Molecular surveillance of drug-resistance associated mutations of Plasmodium falciparum in south-west Tanzania

doi:10.1186/1475-2875-6-2

Malaria Journal

Volume 6

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Schönfeld M
Barreto Miranda I
Schunk M
Maduhu I
Maboko L
Hoelscher M
Berens-Riha N
Kitua A
Löscher T

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Schönfeld M
Barreto Miranda I
Schunk M
Maduhu I
Maboko L
Hoelscher M
Berens-Riha N
Kitua A
Löscher T
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Research

Molecular surveillance of drug-resistance associated mutations of Plasmodium falciparum in south-west Tanzania

Mirjam Schönfeld¹ , Isabel Barreto Miranda¹ , Mirjam Schunk¹ , Ibrahim Maduhu² , Leonard Maboko³ , Michael Hoelscher¹^,3 , Nicole Berens-Riha¹ , Andrew Kitua⁴ and Thomas Löscher¹

¹Department of Infectious Diseases and Tropical Medicine, Ludwig-Maximilians- University (LMU), Munich, Germany

²Department of Paediatrics and Child Health, Mbeya Referral Hospital, Tanzania

³Mbeya Medical Research Programme (MMRP), Mbeya, Tanzania

⁴National Institute for Medical Research (NIMR), Dar es Salaam, Tanzania

author email corresponding author email

Malaria Journal 2007, 6:2doi:10.1186/1475-2875-6-2


Published:	15 January 2007

Abstract

Background

In Tanzania, drug-resistant malaria parasites are an increasing public health concern. Because of widespread chloroquine (CQ) resistance Tanzania changed its first line treatment recommendations for uncomplicated malaria from CQ to sulfadoxine-pyrimethamine (SP) in 2001. Loss of SP sensitivity is progressing rapidly. SP resistance is associated with mutations in the dihydrofolate reductase (pfdhfr) and dihydropteroate synthase (pfdhps) genes.

Methods

In samples from 86 patients with uncomplicated Plasmodium falciparum malaria from Mbeya and Matema, Mbeya region, south-western Tanzania, the occurrence of mutations was investigated in the pfcrt and pfmdr1 genes which are associated with CQ resistance and in pfdhfr and pfdhps, conferring SP resistance, as well in cytb which is linked to resistance to atovaquone.

Results

Pfcrt T76 occurs in 50% and pfmdr1 Y86 in 51.7%. Pfdhfr triple mutations coexisting with pfdhps double mutations were detected in 64.3% of the P. falciparum isolates. This quintuple mutation is seen as a possible predictive molecular marker for SP treatment failure. Mutations of the cytb gene were not detected.

Conclusion

These findings of a high prevalence of mutations conferring SP resistance correspond to data of in vivo SP efficacy studies in other regions of Tanzania and underline the recommendation of changing first-line treatment to artemisinin-based combination therapy.