Plasmodium falciparum: New Developments

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Electron micrograph of Plasmodium falciparum. 2006.


By Charley Myers


Figure 3. Nature Reviews. Life cycle of P. falciparum in both human host and mosquito vector.
Figure 4. Salleres et al 2004. “Infant burial no. 36, an inhumation burial, at the cemetery at Lugnano, in Taverna.”
Figure 5. Yang et al 2017. Immunofluorescence microscopy labeling SPECT and PLP1 proteins in Plasmodium falciparum (Pf).
Figure 6. Yang et al 2017. Measurements of P. falciparum presence in human liver cells. NF54 are wild type while PfPLP1 D2 are the PLP knockout strains of P. falciparum.

Introduction

Plasmodium falciparum is a protozoan of the eukaryotic domain. It is most widely known in today's world as one of the most common malarial parasites. This particular species causes malignant malaria, which leads to the most complications and mortality rates of any other malaria-causing agent. [1]


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Background

Plasmodium falciparum is a protozoan of the eukaryotic domain. It is widely known in today's world as one of the most common malarial parasites. This particular species causes malignant malaria, which leads to the most complications and mortality rates of all malaria-causing agents. It is estimated that between 300 million and 500 million people are afflicted with malaria annually (WHO). The majority of these incidences of malaria occur in sub-Saharan Africa and affect children under 5. According to the CDC, there are 156 species of Plasmodium, four of which are considered parasitic to humans. These include P. falciparum, P. vivax, P. ovale and P. malaria. Plasmodium falciparum has the highest rate of malarial infection among the four species [4]. We know for a fact that P. falciparum is a malarial parasite that targets humans. What is relatively unknown, however, is the exact mechanism by which the protozoa are able to enter the cell and cause disease.


The Physical Microbe

Taxonomy

Kingdom: Protista Subkingdom: Protozoa Phylum: Apicomplexa Class: Sporozoasida Order: Eucoccidiorida Family: Plasmodiidae Genus: Plasmodium Species: Falciparum



Metabolism

Plasmodium falciparum is a highly proliferating organism whose job is very energetically costly. The protozoa must maintain a high metabolic rate in order to infect its various hosts. It is clear that the metabolism of P. falciparum is closely intertwined with that of its host, as the two share a very intimate relationship. The metabolism of the microbe must adapt to its changing environments. For example, when in the blood stage of its lifecycle, P. falciparum acquires most of its energy from oxidizing glucose into lactate through the process of glycolysis. This parasite utilizes up to 75% times more glucose than its uninfected erythrocyte counterparts[5]. Glycolysis alone is not very productive in the gathering of energy, as it generally only produces 2 ATP per molecule of glucose. A reasonable way to generate more ATP would be to carry out the TCA cycle. However, as the mammalian blood is teeming with glucose, it is efficient enough a process to perform glycolysis alone[6].

There is evidence that proposes hemoglobin degradation as an additional form of generating energy in P. falciparum, on top of glycolysis. During the intraerythrotic stage of the P. falciparum life cycle, in which the protozoa is parasitizing a vertebrate, the cytoplasm of the host cell is consumed and between 60% and 80% of the hemoglobin in the cell is degraded[7]. After the degradation the heme moiety is stored as a polymer, known as the malaria pigment hemozoin, instead of being recycled[8]. P. falciparum may then utilize this polymer in order to produce amino acids, which are then integrated into parasite proteins and may also be used in metabolism<ref?[7]</ref>. This is a good example of parasitism because the parasite, P. falciparum is pooling the resources of the host (the hemoglobin) and turning them into an integral part of its own survival (amino acids) (Figure 2).

Figure 2. Hemoglobin degradation pathway in P. falciparum. Francis et al 1997.

Hemoglobin metabolism is not fully sufficient for the metabolism of P. falciparum. But it can be combined with exogenous amino acid synthesis in order to allow for P. falciparum survival[9]. Knowledge about hemoglobin degradation has proven very useful to researchers targeting malaria outbreaks worldwide. This is because the enzymes that are involved in hemoglobin breakdown, or proteolysis, may be potential targets for antimalarial drug therapy (see section on Malarial Drug Therapy).

Section 3

Include some current research, with at least one figure showing data.

Section 4

Conclusion

References



Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2017, Kenyon College.