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Pneumocystis carinii pneumonia in South African children infected with human immunodeficiency virus

Background. Pneumocystis carinii pneumonia (PCP) has been regarded as uncommon in HIV‐infected patients in Africa, but diagnostic difficulties and geographic variability may partly account for this. There is little information on the incidence of PCP in HIV‐infected children in Africa. Aim. To investigate (1) the incidence and associated features of PCP in African HIV‐infected children and (2) the usefulness of sputum induction and nasopharyngeal aspirates (NPAs) for diagnosis of PCP. Methods. HIV‐infected children hospitalized with pneumonia were prospectively enrolled in a 1‐year study in South Africa. History, examination, chest radiology and blood tests (including HIV testing) were performed. Sputum induction (5% NaCl nebulization) or nondirected bronchoalveolar lavage in intubated patients was performed for P. carinii identification using immunofluorescence and silver stain; immunofluorescence was also done on nasopharyngeal aspirates (NPAs). Results. Of 151 HIV‐infected children [47% female; median age, 9 (range, 3 to 23) months], 87 had been previously diagnosed with HIV whereas 64 (42.4%) were found to be HIV‐positive at the time of admission. PCP occurred in 15 children (9.9%; 95% confidence interval, 5.9 to 15.5) and was the AIDS‐defining infection in 13 of 64 (20.3%; 95% confidence interval, 11.8 to 31.5). Only 1 of 59 children receiving prophylaxis (1.7%) developed PCP compared with 14 of 92 (15.2%) not taking prophylaxis [relative risk, 0.11 (0.02 to 0.82), P = 0.007]. PCP‐infected children were younger [3 (range, 3 to 4) vs. 10 (range, 4 to 24) months, P < 0.001] and presented with more severe pulmonary disease as indicated by a higher respiratory rate [63 (range, 60 to 73) vs. 50, (range, 40 to 60) P < 0.001], heart rate [160 (range, 136–180) vs. 140 (range, 120–152) P = 0.025] and a greater incidence of cyanosis (53%vs. 26%, P = 0.025). Clinical signs of HIV infection, occurring in 96% of children, were equally prevalent in both groups. High serum lactate dehydrogenase was the only laboratory investigation that distinguished PCP‐infected from uninfected children [626 (range, 450 to 1098) vs. 307 (range, 243 to 465) units/l], P < 0.001. No radiologic features were found to be diagnostic of PCP. P. carinii was identified in 9 sputa and 6 bronchoalveolar lavage specimens, but all corresponding NPAs were negative. Seven of 15 (47%) children with PCP died while hospitalized compared with 24 of 136 (18%) without PCP [relative risk, 1.21 (range, 0.99 to 1.47), P = 0.008]. Conclusion. PCP is an important pathogen in HIV‐infected infants in South Africa and is associated with a high mortality. Induced sputum is effective for obtaining lower respiratory tract secretions for diagnosis of PCP but an NPA is not useful.