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Sickle cell trait (SCT) began in countries where malaria is common. Sickle cell trait (SCT) is caused by a gene mutation that changes the hemoglobin protein in red blood cells. SCT is also referred to as HbAS. Those with SCT often have no symptoms of malaria. While this SCT mutation protects carriers from severe malaria, it does not offer any benefits to a person not living where malaria is a threat

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5.  Drug resistance is complicating the prevention and treatment of malaria causing parasites

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4. Access to diagnosis and treatment is difficult in poorer countries and rural regions

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3. Understanding local beliefs around malaria. in many countries people are not afraid of malaria as it is so common and many adults have been infected multiple times. It is hard to change behavior in these circumstances.

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2. Poor agricultural conditions will lead to increase standing water where mosquitoes can lay eggs. This will increase risk of mosquitoes carrying diseases.

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1. Microscopy. Parasite-based diagnostic testing by microscopy to detect the malaria-causing parasites (p. falciparum, P. vivax, P. malariae, P. ovale. and P. knowles) using the Giemsa stain,using thin and thick films, is the gold standard to diagnose malaria.

2. Rapid Diagnostic Tests.  RDTs detect specific antigens produced by malaria parasites. Blood is obtained by finger prick and results are available in 15-30 minutes. These RDTs are simple to perform and interpret, require little training and can help manage malaria infections in remote areas with limited access to good microscopy.

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We can ADVOCATE for leaders to invest in funding to eradicate malaria.

We can ACT by raising awareness, voting, and volunteering around the globe to bring medical treatments to people in need.

We can EDUCATE ourselves and others about ways to prevent, identify and treat malaria.

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Diagnosing malaria begins with taking a careful history of symptoms and gathering a detailed travel history. This is vital to case management of malaria especially in a person who has traveled or immigrated from an endemic area.  Even in areas of the world with high incidences of malaria it is very important to get a detailed history and exam as there are many causes of fever around the world.

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1. Poverty makes it harder to eradicate disease thru improved sanitation, water drainage, access to healthcare and then increased rates of malaria and illness increase poverty. This is a terrible cycle.

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Malaria is a disease that occurs  throughout most tropical regions of the world with parasite P. falciparum causing the most disease.  In 2021, there were an estimated 247 million cases and 619.000 deaths worldwide.

Over 95% of malaria occurs in Africa, 2% in Southeast Asia and Eastern Mediterranean regions, with Americas and Western Pacific regions making up the rest.

29 countries account for 96% of cases. Nigeria (27%), Democratic Republic of Congo (12%), Uganda (5%), Mozambique (4%), Angola (3%), Burkina Faso (3%) account for 55% of all cases globally.

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Barriers to Malaria Control and Eradication

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Barriers to Malaria Control and Eradication

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The only approved malaria vaccine is RTS,S  commonly known as Mosquirix. The vaccine was released on October 6, 2021 and by April of 2022, the vaccine has been given to 1 million children living in areas with moderate-to-high malaria transmission. It has been shown to reduce malaria infections and deadly malaria among children.

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Malaria Prevention: Tools and Strategies

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Malaria Prevention: Tools and Strategies

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Malaria is transmitted by the bite of an infected Anopheles Mosquito: What happens next?

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Malaria is transmitted by the bite of an infected Anopheles Mosquito: What happens next?

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Vector Control Methods and Preventive Chemotherapy

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Vector Control Methods and Preventive Chemotherapy

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1.  Using DEET or Picaridin containing bug spray.  DEET and Picaridin inhibit the mosquito's ability to sniff and attack areas of exposed skin. thereby decreasing possibility of bug bites.
2. Wearing long sleeves and pants to cover exposed skin.
3. Insecticide-treated bed nets (shown above). These nets work by killing and repelling mosquitos and other insects.
4. Indoor Residual Spraying. Spraying surfaces of houses with insecticides will kill mosquitoes who rest inside houses after biting an infected human. These malaria vectors will die when they come to rest of the sprayed surface of the houses.
5. Consider intermittent preventive treatment for pregnant women and infants in high risk regions.

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Malaria prophylaxis is highly effective and should be taken by people traveling to endemic areas. Choice of medication depends of region of travel and patterns of drug resistance there. Additionally, one should consider itinerary, length of trip, cost of medication, drug allergies and medical history. Malarone, Doxycycline, and Mefloquine can be taken in areas with chloroquine resistance present (which is now almost universal) and Plaquenil can be taken where chloroquine resistance is not present (much less commonly now).

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Over the last decade, parasite resistance to ACTs and other medicines has emerged as a threat in the fight against malaria, particularly in the Greater Mekong subregion and Africa. Resistance has been shown in 3 of the 5 malaria species known to affect humans: P. falciparum, P. vivax, and P. malariae. However, nearly all patients infected with artemisinin-resistant parasites who are treated with an ACT are fully cured.

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Malaria is treatable if recognized and diagnosed promptly. The most effective malaria medicine available today are Artemisinin-based combination therapies (ACTs). This is the recommended treatment for Plasmodium falciparum malaria (the deadliest malaria parasite globally. ACTs combine 2 active pharmaceuticals with different mechanisms of action, including parts of artemisinin extracted from the plant Artemisia annua and a partner drug. An image of Artemisia annua is pictured above. The role of the artemisinin compound is to lower the number of parasites during the first 3 days of treatment, while the role of the partner drug is to eliminate the remaining parasites.

