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Few studies exist of adherence to guidelines for vaccination of persons infected with human immunodeficiency virus (HIV), especially in the era of highly active antiretroviral therapy (HAART). In a retrospective, cross-sectional analysis in the HIV Outpatient Study sites, 198 (32.4%) of 612 patients eligible for hepatitis B vaccine received at least 1 dose. In multivariate analysis, hepatitis B vaccination was associated with HIV risk category, education level, and number of visits to the HIV clinic per year. Among 716 patients eligible for hepatitis A vaccine, 167 (23.3%) received ⩾1 dose. Response to hepatitis B vaccination was associated with higher nadir CD4+ cell counts (P = .008) and HIV RNA levels less than the level of detection (P = .04), although some response was documented at all CD4+ levels. Although there were low rates of complete hepatitis vaccination in this cohort of ambulatory patients, prompt efforts to vaccinate patients entering care, receipt of antiretroviral therapy, and practice reminder systems may enhance vaccination practices. [ABSTRACT FROM AUTHOR]

To ascertain the impact of hepatitis C virus (HCV) infection on human immunodeficiency virus (HIV) disease progression and associated death in the era of highly active antiretroviral therapy (HAART), we examined mortality rates, the presence of other diseases, and antiretroviral use in an observational cohort of 823 HIVinfected patients with and without HCV coinfection during the period of January 1996 through June 2001. Analyses were used to compare patient characteristics, comorbid conditions, and survival durations in HIVinfected and HIV-HCV-coinfected patients. HIV-HCV-coinfected persons did not have a statistically greater rate of acquired immunodeficiency syndrome or of renal or cardiovascular disease, but they did have more cases of cirrhosis and transaminase elevations. There were proportionately more deaths in the HIVHCV-coinfected group. Age, baseline CD4[sup +] cell count, and duration of HAART were significantly associated with survival, but HCV infection was not. HAART use was a strong predictor of increased duration of survival, suggesting that treatment is more important to survival than is HCV coinfection status. [ABSTRACT FROM AUTHOR]

Parenteral interferon-γ (IFN-γ) activates murine macrophages to inhibit Trypanosoma cruzi multiplication and diminishes parasitemia and mortality in acute infection. To investigate the role of endogenous IFN-γ in acute infection, monoclonal antibody to IFN-γ was injected intraperitoneally into mice. The 6250 neutralizing units given 24 and 96 h after infection reproducibly increased mortality (P < .05). Histology sections showed markedly more nests of T. cruzi in treated mice. BALB/c, Swiss Webster, C57Bl/6, and C3H/HEN mice were susceptible to the effects of anti-IFN-γ. Peritoneal macrophages from mice 4 days after infection and a single dose of 6250 units of anti-IFN-γ had significantly reduced ability to inhibit T. cruzi multiplication. Multiple doses of anti-IFN-γ delayed but did not prevent macrophage activation. These results indicate the critical role of endogenous IFN-γ for macrophage activation and host defense against acute T. cruzi infection in mice. [ABSTRACT FROM PUBLISHER]

The effects of ketoconazole against infection with Trypanosoma cruzi both in vivo and in vitro were examined. In vivo, ketoconazole significantly protected mice infected with lethal inocula of the Y strain of T. cruzi even when treatment was initiated seven days after infection; protection was also demonstrated for three other strains. Although mice had demonstrable parasitemia after completion of therapy, tissue sections of treated mice revealed a complete absence of organisms. Concentrations of ketoconazole as low as 0.001 µg/ml inhibited in vitro replication of intracellular organisms, whereas concentrations of ketoconazole that prevented replication of intracellular amastigotes had no effect on extracellular organisms. This finding and the observation that inhibition of replication of amastigotes occurred in macrophages exposed to ketoconazole before infection suggests that the inhibitory effect depends on interaction of the drug with host cells. Thus ketoconazole should be tested as a therapeutic agent for Chagas' disease in humans. [ABSTRACT FROM PUBLISHER]

Ceftibuten is an oral third generation cephalosporin with potent antimicrobial activity against Enterobacteriaceae, beta-lactamase positive Haemophilus influenzae, Moraxella catarrhalis, Neisseria meningitidis, Neisseria gonorrheae, penicillin-susceptible pneumococci, and beta-hemolytic streptococci. To study the efficacy and safety of ceftibuten for treatment of bronchitis, 58 patients were randomized to therapy with either ceftibuten 400 mg once a day or cefaclor 250 mg every 8 h at a ratio of two to one. Of 45 clinically evaluable patients, 28 (87.5%) of the 32 ceftibuten patients and 12 (92.3%) of the 13 cefaclor patients were clinically improved or cured. Of 33 microbiologically evaluable patients, 21 (87.5%) of the 24 ceftibuten patients and eight (80%) of the ten cefaclor patients were cured. Of 56 patients evaluable for adverse effects, three (7.9%) of the 38 ceftibuten patients and one (5.6%) of the 18 cefaclor patients had adverse reactions. In this small study, once-daily ceftibuten appeared as safe and as effective as cefaclor for the treatment of bronchitis. [ABSTRACT FROM AUTHOR]