The objective of this study was to determine the antimicrobial susceptibility of anaerobic bacteria from the intestinal microflora of healthy children who had not been treated with antimicrobial agents since birth or at 1, 3, 6, 12, 18 and 24 months of age, as well as from children of the same ages treated with the most commonly used antimicrobial agents in Nicaragua. A total of 947 Bacteroides and 745 Clostridium strains were isolated from 67 healthy and 94 antimicrobial-treated children. The minimal inhibitory concentrations of ampicillin, cefoxitin, imipenem, clindamycin, metronidazole and chloramphenicol were determined by the agar dilution method. Detection of ss-lactamase was made by the nitrocefin assay. No bacterial strains resistant to imipenem, clindamycin, metronidazole or chloramphenicol were found. The susceptibility of Bacteroides species to ampicillin and cefoxitin isolated from antimicrobial-treated children decreased progressively as the children reached 24 months of age, from 88% to 78% and from 94% to 81%, respectively. All the Bacteroides strains isolated from the healthy children were 100% susceptible to cefoxitin when they were <=12 months and 92% susceptible after this age; the susceptibility of Bacteroides strains to ampicillin in these children was from 91% at 1 month to 86% at 24 months of age. All Clostridium strains were susceptible to ampicillin and cefoxitin. The ss-lactamase production was seen only in Bacteroides species. These data indicate that a rational use of antimicrobial agents is needed to avoid the development of resistance in anaerobic bacteria.
This subject is important for both the education of health professionals and for preventative measures. Standard and contact-precautions should be employed in professional practice.
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Liver disease may produce significant, albeit highly variable, effects on the pharmacokinetic behaviour of antibiotics in serum. Drug disposition may be altered through several pathophysiological mechanisms including reduced hepatobiliary clearance, and modifications in the volume of distribution induced by albumin synthesis deficiency or portal hypertension-related ascites. Antibacterial agents are not affected by potential alteration in hepatic first-pass effects. Only liver cirrhosis-induced effects on serum pharmacokinetics of antibiotics have been extensively studied, unlike those possibly produced by other forms of liver disease. In liver cirrhosis, pharmacokinetic alterations of nearly all beta-lactam or quinolone agents appear not to be marked enough to require dosage adjustment, provided that renal function stays normal. Adaptation in therapeutic schedule, however, is warranted for those drugs that are substantially cleared by the hepatobiliary system, namely mezlocillin, clindamycin, erythromycin, pefloxacin, enoxacin, antituberculous agents or nitroimidazole derivatives. Special caution should also be exercised when using aminoglycosides or vancomycin because of the wide interpatient variability of their pharmacokinetic disposition and their toxic potential. When renal function is impaired and there is an increased volume of distribution due to ascites, as frequently observed in severe liver insufficiency, the elimination half-life of most antibiotics is markedly prolonged, resulting in potential side effects due to drug accumulation. Accordingly, dosage adjustment applies to all drugs. In this regard, it should be remembered that delineating the dosage guidelines for a given antibiotic on the basis of reported pharmacokinetic parameters in patients with liver cirrhosis is awkward and probably of limited value. This pattern is ascribed to large interpatient variability in the active hepatic cell mass, the degree of portal hypertension and the alteration of serum binding capacity. Furthermore, there is no way of predicting accurately the extent of liver insufficiency in an individual patient. Dosage reduction is thus done empirically in most cases. Whenever possible, direct measurements of serum antibiotic concentrations should be the reasonable approach to manage antibiotic therapy in this kind of clinical condition.
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We previously showed that children attending an inner city pediatric emergency department were sometimes asymptomatically colonized with clindamycin-susceptible community-acquired methicillin-resistant Staphylococcus aureus (MRSA) and borderline methicillin-resistant S. aureus (BRSA) as well. We wished to ascertain whether healthy children attending an outpatient clinic were colonized with these organisms. Therefore to estimate the prevalence of community-acquired MRSA and BRSA nasal colonization in a well child population, we cultured children attending an inner city pediatric outpatient clinic.
Randomly selected strains of beta-lactamase-negative and beta-lactamase-positive Neisseria gonorrhoeae were tested by an agar dilution method for susceptibility to rosamicin, josamycin, erythromycin, clindamycin, and penicillin G. Rosamicin was more active than erythromycin, which was more active than josamycin or clindamycin; the latter two were similar in their activity. The susceptibility to the macrolide antibiotics and clindamycin was independent of beta-lactamase production, but the penicillin minimal inhibitory concentrations were higher in the beta-lactamase-positive group because of the enzyme.
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The initiation of systemic antimicrobial treatment of Pneumocystis jirovecii pneumonia (PCP) is triggered by clinical signs and symptoms, typical radiological and occasionally laboratory findings in patients at risk of this infection. Diagnostic proof by bronchoalveolar lavage should not delay the start of treatment. Most patients with haematological malignancies present with a severe PCP; therefore, antimicrobial therapy should be started intravenously. High-dose trimethoprim/sulfamethoxazole is the treatment of choice. In patients with documented intolerance to this regimen, the preferred alternative is the combination of primaquine plus clindamycin. Treatment success should be first evaluated after 1 week, and in case of clinical non-response, pulmonary CT scan and bronchoalveolar lavage should be repeated to look for secondary or co-infections. Treatment duration typically is 3 weeks and secondary anti-PCP prophylaxis is indicated in all patients thereafter. In patients with critical respiratory failure, non-invasive ventilation is not significantly superior to intubation and mechanical ventilation. The administration of glucocorticoids must be decided on a case-by-case basis.
The objective of this study was to evaluate clinical outcomes and risk factors associated with clinical failure in patients hospitalized with cellulitis with or without abscess.
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Prospective, population-based surveillance for invasive GAS infections was conducted in Ontario from January 1992 until June 2002. All 62 patients meeting clinical and/or histopathologic criteria for invasive GAS who were admitted to the ICUs of four university-affiliated hospitals in Toronto, Canada were included. Demographic and clinical information were obtained retrospectively by chart review. ICU morbidity data included the occurrence of organ dysfunction (renal, hepatic, coagulation, ARDS), treatment, and interventions such as hemodialysis and mechanical ventilation.
Results of treatment of 151 surgical infections with a variety of antimicrobial regimes were retrospectively compared. Diagnoses included diffuse peritonitis (43), severe soft tissue infections (11), septicaemia accompanying abdominal infections (29), intra-abdominal abscesses (36), local peritonitis (27) and other localized infections (5). A total of 211 anaerobic and 130 aerobic strains were isolated. A cure rate of 92% was achieved with metronidazole or ornidazole used alone and 89% with these nitroimidazoles plus an aminoglycoside. Results were equally satisfactory regardless of whether a surgical procedure, such as drainage was performed. Clindamycin and the aminoglycosides had satisfactory results in combination, but not when used alone. Good controlled trials are now justified to define the need for an aminoglycoside and/or surgery in addition to a nitroimidazole.