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Spread of anti-malarial drug resistance: Mathematical model with implications for ACT drug policies

Pongtavornpinyo, W., Yeung, S., Hastings, Ian, Dondorp, A. M., Day, N. P. J. and White, N. J. (2008) 'Spread of anti-malarial drug resistance: Mathematical model with implications for ACT drug policies'. Malaria Journal, Vol 7, p. 229.

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Abstract

Background: Most malaria-endemic countries are implementing a change in anti-malarial drug policy to artemisinin-based combination therapy ( ACT). The impact of different drug choices and implementation strategies is uncertain. Data from many epidemiological studies in different levels of malaria endemicity and in areas with the highest prevalence of drug resistance like borders of Thailand are certainly valuable. Formulating an appropriate dynamic data-driven model is a powerful predictive tool for exploring the impact of these strategies quantitatively.
Methods: A comprehensive model was constructed incorporating important epidemiological and biological factors of human, mosquito, parasite and treatment. The iterative process of developing the model, identifying data needed, and parameterization has been taken to strongly link the model to the empirical evidence. The model provides quantitative measures of outcomes, such as malaria prevalence/incidence and treatment failure, and illustrates the spread of resistance in low and high transmission settings. The model was used to evaluate different anti-malarial policy options focusing on ACT deployment.
Results: The model predicts robustly that in low transmission settings drug resistance spreads faster than in high transmission settings, and treatment failure is the main force driving the spread of drug resistance. In low transmission settings, ACT slows the spread of drug resistance to a partner drug, especially at high coverage rates. This effect decreases exponentially with increasing delay in deploying the ACT and decreasing rates of coverage. In the high transmission settings, however, drug resistance is driven by the proportion of the human population with a residual drug level, which gives resistant parasites some survival advantage. The spread of drug resistance could be slowed down by controlling presumptive drug use and avoiding the use of combination therapies containing drugs with mismatched half-lives, together with reducing malaria transmission through vector control measures.
Conclusion: This paper has demonstrated the use of a comprehensive mathematical model to describe malaria transmission and the spread of drug resistance. The model is strongly linked to the empirical evidence obtained from extensive data available from various sources. This model can be a useful tool to inform the design of treatment policies, particularly at a time when ACT has been endorsed by WHO as first-line treatment for falciparum malaria worldwide.

Item Type: Article
Uncontrolled Keywords: plasmodium-falciparum parasitemia combination therapy malaria parasites treatment failure clinical malaria south-africa transmission children age thailand
Subjects: QV Pharmacology > Drug Standardization. Pharmacognosy. Medicinal Plants > QV 771 Standardization and evaluation of drugs
QW Microbiology and Immunology > Immune Responses > QW 700 Infection. Mechanisms of infection and resistance.
WC Communicable Diseases > Tropical and Parasitic Diseases > WC 750 Malaria
QX Parasitology > Insects. Other Parasites > QX 650 Insect vectors
WB Practice of Medicine > Therapeutics > WB 330 Drug therapy
QX Parasitology > Protozoa > QX 135 Plasmodia
QW Microbiology and Immunology > QW 45 Microbial drug resistance. General or not elsewhere classified.
QX Parasitology > Insects. Other Parasites > QX 600 Insect control. Tick control
QX Parasitology > QX 45 Host-parasite relations
QX Parasitology > Insects. Other Parasites > QX 510 Mosquitoes
Faculty: Department: Groups (2002 - 2012) > Molecular & Biochemical Parasitology Group
Digital Object Identifer (DOI): https://doi.org/10.1186/1475-2875-7-229
Depositing User: Mary Creegan
Date Deposited: 16 Jun 2010 14:52
Last Modified: 06 Feb 2018 13:00
URI: http://archive.lstmed.ac.uk/id/eprint/896

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