Info

Plasmodium vivax

Plasmodium malariae

Plasmodium falciparum

Plasmodium ovale

Persistence of exoerythrocytlc cycle

Yes

No

No

Yes

Relapses

Yes

No, but long-term recrudescences are recognized

No long-term relapses

Possible, but usually spontaneous recovery

Time of cycle

44-48 hr

72 hr

38-48 hr

48 h:

Appearance of parasitized red blood cells; size and shape

11/2 to 2 times larger than normal; oval to normal; may be normal size until ring fills V2 of cell

Normal shape; size may be normal or slightly smaller

Both normal

60% of cells larger than normal and oval; 20% have irregular, frayed edges

Schiiffner's dots (eosinophilic stippling)

Usually present in all cells except early ring forms

None

None; occasionally, commalike red dots are present (Maurer's dote)

Present in all stages, including early ring forms; dots may be larger and darker than in P. vivax

Color of cytoplasm

Decolorized, pale

Normal

Normal, bluish tinge at times

Decolorized, pale

Multiple rings/cell

Occasional

Rare

Common

Occasional

All developmental stages present in peripheral blood

All stages present

Ring forms few, as ring stage brief; mostly growing and mature trophozoites and schizonts

Young ring forms and no older stages; few gametocytes; rare mature schizonts

All stages present

Appearance of parasite; young trophozoite (early ring form)

Ring is Va diameter of cell, cytoplasmic circle around vacuole; heaw chromatin dot

Ring often smaller than in P. vivax, occupying' of cell; heavy chromatin dot vacuole at times "filled in"; pigment forms early

Delicate, small ring with small chromatin dot (frequently 2)*; scanty cytoplasm around small vacuoles; sometimes at edge of red blood cell (appliqué form) or filamentous slender form; may have multiple rings .srcell

Ring is larger and more ameboid than in P. vivax, otherwise similar to £ wax

Growing trophozoite

Multishaped, irregular ameboid parasite; streamers of cytoplasm close to large chromatin dot; vacuole retained until close to maturity; Increasing amounts of brown pigment

Non-ameboid rounded or band-shaped solid forms; chromatin may be hidden by coarse, dark brown pigment

Heavy ring forms; fine pigment grains

Ring shape maintained until late in development; non-ameboid compared to P.vivax

Mature trophozoite

Irregular ameboid mass; 1 or more small vacuoles retained until schizont stage; fills almost entire cell; fine, brown pigment

Vacuoles disappear early; cytoplasm compact, oval, band shaped, or nearly round almost filling cell; chromatin may be hidden by peripheral coarse, dark brown pigment

Not seen in peripheral blood (except in severe infections); development of ail phases following ring form occurs in capillaries of viscera

Compact vacuoles disappear; pigment dark brown, less than in P. malariae

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Schizont (presegmenter)

Progressive chromatin division; cytoplastic bands containing clumps of brown pigment

Similar to P vta except smaller; darker, larger pigment granules peripheral or central

Not seen in peripheral blood (see above)

Smaller and more compact than P. vivax

Mature schizont

Merozoites, 16 (12 to 24) each with chromatin and cytoplasm, filling entire red blood cell, which can hardly be seen

8 (6 to 12) merozoites in rosettes or irregular clusters filling normal-sized cells, which can hardly be seen; central arrangement of brown-green pigment

Not seen in peripheral blood; in rare cases may be seen

3/4 of cells occupied by 8 (8 to 12) merozoites in ' rosettes or irregular clustery I

ill

'If there is a lag time between blood collection (EOTA anticoagulant) and blood film preparation, P. falciparum rings may appear larger than normal.

Figure 49-49 Routine histology micrograph of microsporidian spores in enterocytes, stained with Giemsa stain. Left: Note the fully formed spores. Right: These spores are not fully mature.

