Clostridium perfringens may cause antibiotic -associated diarrhoea

2014 ◽  
Vol 5 (5) ◽  
pp. 303-306
Author(s):  
Anna Doszyń ◽  
Magdalena Dubińska
The Lancet ◽  
1984 ◽  
Vol 323 (8372) ◽  
pp. 305-307 ◽  
Author(s):  
S.P. Borriello ◽  
A.R. Welch ◽  
H.E. Larson ◽  
Fiona Barclay ◽  
M.F. Stringer ◽  
...  

2008 ◽  
Vol 57 (3) ◽  
pp. 343-347 ◽  
Author(s):  
Natassia Camacho ◽  
Carlos Espinoza ◽  
César Rodríguez ◽  
Evelyn Rodríguez

To assess the prevalence of enterotoxigenic Clostridium perfringens among adults suffering from antibiotic-associated diarrhoea in a Costa Rican hospital, faecal samples were analysed from 104 patients by a cultivation approach. The 29 strains obtained, which accounted for an isolation frequency of 28 %, were genotyped and investigated with regard to their in vitro susceptibility to penicillin, imipenem, cefotaxime, chloramphenicol and metronidazole using an agar-dilution method. A multiplex PCR for detection of the toxins α, β and ϵ predictably classified all faecal isolates as biotype A. An agglutination assay revealed that only one isolate synthesized detectable amounts of enterotoxin (detection rate 3 %). This result was confirmed by a PCR targeting the cpe gene. The spores of the only CPE+ isolate did not germinate after incubation for 30 min at temperatures above 80 °C. Most isolates were susceptible to first-choice antimicrobials. However, unusual MICs for penicillin (16 μg ml−1) and metronidazole (512 μg ml−1) were detected in one and three isolates, respectively. The low incidence of enterotoxigenic strains suggests that C. perfringens was not a major primary cause of antibiotic-associated diarrhoea in this hospital during the sampling period.


2009 ◽  
Vol 47 (05) ◽  
Author(s):  
C Kamhuber ◽  
S Hörist-Kollmann ◽  
A Rek ◽  
G Eckhardt ◽  
A Zauner ◽  
...  

1988 ◽  
Vol 59 (02) ◽  
pp. 236-239 ◽  
Author(s):  
Giovanna Barzaghi ◽  
Chiara Cerletti ◽  
Giovanni de Gaetano

SummaryWe studied the aggregating effect of different concentrations of phospholipase C (PLC) (extracted from Clostridium perfringens) on human platelet-rich plasma (PRP). PRP was preincubated with PLC for 3 min at 37° C and the platelet aggregation was followed for 10 min. The threshold aggregating concentration (TAG) of PLC was 3-4 U/ml.We also studied the potentiation of PLC with other stimuli on platelet aggregation. Potentiating stimuli, such as arachidonic acid (AA), ADP. Platelet Activating Factor (PAF) and U-46619 (a stable analogue of cyclic endoperoxides) were all used at subthreshold concentrations. We also studied the possible inhibitory effect of aspirin, apyrase, TMQ, a prostaglandin endoper- oxide/thromboxane receptor antagonist and BN-52021, a PAF receptor antagonist. Only aspirin and apyrase were able to reduce aggregation induced by PLC alone and PLC + AA and PLC + ADP respectively. TMQ and BN-52021 were inactive. In ex vivo experiments oral aspirin (500 mg) partially inhibited platelet aggregation induced by PLC alone, PLC + AA and PLC + ADP 2 and 24 h after administration. Aspirin 20 mg for 7 days also reduced aggregation induced by PLC + AA.


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