General Characteristics

 P. malariae invades primarily the older RBCs, limiting the number of infected cells (see Tables 1 to 3, Figures 1 and 2). The incubation period between infection and symptoms may be much longer than that for P. vivax or P. ovale malaria, ranging from about 27 to 40 days. A regular periodicity is seen from the beginning, with a more severe paroxysm, including a longer cold stage and more severe symptoms during the hot stage. Collapse during the sweating phase is not uncommon.

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.)

A regular periodicity of 72 hours is seen from the beginning of the erythrocytic cycle. The infection may end with spontaneous recovery, or there may be a recrudescence or series of recrudescence (recurrence of symptoms) over many years. These patients are left with a latent infection and persisting low-grade parasitemia for many, many years. The RBCs tend to be normal to small (old RBCs), there is no true stippling, the RBCs may have fimbriated edges, the developing rings tend to demonstrate “band” forms, and the mature schizont contains an average of 6 to 12 merozoites.

Pathogenesis and Spectrum of Disease

 Proteinuria is common in P. malariae infections and may be associated with clinical signs of nephrotic syndrome. With a chronic infection, kidney problems result from deposition within the glomeruli of circulating antigen antibody complexes. A membrane proliferative type of glomerulonephritis is the most common lesion seen in quartan malaria. Because chronic glomerular disease associated with P. malariae infections is usually not reversible with therapy, genetic and environmental factors may play a role in the disease, as well. The patient may have a spontaneous recovery, or there may be a recrudescence or series of recrudescence over many years (>50 years). In these cases, patients are left with a latent infection and persisting low-grade parasitemia.

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