Changes in predominant bacterial populations in human faeces with age and with Clostridium difficile infection.
(57/851)
The bacterial composition of human faeces can vary greatly with factors such as age and disease, although relatively few studies have monitored these events, particularly at species level. In this investigation, bacteria were isolated from faecal samples from healthy young adults and elderly subjects, and elderly patients with Clostridium difficile-associated diarrhoea (CDAD). The organisms were identified to species level on the basis of their cellular fatty acid profiles with the MIDI system. In some groups of bacteria, species diversity was found to change with age despite the overall numbers of organisms being similar at genus level. Bacteroides thetaiotaomicron, B. ovatus and Prevotella tannerae were common gram-negative anaerobes isolated from young adults. Bacteroides species diversity increased in the faeces of healthy elderly people. Bifidobacterial species diversity decreased with age, with Bifidobacterium adolescentis and Bif. angulatum being the most common isolates. CDAD patients were characterised by greater diversity of facultative species, lactobacilli and clostridia, but greatly reduced numbers of bacteroides, prevotella and bifidobacteria. Such bacterial population changes in the normal microbiota could result in metabolic conditions favourable for the establishment of pathogenic micro-organisms, such as clostridia, and would have considerable effects on the biochemical capacity of the large intestine as a whole. Alterations in the community structure of bifidobacteria and lactobacilli have relevance for dietary and therapeutic interventions such as the use of pre- or probiotics that aim to modify the composition or metabolic activities of the intestinal microflora in a beneficial way, particularly in elderly people or individuals at risk of CDAD. (+info)
Anaerobic cellulitis as the result of Clostridium perfringens: a rare cause of vascular access graft infection.
(58/851)
Infection of prosthetic vascular access grafts is the second most common complication of vascular access and represents a challenge encountered by the vascular surgeon. Anaerobic graft infections are rare. We report on a case of a prosthetic vascular access graft infection with Clostridium perfringens. To our knowledge, only one other case with an infected arteriovenous shunt caused by C perfringens has been reported. The patient, a 67-year-old woman with end-stage renal failure as the result of polycystic renal disease, was seen with an infected pseudoaneurysm at the arterial puncture site of the loop graft on the left arm. There was associated purulence at the time of operation. Surgical management consisted of complete graft removal because of the presence of small tunnel abscesses. C perfringens was found in the resected pseudoaneurysm and graft material. Infected pseudoaneurysms most likely are attributable to repetitive punctures in one small area and to a break in sterile technique. A compromised vascular supply, not infrequent in patients for hemodialysis, may lower the oxidation reduction potential, which allows anaerobic bacteria, such as C perfringens, to cause infection. (+info)
Theodore E. Woodward Award. How bacterial enterotoxins work: insights from in vivo studies.
