Plasmodium ovale

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. 

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. 

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). 

Plasmodium ovale—is a rare species. It can cause relapse and is generally seen in West Africa. 

These are usually due to Plasmodium vivax or less commonly to Plasmodium ovale or Plasmodium malar-iae the drug of choice is chloroquine, which should be given by mouth as follows ... 

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 ... 

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) ... 

Primaquine is mainly used to eradicate the exoerythro-cytic stages of Plasmodium vivax and Plasmodium ovale, which if untreated cause late relapse (SEDA-18, 287). There is growing concern about primaquine resistance in P. vivax (SEDA-21, 296). 

Baert, C. B., Deloron, P., Viscogliosi, E., Delgado-Viscogliosi, P., Camus, D., and Dive, D. (1999). Cloning and characterization of iron-containing superoxide dismutase from the human malaria species Plasmodium ovale, P. malariae and P. vivax. Parasitol. Res. 85,1018-1024. 

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. 

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. 

Chloroquine is an excellent suppressive agent for treating acute attacks of malaria caused by Plasmodium vivax and Plasmodium ovale. The drug also is effective for cure and as a suppressive prophylactic for the treatment of Plasmodium malariae and susceptible Plasmodium falciparum. 

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