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Review
. 2004 Nov;48(11):4075-83.
doi: 10.1128/AAC.48.11.4075-4083.2004.

Chloroquine resistance in Plasmodium vivax

J Kevin Baird  1
Affiliations
Review

Chloroquine resistance in Plasmodium vivax

J Kevin Baird. Antimicrob Agents Chemother. 2004 Nov.
No abstract available

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Figures

FIG. 1.
FIG. 1.
Schematic representing the life cycle of plasmodia and the four families of antimalarial agents. Sporontocidal agents kill forms in the mosquito, including infectious sporozoites. Tissue schizonticides kill parasites developing (schizonts) or quiescent (hypnozoites) in the liver. Blood schizonticides kill the asexual blood forms (trophozoites and schizonts) that cause clinical malaria. The gametocytocides kill or sterilize the sexual forms (gametocytes) that infect mosquitoes.
FIG. 2.
FIG. 2.
The three paths to recurrent parasitemia for malarias caused by P. vivax and P. ovale. Sporozoites from mosquitoes reinfect the livers of humans, which yields merozoites that infect blood. Some sporozoites develop to quiescent hypnozoites in the liver and later cause relapse. Subpatent trophozoites in blood cells mature to schizonts that rupture and release merozoites that infect the blood and cause a recrudescence.
FIG. 3.
FIG. 3.
Cumulative incidence of relapses (left y axis) of P. vivax infections after blood schizonticidal therapy with quinine (solid points) or CQ (hollow points) during clinical trials conducted during the 1940s. Data were gathered from various sources (5, 33, 41, 58, 80, 92, 112, 114). The dotted curve represents hypothetical CQ drug levels (right y axis) declining to below the MEC of approximately 100 ng/ml, marked by the hashed line parallel to the x axis.
See this image and copyright information in PMC

References

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