Background. Despite a substantial disease burden. there is little descriptive epidemiology of acute pneumonia in sub-Saharan Africa. We did this study to define the aetiology of acute pneumonia, to estimate mortality at convalescence, and to analyse mortality risk-factors. Methods. We studied 281 Kenyan adults who presented to two public hospitals (one urban and one rural) with acute radiologically confirmed pneumonia during 1994-96. We did blood and lung-aspirate cultures, mycobacterial cultures, serotype-specific pneumococcal antigen detection, and serology for viral and atypical agents. Findings. Aetiology was defined in 182 (65%) patients. Streptococcus pneumoniae was the most common causative agent, being found in 129 (46%) cases; Mycobacterium tuberculosis was found in 26 (9%). Of 255 patients followed up for at least 3 weeks, 25 (10%) died at a median age of 33 years. In multivariate analyses, risk or protective factors for mortality were age (odds ratio 1.51 per decade [95% CI 1.04-2.19]), unemployment (4.42 [1.21-16.11), visiting a traditional healer (5.26 [1.67-16.51), visiting a pharmacy (0.30 [0.10-0.91]), heart rate (1.64 per 10 beats [1.24-2.16]), and herpes labialis (15.4 [2.22-107)). HIV-1 seropositivity, found in 52%, was not associated with mortality. Death or failure to recover after 3 weeks was more common in patients with pneumococci of intermediate resistance to benzylpenicillin, which comprised 28% of pneumococcal isolates, than in those infected with susceptible pneumococci (5.60 [1.33-23.6]). Interpretation. We suggest that tuberculosis is a sufficiently common cause of acute pneumonia in Kenyan adults to justify routine sputum culture, and that treatment with benzylpenicillin remains appropriate for clinical failure due to M tuberculosis, intermediate-resistant pneumococci, and other bacterial pathogens. However, interventions restricted to hospital management will fail associated with socioeconomic, behavioural factors.
Bibliographical noteFunding Information:
This paper is published with the permission of the director of the Kenya Medical Research Institute (KEMRI). The study was supported financially by KEMRI and the UK Wellcome Trust. JAGS was supported by a Wellcome Trust research training fellowship in clinical epidemiology (035375), and KM by a Wellcome Trust senior research fellowship in clinical science (031342). We thank Derrick Crook and staff of the Oxford Vaccine Group and the Public Health Laboratory Service (PHLS), John Radcliffe Hospital, University of Oxford, Oxford, UK, for assistance with speciation of gram-negative pathogens; Malcolm Yates of PHLS Mycobacterium Reference Unit for assistance with speciation of mycobacteria; Salim Mwarumba and Ahenda Hannington for assistance in the Kilifi microbiology laboratory; and Justin Gulani and Christopher Chigiri for administration of questionnaires.
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