Aetiology of uveitis in Sierra Leone, west Africa.

BACKGROUND: In 1992, non-onchocercal uveitis caused 9% of blindness, 8% of visual impairment, and 11% of uniocular blindness among patients visiting an eye hospital in Sierra Leone, west Africa. The aim of this study was to determine the aetiology of uveitis in this population. METHODS: General and ophthalmic examination complemented by serum and aqueous humour analyses for various infectious agents was performed for 93 uveitis patients and compared with serum (n = 100) and aqueous humour (n = 9) analysis of endemic controls. RESULTS: At the initial examination, 45 patients (48%) proved to be severely visually handicapped. After clinical and laboratory analyses, an aetiological diagnosis was established for 49 patients (52%). Toxoplasma gondii was the most important cause of uveitis (40/93; 43%). Anti-toxoplasma IgM antibodies were detected in serum samples of seven of 93 patients (8%) compared with one of 100 controls (1%, p < 0.05). At least six patients (15%) with ocular toxoplasmosis had acquired the disease postnatally. Antibodies against Treponema pallidum were detected in 18 of 92 patients (20%) and in 21 controls (21%). Other causes of uveitis were varicella zoster virus (one patient), herpes simplex virus (two patients), and HLA-B27 positive acute anterior uveitis with ankylosing spondylitis (one patient), while one patient had presumed HTLV-I uveitis. CONCLUSIONS: In a hospital population in Sierra Leone, west Africa, uveitis was associated with severe visual handicap and infectious diseases. Toxoplasmosis proved to be the most important cause of the uveitis. Although the distribution of congenital versus acquired toxoplasmosis in this population could not be determined, the results indicate an important role of postnatally acquired disease. The results further suggested minor roles for HIV, tuberculosis, toxocariasis, and sarcoidosis as causes of uveitis in this population.

Modeling studies of the concurrent growth and neutralization of sulfuric acid aerosols under conditions in the human airways.

A kinetic model of coupled droplet growth, gas uptake, and chemical reaction has been used to examine the possible changes to sulfuric acid aerosols as a result of exposure to respiratory ammonia under the conditions in the human airways. Results for a wide range of initial droplet sizes and concentrations spanning the extremes of likely atmospheric conditions are presented. It is predicted that gas phase reactions of SO2 will not significantly affect the neutralizing capability of airways ammonia. The effects of physical and chemical parameters on aerosol neutralization and growth are discussed and in particular, predictions of neutralization in typical inhalation times for aerosols characteristic of severe persistent London fogs and modern urban conditions are compared. The analysis supports the suggestion that the London fog episodes were unique in the relationship of the acid droplets formed to the neutralizing capability of ammonia in the human airways and that simple extrapolation of mortality and morbidity data from such episodes to modern conditions is unlikely to be valid.