HIV-1 drug resistance mutations in children who failed non-nucleoside reverse transcriptase inhibitor-based antiretroviral therapy.

Non-nucleoside reverse transcriptase inhibitor (NNRTI)-based regimens have recently been used in HIV-1 infected children in resource-limited settings. Treatment failure with this regimen has become more common. A second regimen needs to be prepared for the Thai national program. Genotypic resistance testing was conducted among HIV-1 infected children who experienced virological failure with antiretroviral therapy (ART) using NNRTI-based regimens. Patterns of resistance mutations were studied and options for a second regimen were determined. There were 21 patients with a median (IQR) age of 4.1 (1.9-7.7) years. Sixteen patients were males. The median CD4 cell count and HIV-1 RNA at the time of virological failure were 647 cells/mm3 and 5.3 log copies/ml, respectively. The prevalences of patients with > or =1 major mutation conferring resistance to NRTIs and NNRTIs were 52% and 43%, respectively. Thymidine analoque mutations, M184V/I, and Q151M were observed in 38%, 33%, and 5%. The patterns of resistance mutations suggest that 48% of patients need a protease inhibitor-based regimen for the second regimen and didanosine+lamivudine is the most required nucleoside reverse transcriptase inhibitor backbone.

A patient with penicillin-resistant viridans group streptococcal endocarditis and unusual reactions to vancomycin.

There is a paucity of data regarding the treatment of endocarditis caused by penicillin-resistant viridans group streptococci (PR-VGS). We report a 16-year-old girl who had native-valve endocarditis due to PR-VGS which was identified as Streptococcus mitis. She also had unusual reactions to vancomycin. Eighteen hours after initiation of 50 mg/kg/day vancomycin, she developed a maculopapular rash, then at 48 hours she developed an intermittent high fever and a progressive decrease in peripheral leukocytes and platelets. She developed hypotension on Day 8. Her serum C-reactive protein and procalcitonin levels were high. All reactions improved after vancomycin was discontinued and oral prednisolone was started. This unusual combination of reactions to vancomycin was likely caused by immune and nonimmune mechanisms. Her endocarditis was successfully treated with cefotaxime 200 mg/kg/ day for 4 weeks.