Description:

Malaria persists at low levels on Zanzibar despite the use of vector control and case management. We use a met population model to investigate the role of human mobility in malaria persistence on Zanzibar, and the impact of reactive case detection. The model was parameterized using survey data on malaria prevalence, reactive case detection, and travel history. We find that in the absence of imported cases from mainland Tanzania, malaria would likely cease to persist on Zanzibar. We also investigate potential intervention scenarios that may lead to elimination, especially through changes to reactive case detection. While we find that some additional cases are removed by reactive case detection, a large proportion of cases are missed due to many infections having a low parasite density that go undetected by rapid diagnostic tests, a low rate of those infected with malaria seeking treatment, and a low rate of follow up at the household level of malaria cases detected at health facilities. While improvements in reactive case detection would lead to a reduction in malaria prevalence, none of the intervention scenarios tested here were sufficient to reach elimination. Imported cases need to be treated to have a substantial impact on prevalence.

A young male returned from the Democratic Republic of the Congo (DRC) to India after four months during his official work. Within a week of his arrival, he developed a high-grade fever with nausea and was hospitalized in a private hospital in New Delhi. He was diagnosed with malaria, treated with an artesunate injection as antimalarial, and discharged on day 5th from the hospital. A week later, he was diagnosed with malaria and dengue positive at ICMR-National Institute of Malaria Research, New Delhi. Artesunate with sulphadoxine and pyrimethamine (AS+SP) was administered following India's malaria treatment policy. However, high-grade fever, along with the asexual stage of the P. falciparum parasite, was observed within 28 days of treatment with AS+SP, signifying late treatment failure (LTF). Further, the molecular analysis from both the days of episodes was analyzed using genomic DNA from dried blood spots, revealing resistance to sulphadoxine-pyrimethamine with mutations at codons pfdhfr 51I, pfdhfr 59 R, pfdhfr 108 N, pfdhps 437 A, pfdhps 581 G. No functional mutation associated was found in pfKelch13, but interestingly the sensitive codons to chloroquine (CQ) (wild type pfcrtK76 and pfmdrN86) revealed the probably reversible CQ sensitivity in the sample from DRC. Malaria infection can result in distinct clinical outcomes from asymptomatic to severe. The association between patho-physiological changes and molecular changes in the host, and their correlation with severity of malaria progression is not fully understood.

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Johnson
Journal Coordinator
Global Journal of Research and Review