Features of hemolysis due to Clostridium perfringens infection

Infection by Clostridium perfringens can be an unsuspected cause of hemolysis in emergency room patients. Historically, this condition has been associated with wound contamination and other tissue infections. We report the case of an autistic patient who presented to our emergency department with a distended abdomen and hemolysis of unknown etiology. The patient had no history of recent surgery. Exploration of the abdomen revealed a hepatic abscess. Blood cultures tested culture positive for C. perfringens. We present images demonstrating the salient features of the peripheral blood smear in cases of this uncommon but deadly cause of hemolysis.     

Upper gastrointestinal bleeding related to emphysematous cholecystitis due to Clostridium perfringens

We describe the case of a 46-year-old man admitted for upper gastrointestinal bleeding in the context of cirrhosis. A deep bleeding duodenal ulcer was treated by sclerotherapy. Abdominal pain and fever lead us to perform an abdominal computed tomography, which demonstrated emphysematous cholecystitis. An emergency cholecystectomy was performed and antimicrobial therapy initiated. The patient recovered uneventfully. Links between ulcers and emphysematous cholecystitis are discussed.     

致人腹泻产气荚膜梭菌的分离鉴定与基因分型

目的　研究产气荚膜梭菌与我国人群中引起食物中毒的关系。方法　从江苏扬州三家医院采集腹泻病人临床粪便样品进行细菌分离培养与生化鉴定 ,然后根据ＧｅｎｅＢａｎｋ中已发表的产气荚膜梭菌毒素基因序列 ,设计出针对ｃｐａ、ｃｐｂ、ｅｔｘ、ｉＡ、ｃｐｅ和ｃｐｂ2的 6对引物 ,应用多重ＰＣＲ方法对鉴定出的产气荚膜梭菌进行基因分型。 结果　从 40份样品中分离到 8株 (占 2 0 %)产气荚膜梭菌 ,分型结果均为Ａ型 ,其中 4株还扩增出ｃｐｂ2基因。 结论　产气荚膜梭菌是致人类腹泻的重要病原菌 , β2毒素可能是一重要的致病因子     

Excretion of enterotoxin-producing Clostridium perfringens in feces by patients during and after diarrhea

The excretion in the feces of Clostridium perfringens producing enterotoxin by 48 patients in 3 cases of food poisoning was studied during the illness and 1 and 3 months after the onset. Patients in the first outbreak excreted such strains mostly in the form of spores. In the second outbreak, spores and viable count cells were excreted in nearly equal numbers, and about 50% of the spores were enterotoxigenic. In the third outbreak, the strains were detected both as spores and as viable count cells during the illness. In all three groups, most fecal samples contained at least 10(3) spores per gram. About 1 month after the onset of the illness, (long after recovery from symptoms), 12 colonies producing enterotoxin were detected from five of the 22 samples of feces obtained from subjects in the three groups. There were few C. perfringens organisms, mostly spores, in the feces. Enterotoxin was not detected in the feces. About 3 months after onset, colonies producing enterotoxin could not be detected from feces of 11 of the subjects in the first group. We conclude that persons affected by C. perfringens food poisoning might contaminate food for at least 1 month after the onset.     

Infectious diarrhea

Diarrhea caused by enteric infections is a major factor in morbidity and mortality worldwide. An estimated 2-4 billion episodes of infectious diarrhea occur each year and are especially prevalent in infants. This review highlights the cellular and molecular mechanisms underlying diarrhea associated with the three classes of infectious agents, i.e. bacteria, viruses and parasites. Several bacterial pathogens have been chosen as model organisms, including Vibrio cholerae as a classical example of secretory diarrhea, Clostridium difficile and Shigella species as agents of inflammatory diarrhea and selected strains of pathogenic Escherichia coli (E. coli) to discuss the recent advances in alteration of epithelial ion absorption. Many of the recent studies addressing epithelial ion transport and barrier function have been carried out using viruses and parasites. Here, we focus on the rapidly developing field of viral diarrhea including rotavirus, norovirus and astrovirus infections. Finally we discuss Giardia lamblia and Entamoeba histolytica as examples of parasitic diarrhea. Parasites have a greater complexity than the other pathogens and are capable of creating molecules similar to those produced by the host, such as serotonin and PGE2. The underlying mechanisms of infectious diarrhea discussed include alterations in ion transport and tight junctions as well as the virulence factors, which alter these processes either through direct effects or indirectly through inflammation and neurotransmitters.     

