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Volume 4
Journal of Infectious Diseases and Treatment
ISSN: 2472-1093
Page 16
Euro Infectious Diseases 2018 &
Histopathology 2018
September 27-29, 2018
&
JOINT EVENT
September 27-29, 2018 Rome, Italy
5
th
International Conference on
Histopathology & Cytopathology
10
th
Euro-Global Conference on
Infectious Diseases
Anthony A Azenabor et al., J Infec Dis Treat 2018, Volume 4
DOI: 10.21767/2472-1093-C1-002
Plasmodium falciparum treated with artemisinin-based combined therapy exhibits enhanced
mutation, heightened cortisol and TNF-α induction
Anthony A Azenabor
1
, Abel O. Idowu
12
, Nicole A. Dutton
1
, Maliha R. Ahmad
1
, Sanjib Bhattacharyya
3
, Steve Gradus
3
, Eldin Talundzic4, Naomi Lucci
4
,
Venkatachalam Udhayakumar
4
, Wellington Oyibo
2
, Zenas George
4
, Carolyn M. Black
4
and
Joseph U. Igietseme
4
1
University of Wisconsin, USA
2
University of Lagos, Nigeria
3
City of Milwaukee Health Department Laboratories, USA
4
National Centre for Emerging and Zoonotic Infectious Diseases, Centres for Disease Control and Prevention, USA
T
he 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 andmalaria-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.
Biography
Anthony A Azenabor is full professor at the University of Wisconsin-Milwaukee and an expert in Infection and Immunity, he has approached his research by
explaining the impact of infection on host immune system, relying on my knowledge of Molecular Biochemistry as a major tool. His current research is aimed
at providing greater insights into mechanisms involved in innate immune function during stimulation by both physiologic and infectious agents. His finding have
contributed to the concept that products of activation by therapeutic interventions and the infectious agents play combined roles in the activation, wholly or in part,
of host defence against pathogens and other challenges.
aazenabo@uwm.edu