Differences Between Plasmodium vivax And falciparum


Plasmodium vivax 

Plasmodium vivax is a protozoalparasite and a human pathogen. This parasite is the most frequent and widely distributed cause of recurring malaria. Although it is less virulent than Plasmodium falciparum, the deadliest of the five human malaria parasites, P. vivax malaria infections can lead to severe disease and death, often due to splenomegaly (a pathologically enlarged spleen). P. vivax is carried by the female Anopheles mosquito.

P. vivax are parasites found inhabiting the liver and blood of humans, and salivary glands of mosquitoes at various stages of development and shape. Starting as rings within red blood cells, then trophozoites as they develop within the red blood cells. Next, they form round gametocytes filling the red blood cells and schizonts which are elongated and wormlike, further filling out the red blood cells. Red blood cells infected by P. vivax cause swelling of the cell, increasing the size by approximately 1.5 times the normal size of red blood cells.

Plasmodium falciparum

Plasmodium falciparum is a unicellular protozoan parasite of humans, and the deadliest species of Plasmodium that causes malaria in humans. The parasite is transmitted through the bite of a female Anophelesmosquito and causes the disease’s most dangerous form, falciparum malaria. It is responsible for around 50% of all malaria cases. P. falciparum is therefore regarded as the deadliest parasite in humans, causing 405,000 deaths in 2018. 

