[Hematogenous spondylitis caused by Bacteroides fragilis].
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OBJECTIVE: To explore the mechanism of injurious effect of succinic acid on human fibroblast and it's role in bacteroides fragilis infection. METHODS: In vitro cultured human fibroblasts were challenged by succinic acid in concentrations of 5, 10, 20 and 30 mmol/L (pH5.5), respectively. The cellular activity, apoptosis rate, the collagen synthesis in the supernatant of the cell culture, and the activity of caspase-3 were determined 24 hours after challenge. Isotonic saline challenged fibroblast were employed as control and the changes in the indices before and after succinic acid challenge were observed. RESULTS: Along with the increase in the concentration of succinic acid, the fibroblast proliferation rate was decreased and so was the collagen synthesis. But the apoptosis rate and caspase-3 activity were increased. The activity of caspase-3 was markedly higher than that in normal control when the succinic acid concentration was 10-30 mmol/L. The cellular activity and collagen synthesis were significantly lower and the apoptosis rate was obviously higher than those in control group when the succinic acid concentration was 20 or 30 mmol/L (P < 0.05). CONCLUSION: The proliferation and collagen synthesis in fibroblast culture could be significantly inhibited and the cellular apoptosis could be promoted by succinic acid. The process of wound healing of the wounds infected by bacteroides fragilis would be delayed due to the production of succinic acid by the bacteria.
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A multicenter, open-label randomized trial was conducted to evaluate the efficacy and tolerability of monotherapy with imipenem-cilastatin (I-C) compared with combination therapy with clindamycin and an aminoglycoside (C+A) for treatment of 117 patients with serious intra-abdominal infections. Fifty-three patients (45%) received I-C and 64 patients (55%) received C+A. The overall clinical success rate was 96.2% for the I-C patients and 92.2% for the C+A patients. Clinical failure rates were 3.8% and 7.8%, respectively (P = NS). Eradication or suppression of pathogens was observed in 81.8% and 82.2% of patients, respectively. Uniform bacteriologic response was observed among all infection subgroups. Fourteen of 145 patients experienced adverse symptoms, including six of 66 (9.1%) monotherapy patients and eight of 79 (10.1%) combination-therapy patients (P = NS). The results of this study demonstrate that I-C monotherapy was as effective as C+A combination therapy for the treatment of serious intra-abdominal infections, regardless of the site or severity of infection or the clinical status of the patient. Both regimens also were found to be comparable in tolerability.
Strains of Bacteroides fragilis which produce enterotoxin(s) (ETBF) have been associated with diarrhoeal diseases in young domestic animals and have also been isolated from humans with diarrhoea. We have determined epidemiologically that ETBF are significantly associated with diarrhoea in humans. We studied Apaches, primarily children, with diarrhoea attending an outpatient facility in Whiteriver, Arizona, from July 1986 through July, 1988. Stool cultures for isolation of ETBF and other diarrhoeal pathogens were taken from these persons as well as from age and time-matched control persons who did not have diarrhoea. ETBF were isolated significantly more often from persons with diarrhoea (12%) than from controls (6%), p = 0.03. Isolation was highest (20-24% of stool cultures positive) during the second and third years of life. The diarrhoeal syndrome associated with ETBF was non-specific, and most characteristic of a secretory, rather than inflammatory, type of diarrhoea. ETBF are significantly associated with acute diarrhoea in Apache children, and may be an important newly described cause of diarrhoea in humans.
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A coagglutination technique using indigenous reagents was applied for the rapid identification of Bacteroides fragilis and the black pigmented bacteroides group, using colony suspensions. All the 58 strains of B. fragilis and 42 strains of black pigmented bacteroides tested could be correctly identified by this method. The specificity of the coagglutination reagent was confirmed by the absence of cross reactivity with the related species of bacteroides, viz., B. distasonis, B. ovatus, B. vulgatus and B. thetaiotaomicron as well as other anaerobic and aerobic bacteria. A panel of four antisera against B. fragilis was required for correct identification of the strains tested, indicating the presence of multiple serotypes. On the other hand, all 42 strains of black pigmented bacteroides tested could be identified, using a single reagent as these strains appeared to have no antigenic type variants.
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The evolution of antimicrobial susceptibility of Bacteroides fragilis over a five year period is described. We have studied 30 selected strains isolated each year at the University Hospital of Sevilla (total: 150 strains). We did not find any resistant strain to chloramphenicol, metronidazole or imipenem. Resistance to piperacillin (8%) and cefoxitin (13%) remain constant over the study period. Resistance to cefmetazole, cefotaxime, mezlocillin, ofloxacin, clindamycin and moxalactam ranges from 24% to 37%. A rise in the percentage of resistant strains to ticarcillin (from 17% to 30%) and ceftizoxime (from 0% to 40%) was also seen during the study period. Bacteroides thetaiotaomicron was the overall more resistant species, and B. fragilis the more sensitive.
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Attempts were made to study the virulence factors in some strains of B. fragilis group in the rat model. Subcutaneous wound abscesses could be produced by 10(9) CFU/ml of live cells of all the five species of B. fragilis group tested. For determination of virulence factor cellular components (capsular polysaccharide and lipopolysaccharide) of B. fragilis were separated using gel filtration technique and injected in rats. Abscesses could be produced only by capsular polysaccharide fraction suggesting it to be the virulence factor. Studies with transmission electron microscope showed presence of capsular polysaccharide in B. fragilis and B. thetaiotaomicron, it was doubtful in B. distasonis and absent in B. ovatus and B. vulgatus. This suggested that virulence factors other than capsular polysaccharide may be responsible for pyogenic lesions in the noncapsulated species of B. fragilis group. The abscess could not be produced by 10(9) CFU/ml of heat killed cells of non-capsulated B. ovatus and B. vulgatus indicating that in live bacteria, a heat labile factor was responsible for the development of abscess.
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