General Characteristics

P. vivax infects only the reticulocytes; thus, the parasitemia is limited to approximately 2% to 5% of the available RBCs (Tables 1 to 3, Figures 1 and 2). Splenomegaly occurs during the first few weeks of infection, and the spleen will progress from being soft and palpable to hard, with continued enlargement during a chronic infection. If the infection is treated during the early phases, the spleen will return to its normal size. A secondary or dormant schizogony occurs in P. vivax and P. ovale, which remain quiescent in the liver. These resting stages have been termed hypnozoites.

Table1. Plasmodium spp.: Clinical Characteristics of the Five Human Infections

Table2. Plasmodia in Giemsa-Stained Thin Blood Smears

          Table2. Plasmodia in Giemsa-Stained Thin Blood Smears—cont’d

Table3. Malaria Characteristics with Fresh Blood or Blood  Collected Using EDTA with No Extended Lag Time*

Fig1. The morphology of malaria parasites. Plasmodium vivax: 1, Early trophozoite (ring form). 2, Late trophozoite with Schüffner’s dots (note enlarged red blood cell). 3, Late trophozoite with  ameboid cytoplasm (very typical of P. vivax). 4, Late trophozoite with  ameboid cytoplasm. 5, Mature schizont with merozoites (18) and  clumped pigment. 6, Microgametocyte with dispersed chromatin. 7,  Macrogametocyte with compact chromatin. Plasmodium malariae: 1, Early trophozoite (ring form). 2, Early trophozoite with thick cytoplasm. 3, Early trophozoite (band form). 4, Late trophozoite (band  form) with heavy pigment. 5, Mature schizont with merozoites (9)  arranged in rosette. 6, Microgametocyte with dispersed chromatin.  7, Macrogametocyte with compact chromatin. Plasmodium ovale: 1, Early trophozoite (ring form) with Schüffner’s dots. 2, Early trophozoite (note enlarged red blood cell). 3, Late trophozoite in red  blood cell with fimbriated edges. 4, Developing schizont with irregularly shaped red blood cell. 5, Mature schizont with merozoites (8)  arranged irregularly. 6, Microgametocyte with dispersed chromatin.  7, Macrogametocyte with compact chromatin. Plasmodium falciparum: 1, Early trophozoite (accolé or appliqué form). 2, Early trophozoite (one ring is in headphone configuration/double chromatin  dots). 3, Early trophozoite with Maurer’s dots. 4, Late trophozoite  with larger ring and Maurer’s dots. 5, Mature schizont with merozoites (24). 6, Microgametocyte with dispersed chromatin. 7, Macro gametocyte with compact chromatin. Note: Without the appliqué  form, Schüffner’s dots, multiple rings/cell, and other developing  stages, differentiation among the species can be difficult. It is  obvious that the early rings of all four species can mimic one another  very easily. Remember: One set of negative blood films cannot rule out a malarial infection. (Reprinted by permission of the publisher  from Garcia LS: Diagnostic medical parasitology, ed 5, Washington,  DC, 2007, Copyright by American Society for Microbiology.)

Fig2.  Morphology of malaria parasites. Column 1 (left to right): Plasmodium vivax (note enlarged infected RBCs). (1) Early trophozoite  (ring form) (note one RBC contains 2 rings—not that uncommon); (2) older ring, note ameboid nature of rings; (3) late trophozoite with  Schüffner’s dots (note enlarged RBC); (4) developing schizont; (5) mature schizont with 18 merozoites and clumped pigment; (6) microgametocyte with dispersed chromatin. Column 2: Plasmodium ovale (note enlarged infected RBCs). (1) Early trophozoite (ring form) with  Schüffner’s dots (RBC has fimbriated edges); (2) early trophozoite (note enlarged RBC, Schüffner’s dots, and RBC oval in shape); (3) late  trophozoite in RBC with fimbriated edges; (4) developing schizont with irregular-shaped RBC; (5) mature schizont with 8 merozoites arranged  irregularly; (6) microgametocyte with dispersed chromatin. Column 3: Plasmodium malariae (note normal or smaller than normal infected  RBCs). (1) Early trophozoite (ring form); (2) early trophozoite with thick cytoplasm; (3) late trophozoite (band form); (4) developing schizont;  (5) mature schizont with 9 merozoites arranged in a rosette; (6) microgametocyte with compact chromatin. Column 4: Plasmodium falciparum. (1) Early trophozoites (the rings are in the headphone configuration with double chromatin dots); (2) early trophozoite (accolé or  appliqué form); (3) early trophozoites (note the multiple rings/cell); (4) late trophozoite with larger ring (accolé or appliqué form); (5) crescent shaped gametocyte; (6) crescent-shaped gametocyte. Column 5: Plasmodium knowlesi—with the exception of image 5, these were photographed at a higher magnification (note normal or smaller than normal infected RBCs). (1) Early trophozoite (ring form); (2) early trophozoite  with slim band form; (3) late trophozoite (band form); (4) developing schizont; (5) mature schizont with merozoites arranged in a rosette;  (6) microgametocyte with dispersed chromatin. Note: Without the appliqué form, Schüffner’s dots, multiple rings per cell, and other devel oping stages, differentiation among the species can be very difficult. It is obvious that the early rings of all five species can mimic one another  very easily. Remember: One set of negative blood films cannot rule out a malaria infection. (From Garcia LS: Malaria Clin Lab Med 30:93 129, 2010,with permission. Column 5 courtesy CDC.)

After a few days of irregular periodicity, a regular 48-hour cycle is established. An untreated primary attack may last from 3 weeks to 2 months or longer. Over time, the paroxysms (symptomatic period) become less severe and more irregular in frequency and then cease altogether. In approximately 50% of patients infected with P. vivax, relapses occur after weeks, months, or even after 5 years or more. The RBCs tend to be enlarged (young RBCs), there may be Schüffner’s dots (exclusively found in P. vivax and P. ovale) after 8 to 10 hours, the developing rings are ameboid, and the mature schizont contains 12 to 24 merozoites (Figure 2 [3]).

Pathogenesis and Spectrum of Disease

 In patients who have never been exposed to malaria, symptoms such as headache, photophobia, muscle aches, anorexia, nausea, and sometimes vomiting may occur before organisms can be detected in the bloodstream. In other patients with prior exposure to the malaria, the parasites can be found in the bloodstream several days before symptoms appear.

Severe complications are uncommon in P. vivax infections, although coma and sudden death or other symptoms of cerebral involvement have been reported, particularly in patients with varying degrees of prima quine resistance. These patients can exhibit cerebral malaria, renal failure, circulatory collapse, severe anemia, hemoglobinuria, abnormal bleeding, acute respiratory distress syndrome, and jaundice. Acute cerebral malaria involves changes in mental status and if untreated may result in fatality within 3 days.

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