Differences Between Plasmodium vivax And Plasmodium falciparum In Tabular Form

NumberElements of ComparisonPlasmodium vivaxPlasmodium falciparum
1.Disease CausedBenign tertian malariaMalignant tertian malaria
2.Geographic areaTropics, Africa (rare in West Africa), Middle East, Asia, Central and South America. It is the most common geographically widespread species of Plasmodium causing malaria in human beings.Predominant species, worldwide tropics, but especially sub-Saharan Africa.
3.Type of RBC invadedPrimarily invades reticulocytes, young red cells.Invades all red cells regardless of age.
4.Parasitized red cellsEnlarged, pale. Fine stippling (Schüffner dots).Not enlarged. Coarse stippling (Maurer’s clefts).
5.Color of cytoplasm ( in Giemsa stained thin blood smear)Decolorized, pale.Normal, bluish tinge at times.
6.Level of usual maximum parasitemiaUp to 30,000/μL of bloodMay exceed 200,000/μL;commonly 50,000/μL
7.No. of merozoites released per infected hepatocyte30,00010,000
8.Ring stagetrophozoitesLarge rings (1/3–1/2 red cell diameter). Usually one chromatin granule; ring delicate.Small rings (1/5 red cell diameter). Often two granules; multiple infections common; ring delicate, may adhere to red cells.
9.Pigment in developing trophozoitesFine; light brown; scatteredCoarse; black; few clumps
10.Late TrophozoiteMedium SizedRarely amoeboidVacuole inconspicuous.LargeMarkedly amoeboidVacuole prominent.
11.Late trophozoite shapeVery pleomorphicCompact and rounded
12.SchizontSmall, compact,Single pigmented massSeldom seen in the peripheral blood smearLarge, amoeboid,Pigments coarseCan be seen in the blood smear
13.Mature schizonts (segmenters)More than 12 merozoites (14–24)Usually more than 12 merozoites (8–32). Very rare in peripheral blood.
14.GametocytesRound or ovalCrescentic
15.MicrogametocytesKidney-shaped with blunt round ends.Cytoplasm stains pale blue.Nucleus large.Chromatin diffuse.Granules fine, scattered.Spherical, compact.Cytoplasm stains pale light blue.Chromatin undivided.Granules abundant.
16.MacrogametocytesCrescentic.Cytoplasm stains dark blue.Nucleus compact.Chromatin central.Pigment more compact.Spherical.Cytoplasm stains dark blue.Nucleus small.Pigment diffuse ecoarse.
17.Distribution in peripheral bloodAll formsOnly rings and crescents (gametocytes).
18.Duration of asexual phase in man36-48 hrsUsually 48 hrs48 hrs
19.Duration of sporogony in mosquito22-23 days at 20°C10-12 days at 27°C30 days at 17.5°C10 days at 25-30°C
20.Duration of intrahepatic phase5.5 days8 days
21.Duration of Schizogony12 days14 days
22.Mechanism of Attachment and ReceptorMerozoite (non–complement-mediated attachment), Duffy antigenMerozoite and glycophorin A and B
23.Pigment ColorBlack and Dark BrownYellow or Golden Brown
24.Incubation periodIncubation period (usually 10 to 17 days)Shortest of all the plasmodia, ranging from 7 to 10 days, and does not extend for months to years.
25.Signs and SymptomsPatient experiences vague influenza-like symptoms with headache, muscle pains, photophobia, anorexia, nausea, and vomiting.After the early influenza-like symptoms, P. falciparum rapidly produces daily (quotidian) chills and fever as well as severe nausea, vomiting, and diarrhea. The periodicity of the attacks then becomes tertian (36 to 48 hours), and fulminating disease develops.
26.Symptom periodicity48 hr36-48 hr
27.ComplicationsSevere complications are uncommon in P. vivax infections, although coma and sudden death or other symptoms of cerebral involvement have been reported.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.
28.AnemiaMild to moderateSevere
29.CNS involvementRareVery common
30.Nephrotic syndromePossibleRare
31.Disease featuresP. vivax causes paroxysms of fever and chills every 48 hours; a spectrum of severe, life threatening syndromes similar to that with P. falciparum may be seen; a liver stage may cause relapses and recrudescences.P. falciparum produces daily (quotidian) chills and fever with nausea, vomiting, diarrhea progressing to tertian (36 to 48 hours) periodicity with fulminating disease (malignant tertian); no persistent liver stage.
32.Severity of infectionComparatively less severe infection.Considered the most pathogenic and “deadliest” of all Plasmodium parasites.
33.Mortality and MorbidityRelatively LowerHigher
34.PrevalenceThe most prevalent of the human plasmodia.Comparatively less prevalent.
35.DiagnosisThick and thin blood smears; ring stage in RBCs with Schüffner dotsThick and thin blood smears; banana-shaped gametocytes; double rings in RBCs
36.Main diagnostic criteriaLarge pale red cell; trophozoite irregular; pigment usually present; Schüffner’s dots not always present; several phases of growth seen in one smear; gametocytes appear as early as third day.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.
37.TreatmentChloroquine (where no resistance), otherwise mefloquine or atovaquone/ proguanil, either followed by primaquine for relapse.Chloroquine (where no resistance); quinine sulfate plus doxycycline or plus tetracycline or plus clindamycin; atovaquone/ proguanil, mefloquine, bartesunate plus doxycycline or clindamycin; artemether/ lumefantrine (coartem).
38.Duration of untreated infection5-7 years6-17 months
39.RelapseCan relapse due to hypnozoites in liverNo  relapse
40.Summarized distinguishing characteristics1. 48-hour cycle

2. Tends to infect young cells

3. Enlarged RBCs

4. Schüffner’s dots (true stippling) after 8-10 hours

5. Delicate ring

6. Very ameboid trophozoite.

7. Mature schizont contains 12-24 merozoites
1. 36-48-hour cycle

2. Tends to infect any cell regardless of age, thus very heavy infection may occur.
3. All sizes of RBCs

4. No Schüffner’s dots (Maurer’s dots: may be larger, single dots, bluish)

5. Multiple rings/cell (only young rings, gametocytes, and occasional mature schizonts are seen in peripheral blood)

6. Delicate rings, may have two dots of chromatin/ring, appliqué or accolé forms

7. Crescent-shaped gametocytes

Also Read: Difference Between Red Blood Cells And White Blood Cells