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DIFFERENCE BETWEEN

Plasmodium vivax vs Plasmodium falciparum- 45 Differences

Plasmodium vivax vs Plasmodium falciparum- 45 Differences

Plasmodium vivax and Plasmodium falciparum are two of the most common species of the parasitic protozoan that causes malaria in humans. Malaria is a life-threatening disease prevalent in many tropical and subtropical regions around the world. These two species are responsible for the majority of malaria cases globally and share certain similarities, but they also have distinctive characteristics that set them apart.

Plasmodium vivax

Plasmodium vivax is known to be the most widespread species of malaria parasite, with a significant presence in Asia, Latin America, and parts of Africa. It is estimated to cause around 70-80 million cases of malaria each year. On the other hand, Plasmodium falciparum is responsible for the most severe and deadly form of malaria, primarily prevalent in sub-Saharan Africa, but also found in other regions like Southeast Asia and South America. It accounts for a majority of malaria-related deaths worldwide.

Both P. vivax and P. falciparum are transmitted through the bites of infected female Anopheles mosquitoes. Once inside the human body, the parasites invade and multiply within red blood cells, leading to the characteristic symptoms of malaria, such as fever, chills, headache, fatigue, and in severe cases, organ failure or cerebral complications.

While the clinical manifestations of P. vivax and P. falciparum infections are similar, there are some notable differences between the two species. One significant difference lies in the life cycle of the parasites within the human host. P. vivax has the ability to form dormant stages known as hypnozoites in the liver, which can remain inactive for months or even years before causing a relapse of the infection. This unique feature makes P. vivax infections more difficult to eliminate completely.

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P. falciparum

In contrast, P. falciparum does not form hypnozoites, but it has a higher multiplication rate within the bloodstream compared to P. vivax. This rapid replication can lead to a more rapid onset of severe symptoms and complications, such as severe anemia, cerebral malaria, or multi-organ failure. P. falciparum infections require prompt and aggressive treatment due to their potential for rapid progression and higher mortality rates, particularly in children and non-immune individuals.

Furthermore, the two species also differ in terms of their response to antimalarial drugs. P. falciparum has developed widespread resistance to many commonly used antimalarial medications, posing a significant challenge for treatment and control efforts. P. vivax, while generally susceptible to many antimalarial drugs, has some limitations in terms of drug choices due to its hypnozoite stage.

Plasmodium vivax and Plasmodium falciparum

In conclusion, Plasmodium vivax and Plasmodium falciparum are two major species of malaria parasites that cause significant morbidity and mortality worldwide. While they share some similarities in terms of transmission and clinical presentation, their unique biological characteristics, including the ability of P. vivax to form hypnozoites and P. falciparum’s increased virulence and drug resistance, distinguish them and pose specific challenges for effective prevention, diagnosis, and treatment of malaria.

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Detailed Comparison Plasmodium Vivax vs Plasmodium Falciparum

S.No.

Category

Plasmodium vivax

Plasmodium falciparum

1

Species

Plasmodium vivax is a species of malaria parasite.

Plasmodium falciparum is a species of malaria parasite.

2

Prevalence

Plasmodium vivax is more widely distributed and accounts for the majority of malaria cases outside of Africa.

Plasmodium falciparum is the most prevalent malaria parasite in Africa and causes the majority of severe malaria cases worldwide.

3

Geographical Distribution

Plasmodium vivax is found in many parts of the world, including Asia, Latin America, and the Middle East.

Plasmodium falciparum is primarily found in sub-Saharan Africa, but also occurs in other tropical regions.

4

Life Cycle

The life cycle of Plasmodium vivax involves both human and mosquito hosts.

The life cycle of Plasmodium falciparum also involves both human and mosquito hosts.

5

Duration of Infection

Plasmodium vivax infection can persist in the liver as dormant forms (hypnozoites) that can cause relapses months or years later.

Plasmodium falciparum infection does not have dormant liver forms, and relapses are rare.wikipedia

6

Fever Pattern

Plasmodium vivax infection typically presents with periodic fever spikes every 48 hours (tertian fever).

