Recently, the malaria parasite was for the first time videoed entering and infecting a human red blood cell (via New Scientist TV):
Malaria kills about a million people every year, mostly in the wet tropics. Symptoms include fever, shivering, arthralgia (joint pain), vomiting, anemia, hemoglobinuria, retinal damage and sometimes blindness and convulsions. The classic symptom of malaria is sudden coldness, then stiffness of muscles followed by fever and sweating lasting 4 to 6 hours, which repeats in a cycle for up to a few days.
It is caused by several species of Plasmodium, a group of generally parasitic protists. Protists are single-celled organisms, but they’re not bacteria and so they’re not affected by most antibiotics.
From over 200 known species of Plasmodium, at least 11 infect humans. Other species infect other animals, including monkeys, rodents, birds, and reptiles. The parasite always has two hosts in its life cycle: a mosquito vector and a vertebrate host.
The parasite’s intermediate hosts are humans and other vertebrates. A mosquito picks up the parasite when it feeds on blood from an infected human. Sporozoites form in the mosquito body, and move to the salivary glands, where they may be passed on to a human host during feeding.
Only female mosquitoes feed on blood while male mosquitoes feed only on plant nectar, thus males do not transmit the disease.
The phylum to which Plasmodium belongs probably started out, tens of millions of years ago originated within the Dinoflagellates — a large group of photosynthetic protists. In other words, they were once very similar to plants, like algae.
These ancestors developed the ability to invade the intestinal lining of their predators and eventually lost their photosynthetic ability, as they evolved the ability to feed on the host organism. How do we know?
Because they still have plastids, which are organelles inside the cell where photosynthesis occurs. In some cases, these plastids are absent, but there is evidence of plastid genes within their genomes. In most cases, the plastids are no longer functional for photosynthesis, but certain species of dinoflagellate can invade the bodies of jellyfish and continue to photosynthesise, because jellyfish bodies are almost transparent.
In humans, the parasite infects healthy red blood cells and feeds on them, before spreading throughout the bloodstream.
A team including Dr Jake Baum at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, used transmission electron microscopy, immuno-fluorescence and 3D super-resolution microscopy to record high-definition images of these blood cell invasion events, a process that takes less than 30 seconds.
The team controlled the process using specific drugs to increase their chances of catching a parasite in the act (Riglar DT, Richard D, Wilson DW, Boyle MJ, Dekiwadia C, Turnbull L, Angrisano F, Marapana DS, Rogers KL, Whitchurch CB, Beeson JG, Cowman AF, Ralph SA & Baum J 2011, “Super-resolution dissection of coordinated events during malaria parasite invasion of the human erythrocyte”, Cell Host & Microbe, vol. 9, issue 1, pp. 9-20).
The parasites produce a specific protein called the tight junction marker and use it to attach to and drill into red blood cells. Then they simultaneously make a bubble, called a vacuole, inside the blood cell, and move into it, as well as fire up their engines so they can move around inside the cell.
Before these images were available, it had been assumed that the invasion by the parasites was an orderly process involving many separate steps. But now it seems that the whole process hinges on the marker protein, and it is hoped that switching off that protein will prove be a kill switch to shut down the whole process before it begins.
Then we can all sleep easy or at least have one less reason to hate mosquitoes.