The first English use of the term “parasite” was recorded sometime in the 1530s. Stemming from the Greek parasitos, “a person who eats at the table of another,” the early English term referred to “a hanger-on, a person who lives on others.” It was not until a century later that the term took on its biological meaning, “an organism that benefits at the expense of its host.”
From this definition, Trichuris muris, a nematode, has become a model organism for parasitism. A intracellular parasite of mice, T. muris is biologically similar to its cousin organism, Trichuris trichiura. The latter, also known as whipworm, parasites humans and causes trichuriasis once it has settled within the large intestine. Therefore, T. muris serves as a suitable substitute from which modern biology can explore, by experimentation, the dynamics through which T. trichiura produces the infection, itself a serious concern affecting over one billion persons in rural, low-income, and tropical regions.
Researchers of the Faculty of Life Sciences at the University of Manchester addressed this model parasite by investigating the factors that allow T. muris infection in laboratory mice. Published in Science, Hayes et al. show that the incidence of whipworm infection is dependent upon the microflora of the mammalian intestine. The presence of various bacterial species, namely Escherichia coli, controls the hatching of T. muris eggs.
Phrasing, here, is intentional. Various intestinal bacteria, including E. coli, were found to distribute themselves in clusters near the rounded edges of Trichuris eggs. Rather than illustrating chemical communication from the microflora to the macroflora, experimentation displayed actual physical contact between the bacteria and parasite eggs, whereby the E. coli cells bound to these end-sites of T. muris with their fimbriae, their cell-surface attachment structures. As if the bacteria can direct the physical action of when these parasitic eggs will hatch.
According to Rachel Ehrenberg of Science News, this research “highlights that parasite-host interactions don’t occur in isolation.” The presence of existing E. coli induces the hatching of these eggs, which in turn controls the infection the nematode can cause. Further experimentation demonstrated that the use of antibiotics to control the E. coli population will therefore limit one’s chances of progressing to infectious loads of Trichuris, of trichuriasis. But as with other cases of dealing with this intestinal ecosystem, these researchers and commentators note the limitations and drawbacks of the antibiotic approach, something explored in-depth with the issue of antibiotic-resistant strains of bacteria. A report from Physorg.com notes that “complex and subtle interactions between these different types of organism have evolved to provide an efficient and beneficial ecosystem for all concerned.”
But how, if parasites are indeed “hanger ons,” can their interactions with microflora produce benefits? It would seem a contradiction in terminologies is at hand. But the University of Manchester researchers comment that intestinal roundworm parasites are one of the more common infections throughout the world’s human population, and although the abundant presence of these organisms in our intestine will cause infection, the natural state of affairs may be one where our bodies continually contain these microscopic “persons who eat at the table of another.” While antibiotics may kill these communicative bacteria in the intestine, and reduce our gut load of nematode infection, Hayes et al. build upon various past studies that demonstrated how moderate levels of the parasite’s inhabitation can help the immune system prevent more burdensome infections and deflect other ailments. The low-to-moderate infection supplied by this physical exchange between worm and bacterium is a beneficial one; as University of Manchester’s Professor Ian S. Roberts notes, “Having a few worms knocking around might not be a bad thing.” A clinical study of children in rural Vietnam, published in 2009, helped start an interest in this mode of thinking; like the current findings, the endemic presence of infectious worms was found to prevent higher rates of dust-mite allergies in the subject population.
The existence of parasites offers protection, it seems. Another member of the research team, Richard K. Grencis, has stated that “the gut and its inhabitants should be considered a complex ecosystem, not only involving bacteria but also parasites, not just sitting together but interacting.” This notion, of the human body as an ecosystem, of micro and macroflora contributing to “ecosystem services” of a sort, has manifested as the study of microbiomes. The emerging field has introduced a reconceptualization in the way both medicine and ecology approach the human body. The microbiologist Martin J. Blaser may frame the moment best when he asks the question, “Who are we?” Principally, I find myself most struck by the now-established fact that only one in ten cells within our body is actually of human origin; the other 90 percent, although smaller in size, belong to this plethora of bacteria, fungi, protozoa, and macroflora such as the whipworm. Such new modes of thinking also include viewing processes in the body and of the immune system as analogous to wider processes in a large-scale ecosystem. The effect of a fever on intracellular parasites and microflora such as bacteria becomes akin to the impact a wildfire has on a forest, and the cracks of our skin become likened to the streams and pathways of water in a desert. Additionally, the field has spawned discipline-wide collaborative projects, none more so than the Human Microbiome Project, an attempt to characterize the base microbial composition of the human body, and therefore better understand the nature of infections and our immune defenses.
And the results have been emerging, both from human studies and those investigating other eukaryotic organisms. A recent collaboration by researchers from the Università degli Studi di Milano, Milan, Italy and the Tampere University of Technology, Tampere, Finland suggests that residential bacteria in our mouths may offer protection, as with the case of Trichuris and dust-mite allergies, against upper respiratory tract infections. Another study by Matthew H. Becker and Reid N. Harris, recently published in PLoS One, found that the presence of skin bacteria isolated from redback salamanders and yellow-legged frogs inhibited the in-vitro growth of Batrachochytrium dendrobatidis, an infectious fungus in part responsible for global reductions in amphibian populations.
But to think back to the recent findings on the relationship between E. coli and T. muris, the field of microbiomes also challenges our etymology of this phrase, “parasitism.” Further microbiological research is necessary to answer questions such as, “What does E. coli gain from this interaction with the whipworm? Does E. coli parasite the parasite?” The French philosopher of science, Michel Serres, might have addressed the issue best when, in his book The Parasite, he explored the connection between the triple implication of the word. Unlike its English root, the French le parasite produces three distinct but overlapping meanings: biological parasite, social parasite, and static. One of Serres’s better quotes goes along the lines of, “parasites parasite parasites,” whereby the divide between parasite and host is a gray one. T. triciura parasites the human intestine, but in turn may be limited by E. coli. Additionally, the nematode’s ability to infect is also controlled by poor living conditions and poverty, consequences of what some may consider the second translation of the French parasite, unequal economic circumstance. Serres used a tale from Aesop’s Fables to illustrate the point, in which a city rat visits the home of a country rat. The city rat may here be the parasite, taking the time and resources of the latter mammal, as defined in the 1530s English root of the word. But Serres noted that the country rat is just as much a parasite as the city dweller, as he is parasite to the farmer, whose home he lives within. Likewise, by extension the farmer may be parasite to the land on which he lives, or its primary owner, and so forth. The philosopher therefore asked, “Who exploits who? Who is the host and who is the guest? Where is the gift and where is the debt?”
But the heart of Serres’s philosophy, and its relevance to the communication between bacteria and nematodes, was in his idea of static, of noise, the third meaning of “parasite.” No system, he wrote, can exist without an interrupting force, this babble. Static interrupts, recreates something. Serres argued that even in the history of biomedicine and biology, the existence and obstacles posed by parasitic biological organisms presented an irregularity that had to be addressed, spurring the scientific discovery of the body. To Serres, parasites, in the broadest sense of the French term, are the driving force of progress. And today still, the confounding relationship between the organisms residing within our microbiomes, be them on the skin or in the intestine or mouth, advances our understanding of the human body. Attention to these inhabitants and processes, like the noise E. coli poses to T. muris, is a good starting point.