(59/851)
Clostridium difficile is a spore forming, gram-positive anaerobic bacillus first described in 1935 by Hall and O'Toole as a commensal organism in the fecal flora of healthy newborn infants (1). The organism was given its unusual name because it grew slowly and was difficult to isolate in pure culture. Its presence in the stool of healthy neonates suggested that C. difficile was a nonpathogen, even though it produced toxins in broth culture. Following its original description, C. difficile passed quickly into relative obscurity in the 1960's and 1970's when antibiotic-associated pseudomembranous colitis became prevalent following the introduction into clinical practice of broad spectrum antibiotics. The frequent association of clindamycin and lincomycin therapy with pseudomembranous colitis led to the term "clindamycin colitis" (2). A breakthrough occurred in 1978 when C. difficile was identified as the source of a cytotoxin in the stool of patients with pseudomembranous colitis (3). During the two decades since its rediscovery, a great deal has been learned about the pathophysiology, epidemiology and management of C. difficile infection, yet many challenges remain. Currently this organism infects over 30% of individuals admitted to United States hospitals, making C. difficile colitis one of the most common nosocomial infections (4). It is estimated that approximately 10-12 million adults are infected with this organism each year in the United States, about a third of whom become symptomatic. The disease burden in the elderly is particularly severe as they are hospitalized more frequently and for longer duration. The pathophysiology of C. difficile diarrhea requires alteration of the colonic microflora by antibiotics, colonization by C. difficile, and release of two potent enterotoxins designated A and B (5). The toxins of Clostridium difficile are required virulence factors in both animals and humans since non-toxigenic strains do not cause disease. Recent cloning and sequencing of the toxin genes reveals extensive amino acid homology between them that is reflected in common molecular and cellular mechanisms. Both toxins damage cells by modifying the rho family of proteins, key regulators of cellular actin. C. difficile infection causes a florid acute inflammatory response seen in patients with pseudomembranous colitis. It is now realized that neurons and immune cells of the lamina propria are major determinants of toxin-induced diarrhea and mucosal damage. Early critical events following toxin exposure are release of the neuropeptides substance P and calcitonin gene related peptide (CGRP) from sensory afferent neurons and activation of lamina propria macrophages and intestinal mast cells. These peptides in turn release a complex cascade of other inflammatory mediators from lamina propria cells (5). The importance of the host immune response, specifically serum IgG directed against toxin A, is now recognized as a critical determinant of disease expression in man. (+info)
Organization of the plasmid cpe Locus in Clostridium perfringens type A isolates.
(60/851)
Clostridium perfringens type A isolates causing food poisoning have a chromosomal enterotoxin gene (cpe), while C. perfringens type A isolates responsible for non-food-borne human gastrointestinal diseases carry a plasmid cpe gene. In the present study, the plasmid cpe locus of the type A non-food-borne-disease isolate F4969 was sequenced to design primers and probes for comparative PCR and Southern blot studies of the cpe locus in other type A isolates. Those analyses determined that the region upstream of the plasmid cpe gene is highly conserved among type A isolates carrying a cpe plasmid. The organization of the type A plasmid cpe locus was also found to be unique, as it contains IS1469 sequences located similarly to those in the chromosomal cpe locus but lacks the IS1470 sequences found upstream of IS1469 in the chromosomal cpe locus. Instead of those upstream IS1470 sequences, a partial open reading frame potentially encoding cytosine methylase (dcm) was identified upstream of IS1469 in the plasmid cpe locus of all type A isolates tested. Similar dcm sequences were also detected in several cpe-negative C. perfringens isolates carrying plasmids but not in type A isolates carrying a chromosomal cpe gene. Contrary to previous reports, sequences homologous to IS1470, rather than IS1151, were found downstream of the plasmid cpe gene in most type A isolates tested. Those IS1470-like sequences reside in about the same position but are oppositely oriented and defective relative to the IS1470 sequences found downstream of the chromosomal cpe gene. Collectively, these and previous results suggest that the cpe plasmid of many type A isolates originated from integration of a cpe-containing genetic element near the dcm sequences of a C. perfringens plasmid. The similarity of the plasmid cpe locus in many type A isolates is consistent with horizontal transfer of a common cpe plasmid among C. perfringens type A strains. (+info)
Molecular epidemiology of Clostridium perfringens related to food-borne outbreaks of disease in Finland from 1984 to 1999.
