Parasitology
Bloodstream
Plasmodium ovale


Topic Completed: 1 December 2014

Revised: 4 February 2019

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PubMed Search: Plasmodium ovale[TI] free full text[sb]

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Cite this page: Fadel H. Plasmodium ovale. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/parasitologypovale.html. Accessed October 18th, 2019.
Definition / general
  • Four species of plasmodia causing human malaria are Plasmodium vivax, Plasmodium falciparum, Plasmodium malariae and Plasmodium ovale
Terminology
  • Malaria (from the Italian "mal' aria," meaning "bad air") is an acute and sometimes chronic infection of the bloodstream characterized clinically by fever, anemia and splenomegaly and is caused by apicomplexan parasites of the genus Plasmodium
Epidemiology
  • P. vivax and P. ovale are the least frequent of malaria species; most cases arise in Western Africa, India, South America
Pathophysiology / etiology
  • Spread exclusively by female anopheline mosquitoes
  • Fever paroxysm occurs over 6 - 10 hours and is initiated by the synchronous rupture of erythrocytes with the release of new infectious blood stage forms known as merozoites
  • P. vivax and P. ovale differ from P. falciparum and P. malariae in that true disease relapses of the former species may occur weeks to months following subsidence of previous attacks
  • Transfusion induced malaria may occur when blood donors have subclinical malaria and may prove fatal for the recipient
  • Similarly, congenital malaria may occur in infants born to mothers from endemic areas
  • Infant acquires the infection at birth due to rupture of placental blood vessels with maternal fetal transfusion
  • Liver cells are infected only by sporozoites from the mosquito; thus, transfusion acquired P. vivax or P. ovale infection does not relapse
  • Neither transfusion nor congenital malaria is expected to relapse because exoerythrocytic schizogony does not occur
Diagrams / tables

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Life cycle

Clinical features
  • Defining clinical features of a malarial attack or paroxysm consist of, in order, shaking chills, fever (up to 40° C or higher) and generalized diaphoresis, followed by resolution of fever
  • Involvement of the brain is known as cerebral malaria, in which the patient becomes disoriented, progressing to delirium, coma and often death
Diagnosis
  • Identification of malarial parasites on thin blood films requires a systematic approach
  • Three major factors should be considered: appearance of infected erythrocytes, appearance of parasites and stages found
  • Appearance of RBCs size: enlarged; maximum size may be 1.25 - 1.5 times normal red blood cell diameter; approximately 20% or more of infected red blood cells are oval or fimbriated (border has irregular projections)
  • Schüffner stippling: with all stages except early ring forms
  • Parasite cytoplasm: rounded, compact trophozoites; occasionally slightly ameboid; growing trophozoites have large chromatin mass
  • Appearance of parasite pigment: dark brown, conspicuous
  • Number of merozoites: 6 - 14; average is 8
  • Stages found in circulating blood: all stages
Laboratory
  • Laboratory evaluation of patients suspected of having malaria continues to rely on timely examination of thick and thin blood films to demonstrate the intraerythrocytic parasites
  • More advanced laboratory methods include acridine orange staining and detection of parasite specific DNA
Life cycle
  • Malarial parasites undergo a sexual phase (sporogony) in Anopheles mosquitoes that results in the production of infectious sporozoites, as well as an asexual stage (schizogony) in humans that results in the production of schizonts and merozoites
  • In the bloodstream, some merozoites eventually differentiate into gametocytes (gametogony), which when ingested by female anopheline mosquitoes, mature into male microgametes and female macrogametes
  • Fusion of a microgamete and a macrogamete results in the formation of the motile ookinete, which migrates to the outside of the stomach wall and forms an oocyst
  • Within the oocyst, numerous spindle shaped sporozoites are formed
  • Mature oocyst ruptures into the body cavity, releasing sporozoites, which then migrate through the tissues to the salivary glands, from which they are injected into the vertebrate host as the mosquito feeds
  • Time required for development in the mosquito ranges from 8 - 21 days
  • Sporozoites injected into the vertebrate host reach the hepatic parenchymal cells within minutes and initiate the proliferative phase known as exoerythrocytic schizogony
  • Release of merozoites from ruptured hepatic schizonts initiates the bloodstream infection or erythrocytic schizogony and eventually the clinical symptoms of malaria
  • P. vivax and P. ovale differ from P. falciparum and P. malariae in that true disease relapses of the former species may occur weeks to months following subsidence of previous attacks
  • This occurs as a result of renewed exoerythrocytic and eventually erythrocytic schizogony from latent hepatic sporozoites, which are known as hypnozoites
  • Recurrences of disease due to P. falciparum or P. malariae, called recrudescences, arise from increased numbers of persisting blood stage forms to clinically detectable levels, not from persisting liver stage forms
  • Liver cells are infected only by sporozoites from the mosquito; thus, transfusion acquired P. vivax or P. ovale infection does not relapse
  • Merozoites released from infected hepatocytes subsequently infect erythrocytes
  • Following amplification of parasites in the bloodstream for a period of time and the development of synchrony in their appearance, clinical attacks of malaria occur
  • P. vivax and P. ovale parasites primarily infect young erythrocytes, whereas P. malariae infects older erythrocytes and P. falciparum infects erythrocytes of all ages
  • Morphologic stages seen in erythrocytes include trophozoites (growing forms), schizonts (dividing forms) and gametocytes (sexual forms)
Case reports
Treatment
  • Chloroquine (or hydroxychloroquine) remains an effective choice for all P. vivax and P. ovale infections except for P. vivax infections acquired in Papua New Guinea or Indonesia
Clinical images

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Adult of Anopheles freeborni

Peripheral smear images

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Giemsa, P. ovale

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Wright-Giemsa

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