Bacterial community-acquired pneumonia in HIV-infected patients.

PURPOSE OF REVIEW: In this review, we focus on the clinical features, diagnosis, outcome and management of bacterial community-acquired pneumonia (BCAP) in HIV-infected patients, with particular attention to the most recent findings in this area. RECENT FINDINGS: Clinical features of BCAP are often atypical in HIV-infected individuals, especially when liver cirrhosis is also present. Streptococcus pneumoniae is the most common causative agent and is frequently associated with bacteriemic disease even in low-risk patients according to pneumonia severity index. An etiologic diagnosis is obtained in an average 35% of cases with standard culture methods. In such conditions, urinary antigen test for S. pneumoniae identification may help in reaching a rapid and etiologic diagnosis. CD4 cell count should be carefully considered in HIV patients with BCAP. In consideration of their high mortality risk, patients with a CD4 cell count of less than 200 cells/mul should be hospitalized, whereas those with a CD4 cell count of at least 200 cells/mul could be managed according to pneumonia severity index score. Empiric antibiotic therapy should include a combination of a beta-lactam and a macrolide or a respiratory fluoroquinolone alone. Finally, prevention strategies should include lifestyle modification, highly active antiretroviral therapy access and adherence programs and the implementation of pneumococcal vaccination. SUMMARY: A correct diagnosis and management together with a comprehensive approach to preventive measures, including lifestyle modification, highly active antiretroviral therapy access and adherence programs and the implementation of pneumococcal vaccination, are key factors to reduce BCAP incidence and mortality in HIV-infected patients.

Minor mutations in HIV protease at baseline and appearance of primary mutation 90M in patients for whom their first protease-inhibitor antiretroviral regimens failed.

The association between minor mutations in human immunodeficiency virus (HIV) protease at baseline and development of common primary mutation 90M at virological failure (conferring some resistance to all protease inhibitors [PIs]) was evaluated in 93 previously drug-naive patients experiencing failure of their first PI-based antiretroviral regimens. In logistic regression analysis, the probability of accumulating a new 90M mutation at virological failure was associated with the presence at baseline of minor mutation 36I (naturally occurring in approximately 25% of HIV clade B and in >80% of HIV non-clade-B viruses) (adjusted odds ratio, 13.5 [95% confidence interval, 1.89-95.6]; P=.009) and, possibly, of 10I/V. This suggests a potential role for the presence of 36I at baseline in predicting the appearance of 90M at virological failure.