Plasmodium ovale is a species of parasiticprotozoa that causes tertian malaria in humans. It is closely related to Plasmodium falciparum and Plasmodium vivax, which are responsible for most malaria. It is rare compared to these two parasites, and substantially less dangerous than P. falciparum.
P. ovale has recently been shown by genetic methods to consist of two species, P. ovale curtisi and P. ovale wallikeri.[1]
History
This species was first described by Stephens in a patient from East Africa in 1922.
The reported prevalence is low (<5%) with the exception of West Africa, where prevalences above 10% have been observed.
Clinical features
The prepatent period in the human ranges from 12 to 20 days. Some forms in the liver have delayed development and relapse may occur after periods of up to 4 years after infection.
The developmental cycle in the blood lasts approximately 49 h. An examination of records from induced infections indicated that there were an average of 10.3 fever episodes of > or = 101 degrees F and 4.5 fever episodes of > or = 104 degrees F. Mean maximum parasite levels were 6,944/microl for sporozoite-induced infections and 7,310/microl for trophozoite-induced infections.
Relapses may occur after periods of up to 4 years after infection.
Diagnosis
The microscopic appearance of P. ovale is very similar to that of P. vivax and if there are only a small number of parasites seen, it may be impossible to distinguish the two species on morphological grounds alone. There is no difference between the medical treatment of P. ovale and P. vivax, and therefore some laboratory diagnoses report "P. vivax/ovale", which is perfectly acceptable as treatment for the two are very similar. Schüffner's dots are seen on the surface of the parasitised red blood cell, but these are larger and darker than in P. vivax and are sometimes called "James's dots". About twenty percent of the parasitized cells are oval in shape (hence the species name) and some of the oval cells also have fimbriated edges (the so-called "comet cell"). The mature schizonts of P. ovale never have more than twelve nuclei within them and this is the only reliable way of distinguishing between the two species.
P. vivax and P. ovale that has been sitting in EDTA for more than half-an-hour before the blood film is made will look very similar in appearance to P. malariae, which is an important reason to warn the laboratory immediately when the blood sample is drawn so they can process the sample as soon as it arrives.
Among the species infecting the great apes, Plasmodium schwetzi morphologically appears to be the closest relation to P.ovale. This has yet to be confirmed with DNA studies. The original species has been shown to be two morphologically identical forms - Plasmodium ovale curtisi and Plasmodium ovale wallikeri - which can be differentiated only by genetic means.[11]Both species have been identified in Ghana, Myanmar, Nigeria, São Tomé, Sierra Leone and Uganda. The seperation of the lineages is estimated to have occurred between 1.0 and 3.5 million years ago in hominid hosts.
Life Cycle
Human Infection
Liver Stage
The P. ovale sporozoite enters a hepatocyte and begins its exoerythrocytic schizogony stage. This is characterized by multiple rounds of nuclear division without cellular segmentation. After a certain number of nuclear divisions, the parasite cell will segment and merozoites are formed.
There are situations where some of the sporozoites do not immediately start to grow and divide after entering the hepatocyte, but remain in a dormant, hypnozoite stage for weeks or months. The duration of latency is variable from one hypnozoite to another and the factors that will eventually trigger growth are not known; this explains how a single infection can be responsible for a series of waves of parasitaemia or "relapses".[12]
While similar to P. vivax, P. ovale is able to infect individuals who are negative for the Duffy blood group, which is the case for many residents of sub Saharan Africa. This explains the greater prevalence of P. ovale (rather than P. vivax) in most of Africa.
[14]
^Sutherland CJ, Tanomsing N, Nolder D, Oguike M, Jennison C, Pukrittayakamee S, Dolecek C, Hien TT, do Rosário VE, Arez AP, Pinto J, Michon P, Escalante AA, Nosten F, Burke M, Lee R, Blaze M, Otto TD, Barnwell JW, Pain A, Williams J, White NJ, Day NP, Snounou G, Lockhart PJ, Chiodini PL, Imwong M, Polley SD (2010). "Two nonrecombining sympatric forms of the human malaria parasite Plasmodium ovale occur globally". J Infect Dis. 201 (10): 1544–50. PMID20380562.((cite journal)): CS1 maint: multiple names: authors list (link)
^Cornu M, Combe A, Couprie B; et al. (1986). "[Epidemiological aspects of malaria in 2 villages of the Manyemen forest region (Cameroon, southwest province)]". Med Trop (Mars) (in French). 46 (2): 131–40. PMID3523108. ((cite journal)): Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
^Faye FB, Konaté L, Rogier C, Trape JF (1998). "Plasmodium ovale in a highly malaria endemic area of Senegal". Trans. R. Soc. Trop. Med. Hyg. 92 (5): 522–5. doi:10.1016/S0035-9203(98)90900-2. PMID9861368.((cite journal)): CS1 maint: multiple names: authors list (link)
^Snounou G, Viriyakosol S, Jarra W, Thaithong S, Brown KN (1993). "Identification of the four human malaria parasite species in field samples by the polymerase chain reaction and detection of a high prevalence of mixed infections". Mol. Biochem. Parasitol. 58 (2): 283–92. doi:10.1016/0166-6851(93)90050-8. PMID8479452. ((cite journal)): Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
^Cadigan FC, Desowitz RS (1969). "Two cases of Plasmodium ovale malaria from central Thailand". Trans. R. Soc. Trop. Med. Hyg. 63 (5): 681–2. doi:10.1016/0035-9203(69)90194-1. PMID5824291.
^Radloff PD, Philipps J, Hutchinson D, Kremsner PG (1996). "Atovaquone plus proguanil is an effective treatment for Plasmodium ovale and P. malariae malaria". Trans R Soc Trop Med Hyg. 90 (6): 682. doi:10.1016/S0035-9203(96)90435-6. PMID9015517.((cite journal)): CS1 maint: multiple names: authors list (link)
^Sutherland CJ, Tanomsing N, Nolder D, Oguike M, Jennison C, Pukrittayakamee S, Dolecek C, Hien TT, do Rosário VE, Arez AP, Pinto J, Michon P, Escalante AA, Nosten F, Burke M, Lee R, Blaze M, Otto TD, Barnwell JW, Pain A, Williams J, White NJ, Day NP, Snounou G, Lockhart PJ, Chiodini PL, Imwong M, Polley SD (2010). "Two nonrecombining sympatric forms of the human malaria parasite Plasmodium ovale occur globally". J Infect Dis 201 (10): 1544–1550.
