Disseminated candidiasis with extensive folliculitis in abusers of brown Iranian heroin
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Folliculitis
Malassezia
Folliculitis
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Summary The treatment of 62 dogs with blastomycosis was reviewed to identify prognostic factors and response to various treatment regimens. Severity of lung involvement, as determined by radiography, and the number of nonsegmented neutrophils were useful prognostic factors. Females survived treatment better than did males, but females were more prone to relapse. Ketoconazole treatment at a dose of 10 mg/kg daily for 60 days was not as effective as amphotericin B. The most notable adverse effect of amphotericin B treatment was nephrotoxicosis. Treatment with amphotericin B followed by ketoconazole was as effective as amphotericin B alone and resulted in less nephrotoxicosis. Most dogs that had relapses were retreated effectively with amphotericin B and/or ketoconazole. Canine blastomycosis was shown to be a treatable disease, with a cure rate of approximately 75%.
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The potential of ketoconazole prophylaxis to antagonize the activity of amphotericin B against aspergilli was investigated in vitro and in neutropenic mice. Exposure of Aspergillus fumigatus (six strains) and of Aspergillus flavus or Aspergillus niger to ketoconazole resulted in a uniform increase of the minimal fungicidal activity of amphotericin B, from 0.15–0.63 mg/liter to >2.5 mg/liter in a microwell assay. To test the relevance of this antagonism in vivo, we challenged neutropenic mice iv with a lethal dose of conidia from two strains of A. fumigatus and then treated the mice first with ketoconazole and then with amphotericin B or amphotericin B plus ketoconazole. Pretreatment with ketoconazole for 48 hr completely abolished the protective effect of a subsequent therapy with amphotericin B, whether ketoconazole therapy was stopped (P < .001) or not (P <.001). Ketoconazole given alone had no significant effect on survival. Our data show that ketoconazole not only antagonized the fungicidal activity of amphotericin B in vitro but also abolished in vivo the protective effect of the only drug shown to be useful in the therapy of aspergillosis. The clinical importance of this antagonism, which is not limited to Aspergilli in vitro, requires careful consideration before ketoconazole prophylaxis can be recommended for patients at high risk of developing invasive opportunistic fungal infections.
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Growth inhibition studies were done on an encapsulated and non-encapsulated strain of Cryptococcus neoformans at the minimal inhibitory concentration and one-half the minimal inhibitory concentration of ketoconazole and amphotericin B alone and in combination. Growth of both strains was significantly inhibited by ketoconazole, amphotericin B, and the combined drugs at the minimal inhibitory concentration of each drug over a 5-day period. Calculation of the expected inhibition of growth for both strains with both drugs showed antagonism at 24 h followed by an additive effect and synergy for the remaining 4 days of the assay. Although similar results were obtained for both strains with one-half the minimal inhibitory concentration, an additive effect was observed with the drug combination at 24 h for the encapsulated strain, and an antagonistic effect was observed with the non-encapsulated strain.
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Combinations of amphotericin Band ketoconazole had an additive effect in vitro against Histoplasma capsulatum and Cryptococcus neoformans; ketoconazole combined with flucytosine exerted an indifferent effect against C. neoformans. In vivo studies in athymic nude (nu/nu) mice and their heterozygous (nu/ +) littermates demonstrated that treatment with the ketoconazole-amphotericin B combination resulted in longer survival of mice with cryptococcosis than did treatment with ketoconazole plus flucytosine. However, mice given ketoconazole plus amphotericin B did not survive significantly longer than those given amphotericin B alone (cryptococcosis) or ketoconazole alone (histoplasmosis). Combination chemotherapy with ketoconazole and amphotericin B may offer a modest therapeutic advantage over therapy with either drug alone.
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Interactions among amphotericin B, 5-fluorocytosine, ketoconazole, and micoconazole were tested for all possible paired and triple drug combinations and all four drugs combined against three isolates of Candida albicans, three Candida spp., two isolates of Cryptococcus neoformans, and three isolates Aspergillus fumigatus. An assay for inhibitory activity was developed in which growth in the presence of an antifungal agent was expressed as a percentage of the growth in drug-free cultures. For nearly all of the antifungal combinations, the interaction was additive against most fungal isolates. Drug combinations that included amphotericin B and ketoconazole were most often synergistic, i.e., amphotericin plus ketoconazole, amphotericin plus 5-fluorocytosine plus ketoconazole, and amphotericin plus 5-fluorocytosine plus ketoconazole plus miconazole, whereas the combination of ketoconazole plus miconazole showed the strongest tendency towards antagonism. The data in this screening survey provide a basis for further studies of drug interactions in vivo and in vitro.
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Fungal infections in neutropenic cancer patients have increased in frequency and constitute an important cause of morbidity and mortality. Empiric antifungal therapy is often administered to those patients who have failed to respond to antibacterial antibiotics. We conducted a prospective, randomized trial of amphotericin B and ketoconazole for 172 neutropenic cancer patients with presumed or proven fungal infections. Overall, amphotericin B and ketoconazole were equally effective. Amphotericin B may have been more effective than ketoconazole for the treatment of pneumonia. Also, five of eight Candida tropicalis infections treated with amphotericin B responded, whereas all eight infections treated with ketoconazole failed to respond (P = 0.03). Response rates for localized fungal infections were similar with both drugs. Ketoconazole should not be used as empiric antifungal therapy at institutions where there is a high frequency of infections caused by Aspergillus spp. or C. tropicalis because this agent lacks activity in vitro against these species.
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Objective To detect the MICs of antifungal agents against yeasts, in order to direct the clinician to use antifungal agents accurately. Methods We collected 54 yeast isolates from 2001, 2 - 3, and detected the mimimum inhibitory concentrations (MIC) of amphotericin B, ketoconazole, flu-conazole by micro - dilution. Results The ranges of MICs of amphotericin B fluconazole and ketoconazole against yeasts varied from 0. 25 - 1. 0μg/ml, 2. 0 - 8. 0μg/ml and 16μg/ml, respectively. Conclusion Yeast species resistance to Amphotericin B was lowest (0% ) , and highest to Ketoconazole. Micro - dilution can be used to test antifungal agent susceptibility clinically.
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Folliculitis
Malassezia
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