Plasmodium vivax infection

Mefloquine, a fluorinated derivative of 4-quinoline methanol, is a product of the US Army s antimalarial research program. It is active against chloroquine-resistant Plasmodium falciparum, and has an excellent schizonti-cidal effect in the blood in experimentally induced Plasmodium vivax infections in volunteers. It is not gametocidal. P. vivax infections can persist after successful treatment of the falciparum infection with other drugs the fact that mefloquine is effective against both organisms is thus of practical importance (SEDA-13, 808). 

Cavasini, C. E., Mattos, L. C., Couto, A. A., Bonini-Domingos, C. R., Valencia, S. FI., Neiras, W. C., Alves, R. T., Rossit, A. R., Castilho, L., and Machado, R. L. (2007). Plasmodium vivax infection among Duffy antigen-negative individuals from the Brazilian Amazon region An exception Trans. R. Soc. Trap. Med. Hyg. 101,1042-1044. 

Schmidt, L. H. (1978). Plasmodium falciparum and Plasmodium vivax infections in the owl monkey (Aotus trivirgatus). I. The courses of untreated infections. Am. ]. Trap. Med. Hyg. 27,671-702. 

Pamaquine was synthesized in 1952, this 8-aminoquinoline was the first drug capable of preventing the relapses in Plasmodium vivax malaria. Toxicological concerns led to restrictions in the use of Pamaquine. Primaquine another 8-aminoquinoline derivative has been used since 1950 s for the eradication of liver stages in course of Plasmodium vivax infections. 

Malaria is transmitted by the bite of an infected female Anopheles mosquito, one of the few species of the insect capable of carrying the human malaria parasite. The responsible protozoa ate from the genus P/asmodium of which only four of some 100 species can cause the disease in humans. The remaining species affect rodents, reptiles, monkeys, birds, and Hvestock. The species that infect humans are P/asmodium falciparum Plasmodium vivax Plasmodium malariae and Plasmodium ovale. Note that concomitant multiple malaria infections are commonly seen in endemic areas, a phenomenon that further compHcates choice of treatment. 

Plasmodium vivax, responsible for the most prevalent form of malaria (benign tertian), has an incubation period of 8—27 days (14 average). A variety seen in northern and northeastern Europe has an incubation period as long as 8—10 months. The disease can cause splenic mpture and anemia. Relapses (renewed manifestations of erythrocytic infection) can occur with this type of malaria. Overall, P. vivax is stiU susceptible to chloroquine however, resistant strains have been reported from Papua New Guinea and parts of Indonesia. Plasmodium malariae the cause of quartan malaria, has an incubation period of 15—30 days and its asexual cycle is 72 hours. This mildest form of malaria can cause nephritis in addition to the usual symptoms. It is a nonrelapsing type of malaria but the ted blood ceU infection can last for many years. No resistance to chloroquine by this plasmodium has been reported. Plasmodium ovale responsible for ovale tertian malaria, has an incubation period of 9—17 days (15 average). Relapses can occur in people infected with this plasmodium. No chloroquine resistance has been reported for this parasite. 

Craig, A.A. and Kain, K.C. (1996) Molecular analysis of strains of Plasmodium vivax from paired primary and relapse infections. Journal of Infectious Diseases 174, 373-379. 

Chloroquine is a rapidly acting blood schizonti-cide with some gametocytocidal activity. It is used with primaquine for Plasmodium vivax and Plasmodium ovale infections. It has been widely used prophylactically by traveler s to endemic areas. Its mechanism of action is unclear. It is believed to hinder the metabolism of hemoglobin in the parasite. Presumably chloroquine prevents the formation in the plasmodia of polymers out of free heme which then builds up and becomes toxic. Resistance occurs as a consequence of the expression of a membrane phospho-glycoprotein pump in the plasmodia which is able to expel chloroquine from the parasite. Plasmodium falciparum is the most likely to become resistant. 

Human malaria is caused by four species of Plasmodium namely Plasmodium falciparum, P. vivax, P. malariae and P. ovale. P. vivax is mainly responsible for most of the infections (70%) which results in benign tertian malaria. In P. falciparum and P. vivax infections, the patient has fever with rigors every third day and termed as tertian. The other two, P. ovale and P. malariae are mild in nature in which fever develops every fourth day and termed as benign quartan. Symptoms and complications in P. falciparum malaria are more severe than P. vivax malaria. 

Ling J et al Randomized, placebo-controlled trial of atovaquone/proguanil for the prevention of Plasmodium falciparum or Plasmodium vivax malaria among migrants to Papua, Indonesia. Clin Infect Dis 2002 35 825. [PMID 12228819]... 