An outbreak of enterocolitis due to Clostridium perfringens in a hospital for the severely disabled

We had an outbreak of 14 cases of enterocolitis due to Clostridium perfringens (Cl. perfringens) in a hospital for the severe multiply-disabled, where the 100 disabled were admitted, in summer in 1985. The signs and symptoms shown by this enterocolitis were primarily diarrhea without fever and loss of appetite. The feces of 10 cases were examined bacteriologically. The test showed 10(3) to 10(6) cells of Cl. perfringens per one gram of their feces and all the strains isolated were untypable by the classification of Hobbs. Nine out of 10 cases were randomly selected and all of the 9 cases were proved to have enterotoxin producing strains. All the strains were highly sensitive to many kinds of antibiotics except kanamycin and gentamicin. Eleven out of the 14 cases were admitted in the same ward and the 7 out of the 11 cases were in the same room of this ward. Considering the spreading route of this infection, it is unlikely that this outbreak occurred due to food supplied from kitchen in this hospital, because all of the disabled, admitted in this hospital, had little chance by which some of the disabled only in a specific ward or room were supplied with bacteriologically contaminated meals from the point of view of cooking and supplying system of this hospital. Adding to this fact, if this outbreak was due to food-born infection, the symptoms of most patients should occur within 1-2 days, because the incubation period of this disease is within a day, however, the patients increased day by day for more than a week.(ABSTRACT TRUNCATED AT 250 WORDS)     

Polyarticular Clostridium perfringens pyoarthritis

A woman with rheumatoid arthritis presented with an abdominal mass and Clostridium perfringens septic arthritis in both wrists and shoulders. We believed this to be the first reported case of polyarticular septic arthritis due to Clostridium perfringens. Apatite, lipid, and cholesterol crystals in the shoulder joint effusions were a potential source of diagnostic confusion.     

A hospital outbreak of diarrhea due to an emerging epidemic strain of Clostridium difficile

BACKGROUND: Increased Clostridium difficile-associated disease (CDAD) in a hospital and an affiliated long-term care facility continued despite infection control measures. We investigated this outbreak to determine risk factors and transmission settings. METHODS: The CDAD cases were compared according to where the disease was likely acquired based on health care exposure and characterization of isolates from case patients, asymptomatic carriers, and the environment. Antimicrobial susceptibility testing, strain typing using pulsed-field gel electrophoresis, and toxinotyping were performed, and toxins A and B, binary toxin, and deletions in the tcdC gene were detected using polymerase chain reaction. Risk factors were examined in a case-control study, and overall antimicrobial use was compared at the hospital before and during the outbreak. RESULTS: Significant increases were observed in hospital-acquired (0.19 vs 0.86; P < .001) and long-term care facility-acquired (0.04 vs 0.31; P = .004) CDAD cases per 100 admissions as a result of transmission of a toxinotype III strain at the hospital and a toxinotype 0 strain at the long-term care facility. The toxinotype III strain was positive for binary toxin, an 18-base pair deletion in tcdC, and increased resistance to fluoroquinolones. Independent risk factors for CDAD included use of fluoroquinolones (odds ratio [OR], 3.22; P = .04), cephalosporins (OR, 5.19; P = .006), and proton pump inhibitors (OR, 5.02; P = .02). A significant increase in fluoroquinolone use at the hospital took place during the outbreak (185.5 defined daily doses per 1000 patient-days vs 200.9 defined daily doses per 1000 patient-days; P < .001). CONCLUSIONS: The hospital outbreak of CDAD was caused by transmission of a more virulent, fluoroquinolone-resistant strain of C difficile. More selective fluoroquinolone and proton pump inhibitor use may be important in controlling and preventing such outbreaks.