Parasitology
Bloodstream
Plasmodium vivax


Topic Completed: 1 December 2014

Revised: 4 February 2019

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PubMed Search: Plasmodium vivax[TI] free full text[sb] pathology

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Cite this page: Fadel H. Plasmodium vivax. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/parasitologymalariapvivax.html. Accessed November 17th, 2019.
Definition / general
  • Four species of plasmodia causing human malaria are Plasmodium vivax, Plasmodium falciparum, Plasmodium malariae and Plasmodium ovale
  • 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
  • P. vivax infections occur in both tropical and temperate zones, between 45° N and 40° S (WHO: Malaria [Accessed 10 January 2018])
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
  • 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; the infant acquires the infection at birth due to rupture of placental blood vessels with maternal fetal transfusion
  • Neither transfusion nor congenital malaria is expected to relapse because exoerythrocytic schizogony does not occur
  • Persons who lack certain Duffy blood group determinants are protected against P. vivax infection
Diagrams / tables

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Fever paroxysm

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Life cycle

Clinical features
  • In the early stages of the disease, febrile episodes occur irregularly but eventually become more synchronous, assuming the usual tertian (P. vivax, P. falciparum and P. ovale) or quartan (P. malariae) periodicity
  • Patients with malaria may develop anemia and may have other manifestations, including diarrhea, abdominal pain, headache and muscle aches and pains
  • Patients with P. vivax or P. ovale infection may have relapses after many months or years
Diagnosis
  • Growing trophozoites of P. vivax have irregular shapes and are termed ameboid
  • 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
    • Stages found
  • P. vivax and P. ovale parasites primarily infect young erythrocytes, whereas P. malariae infects older erythrocytes and P. falciparum infects erythrocytes of all ages
  • Appearance of RBC and size:
    • Enlarged
    • Maximum size (attained with mature trophozoites and schizonts); may be up to 2x normal erythrocyte diameter
  • Schüffner stippling: Maurer dots (comma shaped spots, dark blue by Giemsa staining, on RBC surface) are seen with all stages except early ring forms
  • Parasite cytoplasm:
    • Irregular
    • Ameboid in trophozoites
    • Has "spread out" appearance
  • Appearance of parasite pigment: golden brown, inconspicuous
  • Number of merozoites: 12 - 24; average is 16
  • Stages found in circulating blood: all stages; wide range of stages may be seen on any given film
Laboratory
  • Laboratory evaluation relies on timely examination of thick and thin blood films to demonstrate the intraerythrocytic parasites
  • More advanced laboratory methods, including acridine orange staining and detection of parasite specific DNA
Life cycle
  • Morphologic stages seen in erythrocytes include trophozoites (growing forms), schizonts (dividing forms) and gametocytes (sexual forms)
  • Malarial parasites undergo a sexual phase (sporogony) in Anopheles mosquitoes that produces infectious sporozoites and an asexual stage (schizogony) in humans that produces 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 mosquito 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 due to renewed exoerythrocytic and eventually, erythrocytic schizogony from latent hepatic sporozoites, which are known as hypnozoites
  • Recurrence 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. falciparum infects erythrocytes of all ages; P. vivax and P. ovale parasites primarily infect young erythrocytes; P. malariae infects older erythrocytes
Prognostic factors
  • Persons who lack certain Duffy blood group determinants are protected against P. vivax infection
  • Glucose-6-phosphate dehydrogenase (G6PD) deficiency has been associated with protection from malaria but evidence is less striking than with these other genetic abnormalities
Mixed infections
  • ~5% of infections are mixed but diagnosis requires definite evidence of 2 separate populations of parasites
  • Most common mixed infections are P. falciparum and P. vivax
  • Finding gametocytes of P. falciparum in a person obviously infected with P. vivax is diagnostic
Case reports
Treatment
  • Chloroquine remains the treatment of choice for vivax malaria, except in Indonesia's Irian Jaya (Western New Guinea) region and the geographically contiguous Papua New Guinea, where chloroquine resistance is common (up to 20% resistance) (Curr Opin Infect Dis 2009;22:430)
  • Chloroquine resistance is an increasing problem in other parts of the world, such as Korea and India
  • When chloroquine resistance is common or when chloroquine is contraindicated, then artesunate is the drug of choice, except in the U.S., where it is not approved for use
Clinical images

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Adult of Anopheles freeborni

Peripheral smear images

Contributed by Dr. M. E. de Baca, South Dakota

16 year old Caucasian girl, infected despite prophylaxis on vacation in Belize:
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Immature trophozoite (ring) forms

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Immature trophozoite (ring) forms


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Gametocyte forms

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Gametocyte forms


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Gametocyte forms

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Gametocyte forms


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Schizont forms

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Schizont forms

Differential diagnosis
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