Plasmodium falciparum infection presents with periodic fever spikes every 48 or 72 hours (tertian or quartan fever).

7

Malaria Severity

Plasmodium vivax infection is generally less severe compared to Plasmodium falciparum infection.

Plasmodium falciparum infection can cause severe malaria, leading to complications such as cerebral malaria and organ dysfunction.

8

Red Blood Cell Preference

Plasmodium vivax primarily infects reticulocytes (young red blood cells).

Plasmodium falciparum infects both young and mature red blood cells.

9

RBC Invasion Mechanism

Plasmodium vivax uses the Duffy antigen receptor for chemokines (DARC) to invade red blood cells.

Plasmodium falciparum uses multiple receptors, including glycophorins and complement receptor 1 (CR1), to invade red blood cells.

10

Glycophorin Preference

Plasmodium vivax shows preference for binding to specific glycophorin molecules on the surface of red blood cells.

Plasmodium falciparum does not show a specific preference for glycophorin molecules.

11

Malaria Symptoms

Plasmodium vivax infection typically presents with symptoms such as fever, chills, headache, and fatigue.

Plasmodium falciparum infection can present with severe symptoms, including high fever, headache, body aches, and gastrointestinal disturbances.

12

Complications

Plasmodium vivax infection can cause complications such as anemia and splenomegaly.

Plasmodium falciparum infection can lead to severe complications, including cerebral malaria, acute respiratory distress syndrome (ARDS), and multi-organ failure.

13

Drug Resistance

Plasmodium vivax has developed resistance to certain antimalarial drugs, such as chloroquine, in some regions.

Plasmodium falciparum has developed resistance to multiple antimalarial drugs, including chloroquine and sulfadoxine-pyrimethamine, in many parts of the world.

14

Relapse Potential

Plasmodium vivax can cause relapses due to the reactivation of hypnozoites in the liver.

Plasmodium falciparum infection does not typically cause relapses.

15

Merozoite Morphology

Plasmodium vivax merozoites have characteristic band-like structures (Schüffner’s dots) in the cytoplasm.

Plasmodium falciparum merozoites do not have band-like structures.

16

Schizont Appearance

Plasmodium vivax schizonts contain fewer merozoites (8-24) compared to Plasmodium falciparum schizonts.

Plasmodium falciparum schizonts contain a larger number of merozoites (16-32).

17

Hemoglobin Degradation

Plasmodium vivax degrades hemoglobin into a pigment called hemozoin.

Plasmodium falciparum degrades hemoglobin at a higher rate, leading to increased hemozoin production.

18

Gametocyte Production

Plasmodium vivax infection produces gametocytes that are visible in the peripheral blood.

Plasmodium falciparum infection can produce gametocytes, but they are less frequently observed in the peripheral blood.

19

Vector Preference

Plasmodium vivax can be transmitted by multiple Anopheles mosquito species, including Anopheles stephensi and Anopheles dirus.

Plasmodium falciparum is primarily transmitted by Anopheles mosquitoes, such as Anopheles gambiae and Anopheles funestus.

20

Vector Competence

Plasmodium vivax has a lower vector competence (ability to transmit the parasite) compared to Plasmodium falciparum.

Plasmodium falciparum has a higher vector competence, leading to more efficient transmission.

21

Host Immune Response

Plasmodium vivax infection elicits an immune response characterized by production of antibodies and immune memory.

Plasmodium falciparum infection can induce a complex immune response involving both humoral and cellular components.

22

Immune Evasion Mechanisms

Plasmodium vivax employs immune evasion mechanisms, including antigenic variation, to evade the host immune response.

Plasmodium falciparum employs various immune evasion mechanisms, such as antigenic variation, sequestration of infected red blood cells, and suppression of host immune responses.

23

Pregnancy-Associated Malaria

Plasmodium vivax infection is less commonly associated with pregnancy complications compared to Plasmodium falciparum infection.