Plasmodium ovale

Smaller than P. vivax titan P. vivax

Same as macrogametocyte (described above)

Red blood cell enlarged, oval, with fimbriated edges; Schiiffner's dots seen in all

Microgametocyte

Main criteria

Plasmodium vivax

Plasmodium malariae

Plasmodium ovale

Chapter 49 Laboratory Methods for Diagnosis of Parasitic Infections 603 Table 49-20 Plasmodia in Giemsa-Stained Thin Blood Films—cont'd

Macrogametocyte

Rounded or oval homogeneous cytoplasm; diffuse, delicate, light brown pigment throughout parasite; eccentric compact chromatin

Similar to P. vivax, but fewer in number, pigment darker and more coarse

Sex differentiation difficult; "crescent" or"sausage" shapes characteristic; may appear in "showers," black pigment near chromatin dot, which is often central

Smaller than P. vivax

Large pink to purple chromatin mass surrounded by pale or colorless halo; evenly distributed pigment

Similar to P. wax, but fewer in number, pigment darker and more coarse

Same as macrogametocyte (described above)

titan P. vivax

Large, pale red blood cell; trophozoite irregular; pigment usually present; Schiiffner's dots not always present; several phases of growth seen in one smear; gametocytes appear as early as third day

Red blood cell normal in size and color; trophozoites compact, stain usually intense, band forms not always seen; coarse pigment; no stippling of red blood cells; gametocytes appear after a few weeks

Development following ring stage takes place in blood vessels of internal organs; delicate ring forms and crescent-shaped gametocytes are only forms normally seen in peripheral blood; gametocytes appear after 7-10 days

Figure 49-49 Routine histology micrograph of microsporidian spores in enterocytes, stained with Giemsa stain. Left: Note the fully formed spores. Right: These spores are not fully mature.

The asexual and sexual forms circulate in the human bloodstream in three species. However in P. falciparum infections, as the parasite continues to grow, the RBC membrane becomes sticky, and the cells tend to adhere to the endothelial lining of the capillaries of the internal organs. Interference with normal blood flow in these vessels gives rise to additional problems, which are responsible for the different clinical manifestations of this type of malaria.

A number of genetic factors provide some resistance to the various Plasmodium spp. Hemoglobin S, thalassemia, and gIucose-6-phosphate dehydrogenase deficiency are associated with increased resistance to P. falciparum. Apparently, the Duffy-negative RBCs convey

Red blood cell enlarged, oval, with fimbriated edges; Schiiffner's dots seen in all

Figure 49-50 For legend see p. 605

- figura 49-50 The morphology of malaria parasites. Plasmodium vivox I, Early trophozoite (ring form). 2, Late trophozoite with gchuffner's dots (note enlarged red blood cell). 3, Late trophozoite with ameboid cytoplasm (very typical of P. vfww). 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 I Early trophozoite (ring fonn) with Schiiffner's dots. 2t 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 inegularly. 6, Microgametocyte with dispersed chromatin. 7, Macrogametocyte with compact chromatin. Plasmodium falciparum l. Early trophozoite (accolé or appliqué form). 2, Early trophozoite (one ring is in headphone configuration/double chromatin dots). 3, Earl y 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, Macrogametocyte with compact chromatin. Note: Without the appliqué form, Schiiffner'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 spedes can mimic one another very easily. Remember that one set of negative blood films cannot rule out a malarial infection. (Garcia LS: Diagnostic medical parasitology, ed 5, Washington, DC, 2007, Copyright by American Society for Microbiology.)