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The symptoms of malaria include: fever, shaking, chills, headache, muscle ache, fatigue, nausea, and flu-like symptoms.

Physical findings include: pallor from anemia, hepatomegaly, splenomegaly, jaundice (yellowing of skin and eyes) due to the destruction of erythrocytes after they are invaded by the merozoite form of the parasite.

In severe cases, illness can cause seizure, organ failure and death.

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Why does the immune system's attempt to stop malaria often fail?

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Why does the immune system's attempt to stop malaria often fail?

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Malaria parasites have evolved and come up with strategies to avoid and win in attacks from the immune system due to a range of genetic changes such as allelic variation, biomolecular exposure to proteins, and intracellular replication. In order for malaria parasites to enter red blood cells, it changes a critical protein on its surface that it uses as one of several molecular "keys" to enter red blood cells. The gene that codes for this protein inside the parasite's nucleus can switch on and off. This changes its presence on the surface of the parasite which allows it to travel undetected. Once the parasite enters the red blood cell and begins producing daughter parasites, it returns to normal. This process is known as epigenetic regulation. It uses this stealthy on/off mechanism with varying frequencies and in many places in the body to avoid our immune response.

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IFN-y and CD8 T cells inhibit parasite development in hepatocytes. The immune system also sends antibodies to prevent sequestration of infected erythrocytes by preventing binding to adhesion molecules on the vascular endothelium.

Unfortunately, although our immune system puts a lot of effort into attempting to kill malaria parasites, it often fails without medical treatments.

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In some cases, a type of white blood cell (monocyte) can kill certain malaria parasites in the presence of cytophilic IgG3 and IgG1 antibodies (76). These antibodies cause phagocytosis and kill malaria parasites. Phagocytosis is the process by which a phagocyte (a type of white blood cell) surrounds and destroys foreign substances (such as bacteria) and removes dead cells. This is possible since cross-linked FcγR–Fc induce a respiratory burst.

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For people who are repeatedly exposed to malaria, it is possible to develop antibodies against certain stages and development of the malaria parasite. The antibodies found in many adults in malaria infested areas are partly responsible for decreased cases in adults vs. children. As shown in the graph above, children under five amounted to up to 600,000 deaths in 2005. While that same year, people age 50-70+ only had around 100,000 deaths. This shows how prior infections can help develop antibodies and a stronger immune response to prevent severe disease and death from subsequent malarial infections.

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The sporozoites travel to the mosquitos salivary glands. Then, when the mosquito next feeds on a human, they inject the sporozoites into the human host to continue the malaria life cycle.

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The zygotes become capable of motion and elongate (called ookinetes). The difference in shape between the Zygotes and Ookinetes are shown above. These attack the midgut wall of the mosquito after traversing through the chitlin, protein containing peritrophic matrix, and the midgut epithelial cell. Once the ookinetes have made it through to the midgut, they develop into oocysts. These will develop, rupture, and release sporozoites.

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How does this continue to spread back to mosquitoes from the human? 

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How does this continue to spread back to mosquitoes from the human? 

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At this point, some of the parasites differentiate into gametocytes. Gametocytes are the sexual precursor cells that cause the movement of the malaria parasite from the human to the mosquito. Gametocytes mature in the human bone marrow. Then, once a mosquito feeds on the human, they take in gametocytes infected with malaria. The image above shows how the passing of malaria is a cycle depending on both the human and the mosquito to spread.

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Erythrocytic cycle

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Sporogonic cycle

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Anopheles Mosquito takes a blood meal and ingests gametocytes

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Anopheles Mosquito takes a blood meal and ingests gametocytes

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The gametocytes become macrogametes once they undergo meiosis to form mature female sex cells of the malarial parasite. Next, the parasite multiplies in the stomach of the mosquito. The microgametes penetrate the macrogametes. This ends up creating zygotes.

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BLOOD STAGE: Next, the parasites rapidly grow inside erythrocytes, feeding on hemoglobin of red blood cells, developing from immature trophozoites to mature trophozoites to schizonts, ultimately rupturing the red blood cells, and releasing merozoites into the bloodstream to infect other red blood cells. This blood stage is what causes malaria symptoms as toxins are released into the bloodstream.

The parasite goes through asexual multiplication in the erythrocytes, which is called erythrocytic schizogony. This allows the parasite to multiply and spread exponentially, both causing symptoms in the infected human during this blood stage and spreading back to mosquitoes when the sick human is bitten.

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Exo-erythrocytic Cycle

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Mosquito bites human and injects sporozoites

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Mosquito bites human and injects sporozoites

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LIVER STAGE: The protist Plasmodium protozoa cause malaria. Protozoa are single-celled eukaryotes. The Plasmodium protozoa is spread by an infected mosquito. When it bites, a Malaria-infected female Anopheles mosquito inoculates sporozoites into the human. Anticoagulant saliva is injected together with the sporozoites. Then, the parasite travels to the liver and enters the parenchyma cells. This is the incubation period. Once here, they mature into shizonts, which rupture and release Merozoites.

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How does the human immune system respond?

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How does the human immune system respond?

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What is the sequence of events that take place between being bitten by a mosquito and full-blown illness?

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What is the sequence of events that take place between being bitten by a mosquito and full-blown illness?