IVD of Plasmodium falciparum

Background

Plasmodium falciparum, the pathogen that causes falciparum malaria in humans, is primarily transmitted by Anopheles mosquitoes and reproduces asexually in human liver cells. It then invades and consumes nutrients, destroys red blood cells, and causes symptoms such as chills and fever in the body. The pathogenesis of Plasmodium falciparum is mainly related to the period during which it parasitizes red blood cells. The discovery of Plasmodium parasites in peripheral blood red blood cells provides a certain basis for diagnosis.

The life cycle of Plasmodium falciparum.Fig1. The life cycle of Plasmodium falciparum. (Josling G A, et al., 2015)

Main Steps of IVD for Plasmodium falciparum

  • Morphological examination. Take peripheral blood to make thick and thin blood films, then stain them with Ji's or Wright's dye, and examine them under a microscope to find malaria parasites.
  • Immunological examination. The main methods include indirect fluorescent antibody assay (IFA), indirect hemagglutination assay (IHA), ELISA, etc.
  • Molecular biology examination. DNA probes and PCR have high sensitivity and specificity, and can effectively assist in vitro diagnosis (IVD).
  • Serological tests. Circulating antigen testing and circulating antibody testing can diagnose existing patients and carriers.
  • Rapid diagnostic test (RDT).

Differences between Plasmodium falciparum and other Plasmodium

Virulence and Severity

  • Plasmodium falciparum: Causes the most severe form of malaria, often referred to as falciparum malaria. It has a high mortality rate if not treated promptly and correctly.
  • Other Plasmodium Species: Generally cause less severe forms of malaria. For instance, Plasmodium vivax and Plasmodium ovale can cause relapsing malaria due to dormant liver stages (hypnozoites).

Geographic Distribution

  • Plasmodium falciparum: Predominantly found in sub-Saharan Africa, but also present in parts of Southeast Asia, South America, and other regions.
  • Other Plasmodium Species:
  • Plasmodium vivax: More common in Asia, Latin America, and parts of Africa.
  • Plasmodium ovale: Generally found in West Africa.
  • Plasmodium malariae: Has a more widespread but patchy distribution.
  • Plasmodium knowlesi: Primarily found in Southeast Asia and is a zoonotic parasite affecting monkeys and humans.

Life Cycle and Parasitemia

  • Plasmodium falciparum: Has the ability to infect red blood cells (RBCs) at all stages of their development, leading to high levels of parasitemia (up to 50% or more).
  • Other Plasmodium Species: Typically infect reticulocytes (immature red blood cells, as in the case of Plasmodium vivax) or older RBCs (as in Plasmodium malariae), usually resulting in lower parasitemia levels.

Drug Resistance

  • Plasmodium falciparum: Known for its high potential for developing drug resistance, particularly to chloroquine and, recently, artemisinin derivatives.
  • Other Plasmodium Species: Some resistance has been observed, particularly in Plasmodium vivax to chloroquine, but it is generally less of a problem compared to Plasmodium falciparum.

Incubation Period

  • Plasmodium falciparum: Incubation period is shorter, typically around 9-14 days.
  • Other Plasmodium Species: Tend to have longer incubation periods; for example, Plasmodium vivax can take 12-17 days, while Plasmodium malariae can take 18-40 days.

Complications

  • Plasmodium falciparum: Can lead to severe complications such as cerebral malaria, severe anemia, respiratory distress, and multi-organ failure.
  • Other Plasmodium Species: While they can cause serious illness, they are less likely to cause the severe complications seen in falciparum malaria.

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  • High sensitivity, high specificity, and high purity.
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  • A wide range of immunological experiments can be performed with it.

Our Outstanding Advantages

  • High-quality service, high-level experiments, and reliable analysis.
  • As a diagnostic and monitoring tool, IVD proteins provide valuable information on a variety of diseases and conditions.
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Case Study

Case 1: Henshall IG, Spielmann T. Critical interdependencies between Plasmodium nutrient flux and drugs. Trends Parasitol. 2023 Nov;39(11):936-944. doi: 10.1016/j.pt.2023.08.008. Epub 2023 Sep 14. PMID: 37716852; PMCID: PMC10580322.

Nutrient import and waste efflux are critical dependencies for intracellular Plasmodium falciparum parasites. Here the author briefly summarise the nutrient acquisition pathways of intracellular P. falciparum blood-stage parasites and then highlight how these pathways influence many aspects relevant to antimalarial drugs, resulting in complex and often underappreciated interdependencies.

Fig2. Schematic of pathways for nutrient acquisition and waste excretion in Plasmodium falciparum. P. falciparum must import nutrients and export waste across three different membranes. Transport of nutrients across the red blood cell (RBC) membrane is through a mix of host and parasite transport proteins, while passage across the parasitophorous vacuole membrane (PVM) and parasite plasma membrane (PPM) is through parasite-established pathways, either vesicle mediate (endocytosis) or non - vesicular. Solutes may also directly diffuse across the lipid bilayer without assistance. Host transport proteins are indicated in yellow, parasite transport proteins are orange. Arrows indicate transport directions.

Case 2: Baro B, Kim CY, Lin C, Kongsomboonvech AK, Tetard M, Peterson NA, Salinas ND, Tolia NH, Egan ES. Plasmodium falciparum exploits CD44 as a coreceptor for erythrocyte invasion. Blood. 2023 Dec 7;142(23):2016-2028. doi: 10.1182/blood.2023020831. PMID: 37832027; PMCID: PMC10783654.

The malaria parasite Plasmodium falciparum invades and replicates asexually within human erythrocytes. CD44 expressed on erythrocytes was previously identified as an important host factor for P falciparum infection through a forward genetic screen, but little is known about its regulation or function in these cells, nor how it may be used by the parasite. Researchers found that CD44 can be efficiently deleted from primary human hematopoietic stem cells using CRISPR/Cas9 genome editing, and that the efficiency of ex vivo erythropoiesis to enucleated cultured red blood cells (cRBCs) is not affected by lack of CD44.

Fig3. CD44 is dispensable for erythroid differentiation of primary human HSPCs. (D) Cytospin images of CD44-CRISPR vs isogenic WT erythroid cells during the time course of ex vivo erythropoiesis. Cas9, nucleofected with Cas9 only; Mock, nontransfected; scale bar, 10 μm. (E) Representative experiment showing enucleation rate of CD44-null cRBCs upon terminal differentiation, as detected by flow cytometry using the cell-permeable DNA stain Vybrant DyeCycle Violet.