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Association of house spraying with suppressed levels of drug resistance in Zimbabwe

Sungano Mharakurwa1,2 email, Susan L Mutambu3 email, Robert Mudyiradima4 email, Tawanda Chimbadzwa4 email, Steven K Chandiwana5 email and Karen P Day6 email

Department of Molecular Microbiology & Immunology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore MD 21205, USA

The Malaria Institute at Macha, P.O. Box 630166, Choma, Zambia

Blair Research Institute, P.O. Box CY 573, Causeway, Harare, Zimbabwe

Provincial Medical Director (Manicaland), 24 'C' Avenue, Box 323, Mutare, Zimbabwe

Postgraduate Studies School, Faculty of Health Sciences, The University of the Witwatersrand, 7 York Road, Parktown, 2193, Johannesburg, South Africa

Peter Medawar Building for Pathogen Research, Department of Zoology, South Parks Road, Oxford University, Oxford OX1 3SY, UK

author email corresponding author email

Malaria Journal 2004, 3:35doi:10.1186/1475-2875-3-35

Published: 18 October 2004

Abstract

Background

Public health strategies are needed to curb antimalarial drug resistance. Theoretical argument points to an association between malaria transmission and drug resistance although field evidence remains limited. Field observations, made in Zimbabwe, on the relationship between transmission and multigenic drug resistance, typified by chloroquine, are reported here.

Methods

Periodic assessments of the therapeutic response of uncomplicated falciparum malaria to chloroquine in two selectively sprayed or unsprayed health centre catchments, from 1995 – 2003. Cross-sectional analysis of in vivo chloroquine failure events for five sites in relation to natural endemicity and spraying history.

Results

During selective house spraying, the chloroquine failure rate for the sprayed catchment decreased, such that, after four years, the odds of chloroquine failure were 4× lower than before start of spraying in the area (OR 0.2, 95% CI 0.07 – 0.75, p = 0.010, n = 100). Chloroquine failure odds for the sprayed area became 4× lower than contemporaneous failure odds for the unsprayed area (OR 0.2 95% CI 0.08 – 0.65, p = 0.003, n = 156), although the likelihood of failure was not significantly different for the two catchments before selective spraying started (OR 0.5, 95% CI 0.21 – 1.32; p = 0.170, n = 88). When spraying ended, in 1999, the drug failure odds for the former sprayed area increased back 4 fold by 2003 (OR 4.2, 95%CI 1.49 – 11.78, p = 0.004, n = 146). High altitude areas with naturally lower transmission exhibited a 6× lower likelihood of drug failure than low-lying areas (OR 0.16 95% CI 0.068 – 0.353, -2 log likelihood change 23.239, p < 0.001, n = 465). Compared to sites under ongoing annual spraying, areas that were last sprayed 3–7 years ago experienced a 4-fold higher probability of chloroquine failure (OR 4.1, 95%CI 1.84 – 9.14, -2 log likelihood change 13.956, p < 0.001).

Conclusion

Reduced transmission is associated with suppressed levels of resistance to chloroquine and presumably other regimens with multigenic drug resistance. It seems the adoption of transmission control alongside combination chemotherapy is a potent strategy for the future containment of drug-resistant malaria.


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