ABSTRACT
OBJECTIVE: To describe the etiology of lung infiltrates in HIV-infected antiretroviral-naive children with chronic persistent/recurrent lung disease in whom routine cultures were negative and were non-responders to World Health Organization standard antimicrobial therapy. METHOD: Non-bronchoscopic bronchoalveolar lavage (NBBAL) was performed on these non-responders. RESULTS: Fifty children were enrolled. Single isolates on NBBAL were seen in 28 cases, dual pathogens in 5 cases and no growth in 14 cases. Haemophilus influenzae (n = 12), Candida albicans (n = 5) and Mycobacterium spp. other than tuberculosis (n = 4) were the commonest pathogens seen. Eight cases with no growth had segmental or lobar collapse: in five cases, NBBAL was therapeutic and in two cases, a diagnosis of lymphoma was made on open lung biopsy. Thirty-two of the 38 cases (84%) had favorable outcomes on follow-up. CONCLUSION: Haemophilus influenzae, C. albicans and Mycobacterium spp. other than tuberculosis are important pathogens in children with HIV and HIV-associated chronic lung disease.
Subject(s)
Bronchoalveolar Lavage/methods , Candida albicans/isolation & purification , HIV Infections/complications , Lung Diseases/diagnosis , Adolescent , Antiretroviral Therapy, Highly Active , Bronchoalveolar Lavage/adverse effects , Child , Child, Preschool , Chronic Disease , Female , HIV Infections/drug therapy , HIV Infections/epidemiology , HIV Infections/microbiology , Humans , Infant , Lung Diseases/epidemiology , Lung Diseases/etiology , Lung Diseases/microbiology , Male , Sex Distribution , South AfricaABSTRACT
BACKGROUND: HIV-related pneumonia is the main cause of paediatric hospital admissions in southern Africa. We aimed to measure predictors of treatment failure and the cause of non-responsive pneumonia in children admitted to hospital with severe pneumonia in Durban, South Africa. METHODS: We investigated 358 children aged 1-59 months who presented with WHO-defined severe or very severe pneumonia. Children were recruited irrespective of HIV status and started on a standard antimicrobial regimen of benzylpenicillin and gentamicin. All infants also received high-dose trimethoprim-sulfamethoxazole. The primary outcome measure was treatment failure at 48 h. FINDINGS: 242 (68%) children were HIV infected, 41 (12%) HIV exposed, uninfected, and 75 (21%) HIV uninfected. Failure to respond by 48 h was predicted by age under 1 year (adjusted odds ratio 6.38, 95% CI 2.72-14.91, p<0.0001), very severe disease (2.47, 1.17-5.24, p=0.0181), HIV status (HIV infected 10.3, 3.26-32.51; HIV exposed, uninfected 6.02, 1.55-23.38; p=0.0003), and polymicrobial disease (one organism 2.06, 1.05-4.05; two organisms 10.75, 4.38-26.36; p<0.0001) on logistic regression analysis. All children with three organisms failed treatment. 72/110 treatment failures had at least two organisms isolated. Three of nine HIV-exposed, uninfected infants, 29/74 HIV-infected, but no HIV-uninfected infants who failed study therapy had Pneumocystis jirovecii pneumonia. INTERPRETATION: For children younger than 1 year, the WHO guidelines are inadequate and need to be revised since both HIV-infected and HIV-exposed, uninfected infants had more treatment failures than did HIV-uninfected infants. Polymicrobial disease is an important reason for treatment failure, and we need to identify rapid low-cost diagnostic methods to assist clinicians.
