Next...Ms. Rex...Sue Rex?

In this week's PLoS One, Ewan Wolff and colleagues present evidence that a common parasite of birds, Trichomonas, also infected tyrannosaurid dinosaurs, and may have caused several, including the Field Museum's famous "Sue" to have died of starvation. The authors examined 61 tyrannosaurid specimens and found mandibular lesions in 10 of these that were consistent with similar lesions that are observed in modern-day birds that are infected with these parasites. Today, columbiforms are heavily parasitized by Trichomonas gallinae and these birds are likely the source of infection in raptors when they are consumed as prey (if anyone wants a live demonstration of this, come hang out in my office and watch the red-tails pick off pigeons). Wolff et al. argue that although infection via consumption of Trichomonas-laden prey can certainly not be ruled out, many of the specimens that show the lesions also have evidence of bite wounds on their heads, suggesting that face-to-face transmission may be the bigger culprit. While looking up information on T. gallinae, I also came across an interesting article in the Journal of Parasitology from last year that conducted molecular studies of Trichomonas isolates from doves around the U.S. using the parasites' ITS1, 18S and alpha-tubulin genes. The surprise of that paper was that the isolates from doves generally fell into two distinct clades - one similar to T. gallinae, but others that were genetically similar to the human STD, T. vaginalis! Clearly, more sampling of trichomonads should be done as they may play significant roles in the ecology of avian communities...and, as Wolff et al. suggest, may have even been having large impacts on birds' dino ancestors.

Source of a Scourge

We now know that humans are the hosts of five different species of malaria parasites. The most virulent of these is Plasmodium falciparum, which is thought to be responsible for close to two million deaths a year. Early molecular phylogenetic studies proposed that humans acquired this parasite from chickens, but subsequent studies showed that that result was an artifact of taxon sampling and paralogous genes and that the closest relative of P. falciparum is a chimpanzee parasite, named Plasmodium reichenowi, which was discovered in the 1920's. For decades, though, only a single strain of P. reichenowi existed in the lab or in any form from which DNA could be extracted and sequenced. Recently, eight new isolates of P. reichenowi were obtained from wild and wild-born chimps and the phylogenetic history of these lineages was studied and published online yesterday in PNAS by Steve Rich of U Mass Amherst and colleagues. These new results now show very nicely that P. falciparum represents a recent host shift from chimps into humans, which may have occurred as recently as 10,000 years ago. It has long been known that these two parasites cannot be reciprocally cross-reared, i.e., chimps cannot be infected with P. falciparum and humans cannot be infected with P. reichenowi (the discoverers of this species tried to give it to themselves!). Rich et al. cite another recent study that demonstrated a different preference for erythrocyte receptors in the two parasites. Perhaps our human ancestors acquired these mutations for receptors and enjoyed a period of being malaria-free, only to have a new - and deadlier - parasite evolve that preferred the human receptor form. Unfortunately, blood smears were not made from these new chimpanzee samples, so it's not yet possible to confirm that these samples share the same distinctive morphology of P. falciparum, but Rich has assured me that they're working on this. It would also be interesting to add the second "ape" parasite, Plasmodium schwetzi, from gorillas, a species that no one has samples of for DNA analysis. What I liked the best about this new study, though, is that these results mean that P. falciparum as a species should be sunk. Think the medical community could handle that?

More "Parasites Rule"

It's Friday afternoon, so I thought a little parasite distraction might be in order. Over at Mental Floss, there's a nice list of eight different parasites that affect their hosts' behavior, in order to promote their transmission: zombie snails, crabs, caterpillars, grasshoppers, fish, ants, and cockroaches. Good creepy stuff for cocktail party or coffee shop evolutionary chit-chat for sure! The last sentence is a question about whether or not there are parasites that affect human behavior. Clearly these folks need to read up on Toxoplasma!

The Importance of Understanding Evolution for Public Health

While lots of people are scrambling to make [good] phylogenetic trees of the new swine flu sequences in the context of other flu viruses, another paper came out in this week's PLoS Biology that presents a really powerful argument for incorporating evolution into public health. Andrew Read, of Penn State University, and others both at Penn State and at the Open University in the U.K. just published the results of their work on late-life acting (LLA) insecticides, arguing that if you understand a little bit about natural selection, you just might be able to profoundly stack the deck in the global battle against malaria. Mosquitoes as a whole, suffer a high mortality rate - according to Read et al., the figure is around 10% per day or 20-40% per gonotrophic, or egg-laying, cycle. In order to transmit malaria, a mosquito must take one blood meal from an infected person and then survive long enough to need a second one, with the interval between these events being long enough for the parasite to develop to an infective stage. Because development to the infective stage typically takes 10-14 days in malaria-endemic regions, very few infected mosquitoes live long enough to actually vector the disease. The paper argues that conventional insecticides such as DDT and pyrethroids, classes of which are "early-acting" insecticides that kill 80% of mosquitoes they come into contact with, exert tremendous selection pressure on mosquitoes to evolve resistance, because they are robbing a large proportion of the whole population of all of their fitness. Conversely, LLA insecticides, which kill mosquitoes after their first gonotrophic cycle, impose far less natural selection and thus the corresponding selection for resistance is slower to evolve. Crunching some numbers allowed Read et al. to show that an insecticide that killed mosquitoes after 2 or more gonotrophic cycles could reduce the number of malaria-infectious bites by 99.2%. Even the insecticides that took longer to kill mosquitoes still showed drastic reductions: the 4-cycle killers showed a 94.2% drop in deadly bloodmeals. Because evolution of resistance itself bears fitness costs to mosquitoes, LLA could allow for some insecticides to be "evolution proof" - i.e. the time it would take for mosquitoes to evolve resistance to these sprays would be so long as to essentially be immortal.

Hopefully this study and others like it (e.g. Wargo et al., 2007) will be carefully read by those making public health decisions - because thinking long-term - in an evolutionary sense, not just a medical sense - is absolutely critical. And if you're not a public health official, read these studies anyway - they make great examples for teaching the importance of evolution to everyday life.

More Proof that Parasites Rule the World

This week's Nature has an article by Kuris et al. [1] that presents the results of a long-term study of a California estuary that quantified biomass of various groups of organisms. Although as a percentage of the total, parasites are only about 1% of the animal biomass, but it turns out that parasitic trematodes can reach biomasses greater than the birds and fishes in the ecosystem! Some of these parasites are host castrators, thus if one considers these hosts as extended phenotypes of the parasites, the effective biomass of parasites is even higher. One of the things that I found most interesting, though, is that in some snails, the trematode parasites can be 22% of the animal' soft-tissue body weight, a stat published by several members of the same group this year [2]. There has already been a much-hyped instance of researchers accidentally sequencing a gene from a trematode parasite instead of that of the frog they were working on. Now these data are a big caution that the potential for sequencing parasite instead of host can be very high in many invertebrates. Potential for parasite contamination might be very high in EST libraries made from organisms that might be hosts, too...yikes!!

1. Kuris, A.M., R. F. Hechinger, J. C. Shaw et al. 2008. Ecosystem energetic implications of parasite and free-living biomass in three estuaries. Nature 454:515-518.
2. Hechinger, R.F., K. D. Lafferty, F. T. Mancini III, R. R. Warner, and A. M. Kuris. 2008. How large is the hand in the puppet? Ecological and evolutionary factors affecting body mass of 15 trematode parasitic castrators in their snail host. Evolutionary Ecology, in press.

Photo credit: Rodrigo Mexas, on http://nikoninstruments.mediaroom.com/index.php?s=13