Body Hair as Parasite Protection

Does your body hair help you notice when something is crawling around looking for a place to bite? Does it discourage that ectoparasite from biting? Authors Isabelle Dean and Michael T. Siva-Jothy think the answer to both questions is ‘yes.’ A report in Biology Letters reveals the findings of a study that was designed to reveal whether our fine body hairs protect us from ectoparasites such as bedbugs.

Body hair appears to slow bedbugs down; the hairier
you are, the better! Image by Jiří Humpolíček
CC BY-SA 2.5

Bedbugs Are Slower on Hairy Skin

In a study of twenty-nine student volunteers, the researchers noted that bedbugs took longer to select a feeding site on hairy, as opposed to shaven, skin, (and the hairier the better) and that the volunteers were better able to detect the insects on unshaven skin. Thus, having all those fine hairs apparently helps us, in two different ways, to notice the bug before it bites.

Dean and Siva-Jothy point out that it’s already been shown that some insects that bite animals, including bedbug relatives, prefer to bite on relatively hairless parts of the body. It’s easy to see that such behavior would tend to favor bug survival if the bug goes unnoticed. In some circumstances, we can also see that hairier humans might have a survival advantage.

Does Body Hair Slow All Ectoparasites Down?

This study only looked at bedbugs; it would be interesting to see if the same thing happens with ticks (I can attest from personal experience that ticks have an amazing ability to traverse large areas of skin without ever being felt), kissing bugs, mosquitoes, black flies and other biting insects and arachnids.

So we know one possible reason why we have all those fine hairs all over us – and why we perhaps shouldn’t be shaving them off in a time of bedbug resurgence and increased tick-transmitted disease.

Dean, Isabelle, and Michael T. Siva-Jothy. “Human fine body hair enhances ectoparasite detection.” Biology Letters: Published online December 14, 2011, doi: 10.1098/rsbl.2011.0987

Malaria, Cryptosporidium, and Plants

It’s more than a decade now since scientists discovered that Plasmodium spp., agents of malaria, have plastids in their cytoplasm reminiscent of chloroplasts in plants. Chloroplasts are believed to be the descendants of free living cyanobacteria that were ingested by early cells, or invaded those cells, and then became part of cell structure and function. Chloroplasts in green plants provide energy when exposed sunlight.

[caption id="attachment_365" align="alignleft" width="185" caption="Cyanobacteria, NOAA"][/caption]

The plastid in malarial parasites – called an apicoplast – has the same origin as chloroplasts in plants and functions in similar ways. This suggests that Plasmodium spp. and their relatives: Toxoplasma gondii, Cryptosporidium spp., Cyclospora cayetanensis, Isospora belli, and Babesia spp., to name the main ones parasitic in humans, are more like plants than we typically think.

The plastid in Plasmodium spp. and other apicomplexans has lost the ability to produce energy from light, but it remains a vital part of the cell, synthesizing fatty acids, heme and other molecules. The organisms can’t live without their apicoplasts.

Aside from identifying an intriguing connection between some of our worst parasites and the plant kingdom, the discovery of the apicoplast has suggested new ways of treating infections with these parasites. Plasmodium spp. are notorious for developing resistance to antimalarial drugs, while Toxoplasma, Cryptosporidium, and Babesia have proven very challenging to treat and eradicate in the body. It could be that the agents to treat these infections are already in our possession – in the form of herbicides.

Lim, L., et al. The carbon and energy sources of the non-photosynthetic plastid in the malaria parasite. FEBS Lett. (2009),

Life Cycle of Malaria Parasites – A New Twist

The life cycle of Plasmodium spp., agents of malaria, is one of the harder ones for a parasitology student to grasp. It’s full of difficult words such as gametocyte and shizogony, and involves multiplication in both humans and mosquitoes - two hosts about as different from each other as one could imagine. Likewise, the immune system is so complex that most people can only achieve a basic understanding.

Recently, both of these things got more complicated as researchers discovered how malaria may evade the immune system and thereby survive for long periods and cause new bouts of illness later. Aha! Some old mysteries have been solved, but parasitology students will likely groan.

Two species of Plasmodium, P. vivax and P. ovale, have long been known to remain hidden away in the human liver after an initial episode of malaria, returning to the blood weeks, months, or even years later to start the infection all over again. Two other species, P. falciparum and P. malariae, do not stay within liver cells (hepatocytes) but can still mysteriously reappear after all parasites have disappeared from the blood. Where do these parasites, thought to multiply in humans only in red blood cells and hepatocytes, go? At last, we think we know.

A paper by Michelle N. Wykes et al reports that plasmodia can hide within dendritic cells—white cells that are an important part of the immune response intended to eliminate these parasites - in the spleen, multiply inside the cell and return to the bloodstream later to reinitiate malaria (“Rodent blood-stage Plasmodium survive in dendritic cells that infect naive mice.” PNAS 2011).

[caption id="attachment_360" align="alignleft" width="300" caption="Dendritic cell, image by Judith Behnsen et al, Creative Commons 2.5"][/caption]

Plasmodium spp. are not the first parasites known to use the host’s immune system against it in this way: Leishmania sp. parasites invade macrophages, an immune cell intended to kill them, and multiply within the cell before bursting out and spreading to other cells in the body. Other parasites, such as the schistosomes and trypanosomes, trick the immune system in other ways.

This discovery will have implications for the treatment of malaria. Not only will it offer new possible targets for drug therapy or vaccine, it will oblige us to take these infected white cells in the spleen into account in treating infections. The authors suggest that parasites within the dentritic cells may be in a state of “arrested” development and thus able to live a long time before reappearing. I’m wondering what role these arrested parasites might have in the development of drug resistance in Plasmodium spp. parasites.