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Malaria Plasmodium vivax

The causal organisms responsible for malaria belong to the genus plasmodium which is of the class of protozoa known as sporozoa. There are four different species which are accepted as being responsible for human malaria. These are Plasmodium malariae, the parasite of quartan malaria Plasmodium vivax, the parasite of benign tertian malaria, Plasmodium falciparum, the parasite of malignant or sub tertian malaria, and Plasmodium ovale, the parasite that causes a mild type of tertian malaria. [Pg.612]

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. [Pg.270]

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. [Pg.270]

Malaria For the suppressive treatment and treatment of acute attacks of malaria caused by Plasmodium vivax, P. malariae, P. ovale, and susceptible strains of P. falciparum. [Pg.2025]

Four species of plasmodium typically cause human malaria Plasmodium falciparum, P vivax, P malariae, and P ovale. A fifth species, P knowlesi, is primarily a pathogen of monkeys, but has recently been recognized to cause illness, including severe disease, in humans in Asia. Although all of the latter species may cause significant illness, P falciparum is responsible for the majority of serious complications and deaths. Drug resistance is an important therapeutic problem, most notably with P... [Pg.1117]

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]... [Pg.1143]

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). [Pg.206]

Chaudhuri, A., Polyakova, J., Zbrzezna, V., Williams, K., Gulati, S., and Pogo, A. O. (1993) Cloning of the gpD protein cDNA, the major subunit of the Duffy blood group system and the receptor for the Plasmodium vivax malaria parasite. Proc. Natl. Acad. Sci. USA 90, 10,793-10,797. [Pg.97]

Her hemoglobin level was 10.9 g/dL (moderately anemic), white blood cell count was 5200/p.L (normal), and her platelet count was 103,000/pL (the lower limit of normal for platelet count is 140,000/pL). Examination of a peripheral blood smear revealed clear evidence of malaria due to Plasmodium vivax (Figure A.4). [Pg.443]

Question A.7 In general, what are the drugs of choice for the treatment of malaria due to Plasmodium vivax ... [Pg.443]

Plasmodium vivax—is the most geographically widespread and the cause of the most malaria cases in the United States. This species produces less severe symptoms. Relapse is possible as well as the potential for chronic disease. [Pg.445]

Alphonse Laveran, a French Army physician working in North Africa in the 1880s, was the first to observe malarial parasites in human blood. Their mode of transmission was not understood, however, until Ronald Ross, a British medical officer in India, found the organisms within the bodies of Anopheles mosquitoes. Malaria is caused by four species of parasitic protozoa Plasmodium vivax, P. ovale, P. malariae, satid P. falciparum. These organisms have complex life cycles involving several different developmental stages in both human and mos-... [Pg.208]

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 ... [Pg.270]

Mefloquine (t) 21 d) is similar in several respects to quinine although it does not intercalate with plasmodial DNA. It is used for malaria chemoprophylaxis, to treat uncomplicated Plasmodium falciparum (both chloroquine-sensitive and chloroquine resistant) and chloroquine-resistant Plasmodium vivax malaria. Mefloquine is rapidly absorbed from the gastrointestinal tract and its action is terminated by metabolism. When used for prophylaxis, 250 mg (base)/week should be taken, commencing 1-3 weeks before entering and continued for 4 weeks after leaving a malarious area. It should not be given to patients with hepatic or renal impairment. [Pg.273]

Quartan malaria is caused by Plasmodium malariae (incubation period of 18-40 days), tertian malaria by Plasmodium vivax and Plasmodium ovale (incubation period of 10 to 18 days), and tropical malaria by Plasmodium falciparum (incubation period of 7 to 14 days) ... [Pg.489]

Alongside the well-known development of resistance by P. falciparum to chloroquine, the emergence of chloroquine-resistant Plasmodium vivax is now clear (SEDA-13, 801). An increased frequency of cerebral malaria appears to coincide with the growing emergence of the chloroquine-resistant strains in Francophone Africa. [Pg.727]

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. [Pg.2068]

Local transmission of Plasmodium vivax malaria—Virginia, 2002. MMWR 2002 51 921-923. [Pg.2076]

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. [Pg.117]

Malaria. Transient hepatic dysfunction commonly occurs in childhood malaria (P6). Patwari et al. (P6), who studied a group of 80 children with Plasmodium vivax malaria, claimed that serum alkaline phosphatase values were elevated in 46% of patients during the acute attack, with a return to normal within the ensuing 6 weeks. While several abnormalities of liver function have been reported in adult patients with malaria, hyperphosphatasemia has only rarely been observed (G16). Among 81 patients with either falciparum or vivax malaria studied by... [Pg.201]


See other pages where Malaria Plasmodium vivax is mentioned: [Pg.216]    [Pg.216]    [Pg.353]    [Pg.155]    [Pg.491]    [Pg.294]    [Pg.182]    [Pg.559]    [Pg.174]    [Pg.427]    [Pg.586]    [Pg.343]    [Pg.328]    [Pg.360]    [Pg.294]    [Pg.353]    [Pg.272]    [Pg.273]    [Pg.342]    [Pg.718]    [Pg.257]    [Pg.36]    [Pg.29]    [Pg.1]   
See also in sourсe #XX -- [ Pg.719 ]




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