Infectious diseases like tuberculosis, malaria and the human immunodeficiency virus are both preventable and curable but cause about half of the deaths in the developing world. They affect people in the prime of their productive lives, inflicting a very heavy impact on development, opportunities and livelihood. Poverty is the end result with an enormous toll on the economy of developing nations. As such, the community goes for the cheapest medications that work and therefore can report on the effectiveness of drugs as an effect of many activities upstream that cause parasite unresponsiveness to therapy. The aim of this study was to investigate the relationship between community auto-medication and molecular markers of drug resistance in malaria to detect and provide evidence for when the community feels a drug is not or no longer effective. This would propose a better management policy towards decreasing drug resistance. This would be achieved by promoting proper therapy-seeking habits and thus ensure a higher quality of life and a higher productive capacity of workers. A survey was first carried out in 8 localities to observe various aspects of therapy-seeking behaviour. The knowledge and practice of malaria management and prevention were quite poor, favouring the prevalence of drug resistant parasites. To establish an index for community-sensing of drug resistance, the prevalence of the mutation of the dhfr gene at position 108 in parasites was used in which Y = -2.5X + 48, where Y = prevalence of mutations (Pm) and X = level of self-prescription. This was confirmed by the extrapolation of the self-prescription of Fansidar (12%) against a value of 18%. This study shows that the therapy-seeking habits of a community can be used to demonstrate the prevalence of mutations to Fansidar and hence possibly to other antimalarial drugs presenting resistance.
Key words: Therapy-seeking behaviour, auto-medication, community-sensing, molecular markers, surveillance indicators, drug resistance.
AluI, Arthrobacter luteus I; ApoII, Arthrobacter protophormiae II; Bsr I, Bacillus stearothermophilus I; CDC, Centers for Disease Control and Prevention; CTE, Cameroon Tea Estate; dhfr, dihydrofolate reductase gene; DNA, deoxyribonucleic acid; dNTP, deoxynucleotide triphosphate; HaeIII, Haemophilus aegyptius III; HindIII, Haemophilus influenzae III; HIV, human immunodeficiency syndrome; P. falciparum, Plasmodium falciparum; PCR, polymerase chain reaction; PCR-RFLP, polymerase chain reaction-restriction fragment length polymorphism; Pfcrt, Plasmodium falciparum chloroquine resistance transporter gene; Pm, prevalence of mutations; PR, prevalence of resistance; RDT, rapid diagnostic tests; RFLP, restriction fragment length polymorphism; Taq, Thermophilus aquaticus; UV, ultraviolet; WBC, white blood cell; WHO, World Health Organization.