Quiescence

How does a vampire avoid that which kills him? He plays dead.

Plasmodium falciparum, a deadly disease known as malaria, proves just as apt to play dead as a fictive vampire facing the sunlight. Humans had a secret weapon against malaria. "Artemisinin (ART), a substance extracted from a Chinese plant," was "the first-line drug for malaria," since other compounds lost their efficacy from overuse and parasite mutation. Artermisinin-based Combination Therapies (ACT) were "the most effective treatment for malaria, achieving a 95% cure rate."

Then, malaria played dead.

In July 2009, artemisinin-resistant malaria was identified in South East Asia. Scientists, desperate to determine how malaria avoided their once brutal weapon, ran laboratory studies.

Françoise Benoit-Vical and his team at Laboratoire de Chimie de Coordination (CNRS) "sought to isolate ART-resistant strains in an experimental manner. This feat was achieved at the end of 2009 when the scientists managed to obtain a strain of Plasmodium falciparum that was resistant to this compound and some of its derivatives, and the first to be adapted to in vitro culture." In the process, the "researchers also identified and characterized a new mode of parasite resistance. To evade the action of ART, Plasmodium falciparum arrested its development and entered a so-called state of quiescence [temporary inactivity]. It thus functioned at a slow metabolic rate until the drug was eliminated", at which time, it would reawaken and wreak havoc again.

"Malaria still continues to kill nearly a million people each year throughout the world. There is no vaccine against this infectious disease", which is caused by a blood parasite and transmitted by mosquitoes."

This study demonstrated "a novel resistance mechanism" and provides "important tool that will allow a clearer understanding of the mechanisms of resistance to antimalarial drugs". Scientists plan further studies in order to "identify the genes responsible for the acquisition of ART resistance."

Sources:
Physorg.com. "How the parasite responsible…" 5 May 2010. http://www.physorg.com/news192300284.html
Witkowski B, Leličvre J, López Barragán MJ, Laurent V, Su XZ, Berry A, Benoit-Vical F. "Increased tolerance to artemisinin in Plasmodium falciparum is mediated by a quiescence mechanism." Antimicrobial Agents and Chemotherapy. Mai 2010.

War of the parasites

Malaria, a disease that reportedly causes "more than 1 million deaths annually", is caused by a mosquito-borne parasite. But, another blood parasite--this one carried by ticks--may provide malaria resistance.

Like malaria, Babesia parasites "infect a wide variety of mammalian hosts". Of the human "population infected with Babesia microti, 25% of adults and 50% of children remain asymptomatic" (without noticeable symptoms). "A new study suggests that monkeys chronically infected with babesiosis, a tick-borne parasite, are able to suppress malaria infection when exposed to a simian malaria parasite." Other coinfection studies in rodents indicate cross-protection. Researchers conclude that "ongoing infection with B. microti parasites leads to suppression of malaria infection" and may provide a way to combat malaria.

Source:
American Society for Microbiology (2010, March 24). Infection with tickborne parasite may suppress malaria. Retrieved March 25, 2010.

Pirate parasites

Parasitic Plasmodium invaders swarm the bloodstream, set up a base camp in the liver, and commandeer healthy red blood cells. These parasites "enter the body from the saliva of a mosquito" and send plague upon their victim (American). Malaria, the deadly and devastating disease that kills nearly a million people every year, is caused by the Plasmodium parasites as they pillage the human body for their own reproduction and survival.

"Inside the blood cells" of the malaria patient, "the parasites replicate and also begin to expose adhesive proteins on the cell surface that change the physical nature of the cells in the bloodstream" (American). Medical experiments "show that infected red blood cells are stiffer and stickier than normal ones." In "later stages of the disease" the cells can be "up to 10 times stiffer" than healthy red blood cells. These infected cells may also anchor onto "endothelial cells lining the vasculature, affecting the normal blood flow. This explains some of the common symptoms of malaria, such as anemia and joint pain" (American).

The parasites avoid a whirlpool of blood cell death in the spleen by anchoring in the safe harbors of the blood vessels. "Sticking to the walls of blood vessels is a survival mechanism for the parasite. In order to develop completely, it needs several days inside a red blood cell. Even though parasitized cells are nearly invisible for the immune system, they may be destroyed in the spleen while circulating freely in the bloodstream" (American).

Brown University professor George Karniadakis and student Dmitry Fedosov study "how malaria infections affect the physical properties of red blood cells, and alter normal blood flow circulation. In particular, they examine an increase in blood flow resistance, and dynamics of infected cells in the bloodstream." The properties that they measure are "used in modeling the flow of red blood cells in people infected with malaria" (American).

Fedosov says, "Our model predicts the dynamics of malaria-infected RBCs in the bloodstream, which anticipates the possible course of the disease." Each infected human contains a slightly different map and provides a unique environment that the parasites must navigate. The researchers recently discovered "that temperature fluctuations of infected red blood cell membranes measured in experiments are not directly correlated with the reported cell properties, hence, suggesting significant influence of metabolic processes" (American).

Hypothesizing on the metabolic processes that affect the patients' body temperatures, the researchers "measured an increase in resistance to blood flow in the capillaries and small arterioles during the course of malaria and found that parasitized red blood cells have a "flipping" motion at the vessel wall that appears to be due to stiffness of the infected cells. The developed models will aid to make realistic predictions of the possible course of the disease, and enhance current malaria treatments" (American).

Play the parasite game (NobelPrize.org site), and see if you can navigate your way to the liver.

Sources:
American Institute of Physics. "Measuring and Modeling Blood Flow in Malaria." ScienceDaily 22 November 2009. 27 November 2009 .