Parasitology

Research Article

Characterization and application of multiple genetic markers for Plasmodium malariae

M. C. BRUCEa1 c1, A. MACHESOa2, M. R. GALINSKIa3 and J. W. BARNWELLa4

a1 Division of Infection and Immunity, Institute of Biomedical and Life Sciences, Glasgow Biomedical Research Centre, Glasgow University, 120 University Place, Glasgow G12 8TA, UK

a2 Ministry of Health and Population, Government of Malawi, currently at Management Sciences for Health Malawi Program, Lilongwe

a3 Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, 938 Gatewood Road, Atlanta, Georgia, USA

a4 Malaria Laboratory Research and Development Unit, Malaria Branch, Division of Parasitic Diseases, Centers for Disease Control and Prevention, 4077 Buford Highway, NE, Atlanta, Georgia 30341, USA

SUMMARY

Plasmodium malariae, a protozoan parasite that causes malaria in humans, has a global distribution in tropical and subtropical regions and is commonly found in sympatry with other Plasmodium species of humans. Little is known about the genetics or population structure of P. malariae. In the present study, we describe polymorphic genetic markers for P. malariae and present the first molecular epidemiological data for this parasite. Six microsatellite or minisatellite markers were validated using 76 P. malariae samples from a diverse geographical range. The repeat unit length varied from 2 to17 bp, and up to 10 different alleles per locus were detected. Multiple genotypes of P. malariae were detected in 33 of 70 samples from humans with naturally acquired infection. Heterozygosity was calculated to be between 0·236 and 0·811. Allelic diversity was reduced for samples from South America and, at some loci, in samples from Thailand compared with those from Malawi. The number of unique multilocus genotypes defined using the 6 markers was significantly greater in Malawi than in Thailand, even when data from single genotype infections were used. There was a significant reduction in the multiplicity of infection in symptomatic infections compared with asymptomatic ones, suggesting that clinical episodes are usually caused by the expansion of a single genotype.

(Received October 08 2006)

(Revised October 15 2006)

(Accepted October 16 2006)

(Online publication December 04 2006)

Correspondence:

c1 *Corresponding author: Division of Infection and Immunity, Institute of Biomedical and Life Sciences, Glasgow Biomedical Research Centre, Glasgow University, 120 University Place, Glasgow G12 8TA, UK. Tel: +0141 330 2829. Fax: +0141 330 4600. E-mail: m.bruce@bio.gla.ac.uk

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