Figure 49-51 Life cycle of Plasmodium. (Modified from Wilcox A: Manual for the microscopical diagnosis of malaria in man, U.S. Public Health Service, Washington, DC, 1960. Illustration by Nobuko Kitamura.)

increased resistance to infection with P. vivax. Plasmodium spp. can be transmitted from shared needles, blood transfusions, and congenital infections. These former infections, as well as mosquito vectors, are still seen within the United States.1'10,18-23 The request for examination of blood flhns for parasites is always considered a STAT request.6'21

Babesiosis

Babesia are tickborne (they can also be transmitted via a blood transfusion or organ transplantation) sporozoan parasites that can cause disease in humans, especially in those who have been splenectomized or tend to be compromised for other reasons. However, immunocompetent persons can also become infected; several different Babesia species can be found within the United States.6,15 Babesia organisms infect the RBCs and appear as pleomorphic, ringlike structures when stained with any of the recommended stains used for blood films (Figure 49-53) (see also Tables 49-4 to 49-7). They may be confused with the ring forms in Plasmodium infections; however, in a Babesia infection, four or five rings

Figure 49-52 Plasmodium falciparum, early ring forms.

Figure 49-53 Babesia in red blood cells may be seen per RBC, and the individual rings are small and pleomoiphic compared with those found in malarial infections.

Hemoflagellates

Hemoflagellates are blood and tissue flagellates, two genera of which are medically important for humans: Leishmania and Trypanosoma (Figures 49-54 to 49-59) (see also Tables 49-4 to 49-7). Some species may. circulate in the bloodstream or at times may be present in lymph nodes or muscle. Other spedes tend to parasitize the reticuloendothelial cells of the hematopoietic

Figure 49-55 Leishmania donovani parasites in Kiipffer cells of liver (2000x).

Trypomastigote * «

Figure 49-54 Characteristic stages of species of Leishmania and Trypanosoma in human and insect hosts. (Illustration by Nobuko Kitamura.)

Promastigote

Figure 49-55 Leishmania donovani parasites in Kiipffer cells of liver (2000x).

organs. The hemoflagellates of humans have four morphologic types (see Figure 49-54): amastigote (leishmanial form, or Leishman-Donovan [L-D] body)-promastigote (leptomonal form), epimastigote (critbi-dial form), and trypomastigote (trypanosomal) form.

The amastigote form is an intracellular parasite in the cells of the reticuloendothelial system and is oval, measuring 1.5 to 5 jxm, and contains a nucleus and kinetoplast. Leishmania spp. exist as the amastigote form in humans and as the promastigote form in the insect host. The life cycle is essentially the same for all species; however, clinical symptoms vary. As the vector takes

Promastigote

Trypomastigote * «

Figure 49-54 Characteristic stages of species of Leishmania and Trypanosoma in human and insect hosts. (Illustration by Nobuko Kitamura.)

Figure 49-57 Trypanosoma gambiense in blood film.

blood meal, promastigotes are introduced into the human host, thus initiating the infection. Depending on the species, the parasites then move from the bite site to the organs within the reticuloendothelial system (bone marrow, spleen, liver) or to the macrophages of the skin or mucous membranes (see Figure 49-55).

Many strains make up the three main groups. L. tropica causes oriental sore or cutaneous leishmaniasis of the Old World, L. braziliensis causes mucocutaneous leishmaniasis of the New World, and L. donovani causes' visceral leishmaniasis (kala-azar) (see Figure 49-56).617 Diagnosis of leishmanial organisms is based on the

Figure 49-59 A, Trypanosoma cruzi in blood film (1600x). B, Trypanosoma cruzi parasites in cardiac muscle (2500x).

figun 19-58 Trypanosoma cruzi trypomastigote.

Figure 49-59 A, Trypanosoma cruzi in blood film (1600x). B, Trypanosoma cruzi parasites in cardiac muscle (2500x).

Humans

Adult worms In intestine

Taenia saginata \ Taenia solium

uncooked Taenia solium \ Cysticera beef no* Eggs/proglottids in muscle,

ir,9ested * ^^ Eggs ingested in muscle^ cattle, pigs by humans

Figure 49-60 Life cycle of Taenia saginata and Taenia solium.

Adult worms have matured in intestine.

Ingested by Eggs/proglottids definitive host (dog) infeces

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