Plasmodium falciparum infection is a major cause of pregnancy-associated malaria, leading to adverse outcomes like maternal anemia and low birth weight.

24

Glycosylphosphatidylinositol (GPI) Anchors

Plasmodium vivax merozoites lack GPI anchors on their surface proteins.

Plasmodium falciparum merozoites possess GPI anchors, which play a role in parasite adhesion and immune evasion.

25

Antigen Diversity

Plasmodium vivax exhibits less antigenic diversity compared to Plasmodium falciparum.

Plasmodium falciparum exhibits high antigenic diversity, contributing to immune evasion and repeated infections.

26

Glycosylphosphatidylinositol (GPI) Anchored Proteins

Plasmodium vivax erythrocyte membrane protein 1 (PvEMP1) family proteins lack GPI anchors.

Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) family proteins possess GPI anchors and play a role in cytoadherence to endothelial cells.

27

Malaria Eradication Potential

Plasmodium vivax elimination and eradication are challenging due to relapses and the presence of dormant liver stages.

Plasmodium falciparum elimination and eradication efforts are also challenging due to its higher virulence and drug resistance.

28

Genetic Diversity

Plasmodium vivax has lower genetic diversity compared to Plasmodium falciparum.

Plasmodium falciparum exhibits higher genetic diversity, contributing to antigenic variation and drug resistance.

29

Malaria Vaccine Development

Developing a malaria vaccine against Plasmodium vivax is challenging due to the presence of hypnozoites and antigenic diversity.

Developing a malaria vaccine against Plasmodium falciparum is complex due to its antigenic diversity and immune evasion mechanisms.

30

Drug Treatment

Plasmodium vivax is susceptible to chloroquine and primaquine for the treatment of blood-stage infection and elimination of hypnozoites, respectively.

Plasmodium falciparum has developed resistance to multiple antimalarial drugs, and treatment guidelines often involve combination therapies, such as artemisinin-based combination therapies (ACTs).

31

Antimalarial Drug Choices in Pregnancy

Plasmodium vivax infections during pregnancy can be treated with chloroquine and primaquine, following careful assessment of risks and benefits.

Plasmodium falciparum infections during pregnancy require prompt treatment with antimalarial drugs that are effective against the parasite and safe in pregnancy.

32

Impact on Global Malaria Burden

Plasmodium vivax contributes significantly to the global malaria burden, accounting for a considerable number of cases outside of Africa.

Plasmodium falciparum is responsible for the majority of malaria-related deaths worldwide and has a major impact on the malaria burden in Africa.

33

Genomic Sequencing

Plasmodium vivax genome sequencing has provided insights into its biology and potential drug targets.

Plasmodium falciparum genome sequencing has been crucial for understanding its genetic diversity, drug resistance, and vaccine development.

34

Relapse Prevention

Primaquine is used for radical cure and prevention of relapses in Plasmodium vivax infection.

Relapses are rare in Plasmodium falciparum infection, and there is no specific medication for preventing relapses.

35

Glycophorin Binding Proteins

Plasmodium vivax has a specific Duffy binding protein (DBP) involved in binding to the Duffy antigen on red blood cells.

Plasmodium falciparum uses multiple erythrocyte binding antigens (EBAs) for binding to various erythrocyte receptors.

36

Host Immune Response Factors

Plasmodium vivax infection induces specific host immune response factors, such as gamma interferon (IFN-γ) and interleukin-10 (IL-10).

Plasmodium falciparum infection induces a complex immune response involving cytokines, chemokines, and immune cell activation.

37

Drug Resistance Molecular Markers

Molecular markers for drug resistance in Plasmodium vivax, such as mutations in pvdhfr and pvdhps genes, have been identified.

Molecular markers for drug resistance in Plasmodium falciparum, such as mutations in pfcrt, pfmdr1, and pfdhps genes, have been extensively studied.

38

Submicroscopic Infections

Plasmodium vivax infections can often be submicroscopic, meaning they cannot be detected by routine microscopy.

Plasmodium falciparum infections are typically detectable by microscopy due to high parasite densities.

