be moved to a major trauma center with the capability for hyperbaric oxygen therapy.
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Toxin genotypes of 95 C. perfringens strains collected within a 45-year period were analysed by a multiplex PCR. A set of primers designed for 4 different genes encoding the alpha, beta, epsilon, and iota toxins was used in a single reaction with a sensitivity of gene detection of 200 fg for DNA extracted from pure culture. Most of the strains (97%) conformed to the A biotype, and the remaining to the C or E biotypes. For biotype determination, seroneutralization of lethality in mice was performed by intravenous injection. Toxin phenotype and genotype profile were concordant in 94% of strains. Our results documented the presence of rare toxin genotypes of C. perfringens in a Polish geographical region and indicated the suitability of multiplex PCR as a method supplementing classical techniques and providing better insight into the prevalence of toxinogenic C. perfringens strains.
Clostridium tertium is infrequently isolated from blood in patients with underlying diseases. Laboratory diagnosis is often delayed because Clostridium tertium is aerotolerant and resistant to metronidazole. Clinically it is a problem because it is commonly resistant to metronidazole, clindamycin and cephalosporins. We present 3 cases illustrating these characteristics.
The tools available for monitoring necrotic enteritis caused by Clostridium perfringens in broiler chickens have been limited, particularly for identifying subclinical disease. In this study, a modified enzyme-linked immunosorbent assay was used to quantify levels of specific immunoglobulin G to C. perfringens alpha-toxin in serum from broilers. We found significantly higher antibody levels in broilers with a history of subclinical necrotic enteritis compared with a zinc-bacitracin-treated group with a low level of gut lesions. Furthermore, in 4.5-week-old commercial broiler flocks, there was an association between the occurrence of C. perfringens-associated hepatitis at slaughter and the immune response to alpha-toxin. Practical solutions for defining cut-off levels for positive serum samples at individual and flock levels are proposed, and were found to be useful on a set of samples available from flocks with different histories regarding the occurrence of C. perfringens-associated disease. This serological approach seems promising as a diagnostic tool in research and disease monitoring regarding C. perfringens-associated disease.
Sporadic outbreaks of fatal enteritis occurred among free-living wild crows ('large billed' or 'wok' crow; Corvus macrorhynchos) in an open-air park in Japan in 2002. Eight crows were found dead during February, followed by two more in September, and five of the eight were examined histopathologically. At necropsy, all cases showed a markedly dilated small intestine, especially the jejunum and ileum, with large amounts of gas, and dark red to greenish-brown soft content. The necrotic intestinal wall was markedly thickened with multifocal haemorrhages. All cases had multifocal white foci in the liver, and four cases showed marked splenomegaly. Histologically, there was severe necrotic enteritis characterized by extensive mucosal necrosis and multifocal haemorrhages, as well as inflammatory cell infiltrations. A prominent pseudo-membrane formation was noted in the affected intestine. Severe adhesive peritonitis was also observed in three cases. Gram-positive bacilli were present in large numbers in the lumen, and in and around necrotic lesions in the affected intestine. The bacilli were positive for Clostridium perfringens enterotoxin type A by immunohistochemistry, and were also positive for C. perfringens type A using the immunofluorescence method. C. perfringens was isolated by anaerobic culture from the intestinal contents. The present enteritis was thought to be induced by proliferated C. perfringens in the intestine, and to be the cause of death.
The aim of this study was to investigate the relationship between mucosal gizzard lesions and caecal Clostridium perfringens counts. Gross pathological changes in the gizzard and small intestine, and caecal C. perfringens counts from 1217 meat-type chickens were recorded during the course of six experiments and were statistically analysed. C. perfringens counts increased significantly (P < 0.001) with the severity of mucosal gizzard lesions. Mucosal gizzard lesions were more prevalent than necrotic enteritis. Correcting for the pen and necrotic enteritis within experiment, mucosal gizzard lesions explained 31.8% of the variation in C. perfringens counts. Mucosal gizzard lesions and age together explained 59.1% of the variation in C. perfringens counts. The mean ages of birds with moderate and severe mucosal gizzard lesions were 1.7 and 0.8 days lower than the mean age of birds with necrotic enteritis, respectively. The association between mucosal gizzard lesions and high C. perfringens counts might be of importance when attempting to improve production efficiency, health and the welfare of the chickens.
The inclusion of antibacterial feed additives has until now been the major strategy for controlling Clostridium perfringens-associated necrotic enteritis in broilers. In the present study, the effect of maternal immunization against the disease was examined. Broiler breeder hens were injected intramuscularly with candidate vaccines based on C. perfringens type A and type C toxoids adjuvanted with aluminium hydroxide. Vaccination resulted in a strong serum immunoglobulin G response to C. perfringens alpha-toxin in parent hens, and specific antibodies were transferred to their progeny. Subclinical necrotic enteritis in broilers was induced under field conditions or in a disease model, and the occurrence of specific enteric and hepatic lesions was evaluated in randomly selected birds. In three experiments, estimates of odds ratio for developing such lesions were 0.23, 0.33 and 0.56 in maternally toxoid C-immunized broilers compared with non-immunized controls. In toxoid A-immunized birds, odds ratios were estimated at 0.41, 0.61 and 0.63. From these results, immunoprophylaxis seems to be an interesting alternative for the control of necrotic enteritis in broilers.
We describe a fatal case of a 74-year old man with acute myeloid leukemia complicated by massive intravascular hemolysis due to Clostridium perfringens sepsis.
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An outbreak of gastroenteritis at a large teaching hospital affected at least 52 workers. Investigation implicated a tuna salad, and the circumstances suggested Clostridium perfringens as the etiologic agent. The risk of such outbreaks may be reduced by cooling of ingredients prior to mixing and refrigeration in small steel containers.
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The case of a patient with fulminant Clostridium perfringens septicemia and intravascular hemolysis is presented. The organisms in the blood stream were in sufficient quantity to be detected on a peripheral blood smear, and some were found to be within leukocytes. In vivo spore formation by C. perfringens is thought to be uncommon; however, in this patient probable spore formation by this organism was observed within peripheral blood leukocytes. The peripheral polymorphonuclear leukocytes from this patient were also markedly vacuolated.