(61/851)
From 1975 to 1999, Clostridium perfringens caused 238 food-borne disease outbreaks in Finland, which is 20% of all such reported outbreaks during these years. The fact that C. perfringens is commonly found in human and animal stools and that it is also widespread in the environment is a disadvantage when one is searching for the specific cause of a food-borne infection by traditional methods. In order to strengthen the evidence-based diagnostics of food poisonings suspected to be caused by C. perfringens, we retrospectively investigated 47 C. perfringens isolates by PCR for the cpe gene, which encodes enterotoxin; by reversed passive latex agglutination to detect the enterotoxin production; and by pulsed-field gel electrophoresis (PFGE) to compare their genotypes after restriction of DNA by the enzymes SmaI and ApaI. The strains were isolated during 1984 to 1999 from nine food-borne outbreaks of disease originally reported as having been caused by C. perfringens. In seven of the nine outbreaks our results supported the fact that the cause was C. perfringens. Our findings emphasize the importance of a more detailed characterization of C. perfringens isolates than mere identification to the species level in order to verify the cause of an outbreak. Also, to increase the probability of finding the significant cpe-positive C. perfringens strains, it is very important to isolate and investigate more than one colony from the fecal culture of a patient and screen all these isolates for the presence of the cpe gene before further laboratory work is done. (+info)
Enteric coronavirus infection in a juvenile dromedary (Camelus dromedarius).
(62/851)
A case of an enteric coronavirus infection in a 6-week-old dromedary calf is described. The animal had diarrhea for 5 days and died despite symptomatic treatment. Numerous viral particles, approximately 140 nm in diameter, with club-like projections were detected in the feces by electron microscopy. These characteristics were consistent with a coronavirus. Immunohistochemical reactivity with 2 antigenic group II coronavirus-specific antibodies confirmed the presence of viral antigen in colonic epithelial cells. The death of the animal was attributed to a neutrophilic and emphysematous colitis that likely was caused by an infection with a Clostridium sp. (+info)
Trends in indigenous foodborne disease and deaths, England and Wales: 1992 to 2000.
(63/851)
BACKGROUND: Commitment to food safety is evidenced by high profile governmental initiatives around the globe. To measure progress towards targets, policy makers need to know the baseline from which they started. AIM: To describe the burden (mortality, morbidity, new presentations to general practice, hospital admissions, and hospital occupancy) and trends of indigenous foodborne disease (IFD) in England and Wales between 1992 and 2000. METHODS: Routinely available surveillance data, special survey data, and hospital episode statistics were collated and arithmetic employed to estimate the burden and trends of IFD in England and Wales. Adjustments were made for underascertainment of disease through national surveillance and for foreign travel. The final estimates were compared with those from the USA. RESULTS: In 1995 there were an estimated 2,365,909 cases, 21,138 hospital admissions, and 718 deaths in England and Wales due to IFD. By 2000 this had fallen to 1,338,772 cases, 20,759 hospital admissions, and 480 deaths. In terms of disease burden the most important pathogens were campylobacters, salmonellas, Clostridium perfringens, verocytotoxin producing Escherichia coli (VTEC) O157, and Listeria monocytogenes. The ratio of food related illness in the USA to IFD in England and Wales in 2000 was 57:1. Taking into account population rates, this ratio fell to 11:1 and converged when aetiology and disease severity were considered. CONCLUSION: Reducing IFD in England and Wales means tackling campylobacter. Lowering mortality rates however also requires better control and prevention of salmonellas, Cl perfringens, L monocytogenes, and VTEC O157. (+info)
Laboratory diagnosis of Clostridium perfringens antibiotic-associated diarrhoea.
(64/851)
Clostridium perfringens has been reported as the cause of up to 15% of cases of antibiotic-associated diarrhoea (AAD) and may be diagnosed by detection of enterotoxin (CPEnt) in faeces. The performance of a commercial ELISA method for CPEnt, with culture and PCR methods to confirm the presence of enterotoxigenic C. perfringens, was evaluated in 200 consecutive specimens from patients with clinical details suggestive of AAD: 8% of the specimens were positive for CPEnt, 16% were positive for C. difficile cytotoxin and 2% gave positive test results for both C. perfringens and C. difficile toxins. Culture and PCR results confirmed the majority of ELISA results, although 2 (12.5%) reactive specimens were only weakly positive. C. perfringens is a potentially important cause of infective AAD and can be detected with the C. perfringens enterotoxin ELISA kit, although weak positive results should be considered with caution. (+info)