39

Antibody Response Targets

Plasmodium vivax antibody responses primarily target proteins expressed on the surface of infected red blood cells.

Plasmodium falciparum antibody responses target various parasite antigens, including surface proteins and variant antigens like PfEMP1.

40

G6PD Deficiency Risk

Primaquine treatment for Plasmodium vivax elimination poses a risk of hemolysis in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.

Hemolysis risk due to primaquine treatment is not as significant in Plasmodium falciparum infection.

41

Hypnozoite Dormancy Duration

Hypnozoites in Plasmodium vivax infection can remain dormant in the liver for months to years.

Plasmodium falciparum does not form hypnozoites, and the duration of dormancy is not applicable.

42

Pathology in Brain

Plasmodium vivax infection is generally not associated with cerebral malaria or significant brain pathology.

Plasmodium falciparum infection can cause cerebral malaria, characterized by sequestration of infected red blood cells in the brain microvasculature.

43

GPI Anchored Merozoite Proteins

Plasmodium vivax merozoites lack GPI-anchored proteins, such as MSP1 and MSP2, on their surface.

Plasmodium falciparum merozoites express GPI-anchored proteins, including MSP1, MSP2, and MSP3, involved in invasion and immune evasion.

44

Pregnant Women Susceptibility

Pregnant women are generally less susceptible to Plasmodium vivax infection compared to Plasmodium falciparum infection.

Pregnant women are highly susceptible to Plasmodium falciparum infection, which can have severe consequences for both the mother and the fetus.

45

Relapse Prevention Treatment Duration

Primaquine treatment to prevent relapses in Plasmodium vivax infection usually lasts for 14 days.

Relapse prevention treatment is not applicable for Plasmodium falciparum infection.

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Frequently Asked Questions (FAQs)

What are the main differences between Plasmodium vivax and Plasmodium falciparum?

Plasmodium vivax forms dormant stages called hypnozoites in the liver, while Plasmodium falciparum does not. P. falciparum is more virulent and causes severe malaria, whereas P. vivax is less severe but can cause relapses.

Where are Plasmodium vivax and Plasmodium falciparum commonly found?

Plasmodium vivax is widespread in Asia, Latin America, and parts of Africa, while Plasmodium falciparum is prevalent in sub-Saharan Africa, but also found in Southeast Asia and South America.

How are Plasmodium vivax and Plasmodium falciparum transmitted?

Both species are transmitted through the bites of infected female Anopheles mosquitoes.

What are the symptoms of malaria caused by Plasmodium vivax and Plasmodium falciparum?

The symptoms include fever, chills, headache, fatigue, and in severe cases, organ failure or cerebral complications.

Can Plasmodium vivax and Plasmodium falciparum be treated with the same drugs?

While both species can be treated with certain antimalarial drugs, P. falciparum has developed resistance to many commonly used medications, making treatment more challenging.

Are Plasmodium vivax infections more difficult to eliminate compared to Plasmodium falciparum?

Yes, P. vivax infections can be more challenging to eliminate due to the formation of hypnozoites, which can remain dormant and cause relapses even after treatment.

Which species of malaria parasite is responsible for the majority of malaria-related deaths?

Plasmodium falciparum is responsible for the most severe and deadly form of malaria, and it accounts for the majority of malaria-related deaths worldwide.

Are Plasmodium vivax and Plasmodium falciparum equally prevalent in all age groups?

Plasmodium vivax infections are more common in younger individuals, while Plasmodium falciparum infections can affect individuals of all age groups.

Can malaria caused by Plasmodium vivax or Plasmodium falciparum be prevented?

Yes, malaria prevention measures such as the use of bed nets, insect repellents, and antimalarial medications can help prevent both P. vivax and P. falciparum infections.

 Are there any vaccines available for Plasmodium vivax or Plasmodium falciparum?

While there is currently no licensed vaccine for malaria, several vaccine candidates are being developed, including those targeting both P. vivax and P. falciparum. However, more research is needed before an effective vaccine becomes widely available.

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