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10th Euro-Global Conference on Infectious Diseases

Rome, Italy

Anthony A Azenabor

Anthony A Azenabor

University of Wisconsin, USA

Title: Plasmodium falciparum treated with artemisinin-based combined therapy exhibits enhanced mutation, heightened cortisol and TNF-α induction

Biography

Biography: Anthony A Azenabor

Abstract

The artemisinin-based combined therapy (ACT) post-treatment illness in Plasmodium falciparum-endemic areas is characterized by vague malaria-like symptoms. The roles of treatment modality, persistence of parasites and host proinflammatory response in disease course are unknown. We investigated the hypothesis that ACT post-treatment syndrome is driven by parasite genetic polymorphisms and proinflammatory response to persisting mutant parasites. Patients were categorized as treated, untreated and malaria-negative. Malaria positive samples were analyzed for Pfcrt, Pfmdr1, K13 kelch gene polymorphisms, while all samples were evaluated for cytokines (TNF-α, IL-12p70, IL-10, TGF-β, IFN-γ) and corticosteroids (cortisol and dexamethasone) levels. The treated patients exhibited higher levels of parasitemia, TNF-α, and cortisol, increased incidence of parasite genetic mutations, and greater number of mutant alleles per patient. In addition, corticosteroid levels declined with increasing number of mutant alleles. TGF-β levels were negatively correlated with parasitemia, while IL-10 and TGF-β were negatively correlated with increasing number of mutant alleles. However, IL-12 displayed slight positive correlation and TNF-α exhibited moderate positive correlation with increasing number of mutant alleles. Since post-treatment management ultimately results in patient recovery, the high parasite gene polymorphism may act in concert with induced cortisol and TNF-α to account for ACT post-treatment syndrome. In conclusion, the ACT-meted-syndrome consists of post-treatment malaria-like-illness, enhanced genetic polymorphism in parasite that may not be effective phenotypes, and proinflammatory conditions accompanied by regulatory cytokine impairment.