Four principal species from the genus Plasmodium cause natural human infection Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, and Plasmodium falciparum. P. falciparum is the most lethal as it causes approximately 90% of malaria-related deaths (1). An additional species, Plasmodium knowlesi, which generally infects macaques, has also been shown increasingly to infect humans as well (4). As more sophisticated diagnostic tests are now able to easily distinguish one species of Plasmodium from another, it is thought that infection with P. knowlesi has heretofore been underreported because this species morphologically resembles other Plasmodium species in blood smears (5). 

The total dose of chloroquine base over 3 days should be approximately 25 mg/kg base. This is sufficient for Plasmodium malariae infection but, for Plasmodium vivax and Plasmodium ovale eradication of the hepatic parasites is necessary to prevent relapse, by giving ... 

Must reading are the papers of L. H. Schmidt summarizing his development of the owl monkey model for the evaluation of potential drugs against Plasmodium falciparum and P. vivax infections. ... 

Blood group antigen-bearing proteins also serve as receptors for infection agents (Table 10-7). A notable example is the presence of receptors in the Duffy blood group antigens to Plasmodium vivax and Plasmodium knowlesi. Individuals who do not express Duffy antigens are resistant to infection by these malarial parasites. 

The exact geographic distribution of the various species is not well documented however, it is reported that Plasmodium vivax is more prevalent in India, Pakistan, Bangladesh, Sri Lanka, and Central America, whereas P. falciparum is predominant in Africa, Haiti, Dominican Republic, the Amazon region of South America, and New Guinea. Both P. falciparum and P. vivax are prevalent in aU of Southeast Asia, South America, Middle East, North Africa, Ethiopia, Somalia, and Sudan. Most of the infections with P. ovale occur in Africa, and the distribution of P. malariae is considered worldwide. 

MALARIA is a disease mostly in tropical areas, where it is a major medical problem. Malaria is caused by a parasitic protozoa of the genus Plasmodium and is transferred when an infected female mosquito of the genus Anopheles bites a person and Plasmodium sporozoites enter the blood, where they first reach the liver and develop into merozoites over a period of 5-7 days without giving any symptoms. Then the immature merozoites penetrate the red blood corpuscles, where they divide asexually to form merozoites. When this process is complete, the blood corpuscles rupture and the merozoites enter the blood plasma. The rupture of the erythrocyte membrane provokes a fever, which occurs every second day after infection with Plasmodium vivax, every third after infection with Plasmodium malaria after infection with the severe Plasmodium falciparum fever is more irregular, because the parasites of this species do not develop simultaneously. 

Collins, W. E. (2002b). Nonhuman primate models. II. Infection of Saimiri and Aotus monkeys with Plasmodium vivax. Methods Mol. Med. 72,85-92. 

Hydroxychloroquine sulfate is a 4-aminoquinoline compound that interferes with parasitic nucleoprotein (DNA/ RNA) synthesis and parasite growth or causes lysis of parasite or infected erythrocytes. In rheumatoid arthritis, it may suppress formation of antigens responsible for symptom-producing hypersensitivity reactions. It is indicated for prophylaxis and treatment of acute attacks of malaria caused by Plasmodium vivax, Plasmodium malariae, and Plasmodium ovale, and susceptible strains of Plasmodium falciparum. It is also used for treatment of chronic discoid and systemic lupus erythematosus (SLE) and acute or chronic rheumatoid arthritis in patients not responding to other therapies. 

Clinical malaria is characterised by periodic fever, which follows the lysis of infected erythrocytes, and caused mainly by the induction of cytokines interleukin-1 and tumour necrosis factor. P. falciparum infection can have serious effects, for example anaemia, cerebral complications (from coma to convulsions), hypoglycaemia and glomerulonephritis. The disease is most serious in the non-immune, including children, pregnant women and tourists. Humans in endemic areas, who have survived an attack of malaria, are semi-immune and disease can be characterised by headache and mild fever. Infection by the other species of Plasmodium is normally self-limiting although relapses may occur, particularly in P. vivax infections. The species of parasite and the age and immune status of the patient are important in considerations of treatment and interpretation of the effects of all medicines. 

Plasmodium vivax (benign tertian) is the most prevaient form of malaria. It has an incubation period of 1 to 4 weeks (average, 2 weeks). This form of maiaria can cause spleen rupture and anemia. Reiapses (renewed manifestations of erythrocytic infection) can occur. This results from the periodic reiease of dormant parasites (hypnozoites) from the iiver cells. The erythrocytic forms generaiiy are considered to be susceptibie to treatment. 

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