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Does Pneumocystis carinii occur in Kenya?

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Page 1: Does Pneumocystis carinii occur in Kenya?

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TRANSAC~~NS OF THE ROYAL SOCIETY OF TROPICAL. MEDICINE AND HYGIENE, VOL. 76, No. 2, 1982

Does Pneumocystis carinii occur in Kenya?

LESLEY GRIFFIN’ AND S. B. LUCAS’

‘Dept. of Medical Microbiology and 2Dept. of Pathology, Unjversity of Nairobi, Box 30588, Nairobi, Kenya

Summary An experiment was carried out exposing immuno-

suppressed mice to the atmosphere to determine if transmission of Pneumocystis car&ii occured in Kenya. Mice were killed at weekly intervals for four months and the lungs examined histologically for the presence of these parasites. None of the mice contracted even light infections and this, together with the lack of clinical evidence of this disease in immunosuppressed or neonatal cases, suggests that this parasite does not occur in Kenya. Possible reasons for this are dis- cussed.

Introduction Pneumocystis~caritii is an important complication in

infants and immunosuppressed patients, usually pro- ducing an interstitial pneumonia. Experimentally the infection has been produced in laboratory rats and mice treated with cortisone (WALZER et hl., 1979; VOSSEN et al.. 1978; MASUR & TONES. 1978). and latent P. car&ii has been found in a variety of wild mammals including rats, shrews and ferret badgers (CROSS & HUNG. 1975) foxes. monkevs and rabbits. Administration of cortisone is thought to activate a latent infection already present in the host (FRENKEL et al., 1966).

Although the exact mode of transmission of P. carinii is unclear, presumptive evidence suggests that inhalation of the spores in droplets of moisture is the most likely. Thus, two reports described the sequen- tial develonment of the disease in immunosuunressed patients occupying adjoining beds in hospii$ (RUS- KIN 81 REMINGTON, 1967; BRAZINSKY & PHILIPS, 1969) and another describes the infection in three members of a single family in which one member suffered from leukaemia (WATANABE et al., 1965).

The parasite appears to be ubiquitous in nature as the distribution of human cases is worldwide. In Africa the disease has been reported from Nigeria (ABIOYE, 1967), Congo (THUS & JANSSENS, 1963) and South Africa (PEPLER, 1958). However, as yet there are no reports of P. cur&ii occuring in Kenya. At Kenyatta National Hospital in Nairobi about 50 cancer patients are being treated with immunosup- pressive regimes at any one time. About 50 such patients are autopsied annually. Further, about 150 neonates and infants are examined post mortem each year. None the less, in spite of careful histological examination of the lungs, P. carinii has never been observed. Each year about six to eight sputum samples from patients with pneumonia thought to be due to P. car&ii are examined in the parasitology section but all have been negative.

An experiment was therefore done following the procedure described by WALZER et al. (1979), using immunosuppressed mice to determine if the spores of

P. carinii occur naturally in the atmosphere at a level likely to be transmitted by inhalation to suitable susceptible hosts.

Method 80 female brown C.B.A. outbred mice were

housed, six to a cage, in standard cages in a room open to the air and used by other investigators. The mice were fed on proprietary mouse pellets and given water to which 1 mg/ml tetracycline was added. Each animal was treated twice weekly with subcutaneous injections of 1 mg hydrocortisone succinate. After one month five animals were killed each week and the lungs examined histologically for the presence of P. carinii. After three months the cortisone dose was doubled on the remaining animals for the last month, by which time all the animals had been killed.

Results No infections of P. carinii were observed in the

lungs of any of the 80 mice examined, even in those on high doses of cortisone and left exposed for four months. Atrophy of lymph nodes and thymus, and stunting of growth in the mice, indicated that the animals were immunosuppressed.

Discussion All eight strains of immunosuppressed mice used

by WALZER et al. (1979) became infected with P. curinii, to varying degrees depending on the strain. The drug regime and maintenance of the mice in this study were the same as those described by Walzer and his co-workers. However, the failure of any of the immunosuppressed mice to contract even light infec- tions, together with the absence of clinical or histo- pathological evidence of natural infections suggests that P. cur&ii is not present in Kenya. If this is so, the obvious question is why it is absent in Kenya and, indeed, why there are so few reports of the disease from Africa. Speculation may suggest that climatic factors could be important in the transmission of the disease or indeed that transmission other than by inhalation of spores in droplets of moisture may occur. It has been suggested that Pneumocystis pneumonia may be a zoonotic disease and that domestic pets may act as a reservoir of infection (RUSKIN, 1976). Indeed most of the reports come from Europe or America where pets are often an integral part of the family group-and live in close nroximitv to the members of the familv. It is nossible ihat the &e-cycle and transmission of fi. cur&i would bear closer investigation than has hitherto been carried out.

Page 2: Does Pneumocystis carinii occur in Kenya?

LESLEY GRIFFIN AND S. B. LUCAS 199

Acknowledgement The authors are grateful to the Director of the

Wellcome Trust Laboratories for providing the ex- perimental mice and maintenance facilities, and for supplying the drugs.

References Abioye, A. A. (1967). Interstitial plasma cell pneumo-

ma (Pneumocystis cat&ii) in Ibadan. West African Medical 30urna1, 16, 130.

Brazinsky, J. H. & Philips, J. E. (1969). Pneumo- cystis pneumonia transmission between patients with lymphoma (Correspondence). Journal of the American Medical Association, 209, 1527.

Cross, J. H. & Hung, C. K. (1975). Latent Pneutno- cystis carinii infection in some mammals from Tapei Hsien, Taiwan. Journal of the Formosan Medical Association, 74, 564-567.

Frenkel, J. K., Good, J. T. & Schultz, J. A. (1966). Latent Pneumocystis infection of rats, relapse and chemotherapy. Laboratory Investigatzon, 15, 1559- 1577.

Masur, H. & Jones, T. C. (1978). The interaction in vitro of Pneumocystis car&ii with macrophages and L-cells. Journal of Experimental Medicine, 147, 157-170.

Pepler, W. J. (1958). Pneumocystis pneumonia. South African Medical Journal, 32, 1003.

Ruskin, J. (1976). Pneumocystis car&ii. In: “Infec- tious Diseases of the Fetus and the Newborn Infant”. Remmington & Klein. (Editors) London: Saunders, Chap. 16, p. 701.

Ruskin, J. & Remmington, J. S. (1967). The compromised host and infection. I. Pneumocystis carinii, pneumonia. Journal of the American Medi- cal Association, 102, 1070.

Thijs, A. & Jansens, P. G. (1963). Pneumocytosis in Congolese infant. Tropical and Geographical Medi- cine, 15, 158.

Vossen, M. E. M. H., Beckers, P. J. A., Meuwissen, J. H. E. T. & Stadhoulders, A. M. (1978). Developmental biology of Pneumocystis carinii, an alternative view on the life cycle of the parasite. Zeitschrtft ,fur Parasitenhunde, 55, 101-l 18.

Walzer, P. D., Powell, R. D. & Yoned, K. (1979). Experimental Pneumocystis carinii pneumonia in different strains of cortizonised mice. Infection and Immunity, 24, 939-947.

Watanabe, J. M., Chinchinian, H., Weitz, C. & McIlvanie, S. K. (1965). Pneumocystis carinii pneumonia in a family. Journal of the American Medical Association, 193, 685.

Accepted for publication 7th August, 1981.