A fungus called Cryptococcus gattii, has long known to be infective to humans… even though it’s found on trees.
This has particularly been a problem in Southern California, where people have been getting sick from C. gattii for yeas, and no one knew which tree was harboring the fungus. Find out who the culprit is and how they figured it out!
Here at Nothing in Biology Makes Sense, we’re fascinated by all the weird, baroque ways that living things influence and coevolve with each other—so Ed Yong’s new TED talk about mind-controlling parasites is right up our alley. Just like his writing—currently on display at National Geographic‘s Phenomena, among many other venues—it’s a compendium of nifty natural history punctuated with highly educational gross-outs and the occasional black-belt level pun.
Brood parasites are definitely the bullies of the avian world. They lay their eggs in the nests of other birds, sometimes destroying the host’s own eggs or just waiting for their nestlings to do the dirty work after they hatch. They then outcompete any surviving host nestlings for food, while the poor host parents are worked to the bone to feed the monstrous nest invader.
In spite of the steep costs of nest parasitism, most avian host species do not have effective mechanisms for detecting and removing brood parasites from their nests. So, why don’t mama birds notice they have a GIANT intruder in their nest and carry out some infanticide of their own? One hypothesis is that the cost of a mother bird making a mistake and pushing the wrong baby out (i.e. her own) outweighs the benefit of developing such a behavior.
This week in Science, Canestrari et al. published evidence for another hypothesis – that sometimes, it might actually be good to have your nest parasitized.
Evolutionary change by means of Natural Selection needs a couple of things in order to happen: heritability and variation in fitness. That is, offspring need to resemble their parents at least a little (heritability) and individuals need to differ in their survival and offspring production (fitness). We’ll worry about heritability in another post, but variation is something that seems like it might be hard to maintain. Some forms of Natural Selection will reduce variation as more fit individuals become frequent and all the different kinds of less fit individuals are eliminated from the population. However, there is a force, common in nature, which may maintain variation, parasites.
Interactions between hosts and parasites can generate strong selective pressures on each player, especially if your life depends on infecting a host. Often, biologists make an analogy to an arms race where players are developing bigger and better defenses or weapons. Antagonistic interactions may also generate negative frequency dependence where a rare host type is favored because the parasites are adapted to a common type. You can learn more by checking out CJ’s post on the Red Queen Hypothesis or Jeremy’s post on a different coevolutionary puzzle. A key component for maintaining variation via negative frequency dependent selection is specificity. There must variation in the interaction among different host genotypes and parasite genotypes. This is sometimes referred to as a GxG interaction. If parasites can infect all the hosts, there is no specificity. Specificity allows different hosts to be favored over time depending on the composition of the parasite population.
Theoreticians love to use different models of interactions between hosts and parasites, but without empirical evidence, there seems little point. In a recent paper by Rouchet and Vorburger (2012), the authors looked for evidence of just the kind of genetic specificity would result in the maintenance of genetic variation.
Conventional wisdom suggests that pathogens and parasites are more rapidly evolving because of various reasons such as short generation time or stronger selection. Yet somehow, they have not completely won the battle against the host. Recently, a theoretical paper on coevolution in Nature caught my eye (Gilman et al., 2012). Here the authors address this paradox: “How do victim species survive and even thrive in the face of a continuous onslaught of more rapidly evolving enemies?”
Instead of treating a coevolutionary interaction between two species as the interaction of only two traits, the authors investigate the nature of an interaction among a suite of traits in each species. It’s not hard to think of a host having a fortress of defenses against attack from a parasite with an arsenal loaded with many weapons.
A reed warbler feeds a cuckoo chick
Brood parasitism, the reproductive strategy of choice for cuckoos and cowbirds, sounds like a lazy approach to parenting: lay your eggs in another bird’s nest, and let the unwilling adoptive parents take the trouble to raise your chicks. But contracting out parental care like this comes with many of its own complications. Chicks raised by parents of a different species have to eliminate competition from their adoptive nestmates, and may grow up a bit confused; reluctant host birds may need to be told, and reminded, that raising cuckoo chicks is an offer they can’t refuse.
But before crossing all those hurdles, a brood parasite’s first task is to lay eggs in the nest of a host who won’t immediately recognize and reject them. The strong natural selection imposed by host rejection has led cuckoos to evolve “host races” that lay eggs whose color and spotting pattern matched to those of their preferred host species. This kind of broad-scale pattern could arise without much direct effort by female cuckoos—those who lay eggs in the nest of the best matching host species would simply be the ones most likely to have chicks that survive to the next generation. But is it possible that cuckoos do take an active role in matching up to their hosts, seeking out host nests containing eggs that look like their own?
The answer, according to a series of studies over the last several years, is yes—probably.
A red flour beetle. (Image via Wikimedia Commons.)
When evolutionary biologists think about sex, we often think of parasites, too. That’s not because we’re paranoid about sexually transmitted infections—though I’d like to think that biologists are more rigorous users of safer sex practices than the general population. It’s because coevolution with parasites is thought to be a major evolutionary reason for sexual reproduction.
This is the Red Queen hypothesis, named for the character in Lewis Carroll’s Through the Looking Glass who declares that “it takes all the running you can do to keep in the same place.” Parasite populations are constantly evolving new ways to infest and infect their hosts, the thinking goes. This means that a host individual who mixes her genes with another member of her species is more likely to give birth to offspring that carry new combinations of anti-parasite genes.
But although sex is the, er, sexiest prediction of the Red Queen, it’s not the whole story. What matters to the Red Queen is mixing up genetic material—and there’s more to that than the act of making the beast with two genomes. For instance, in the course of meiosis, the process by which sex cells are formed, chromosomes carrying different alleles for the same genes can “cross over,” breaking up and re-assembling new combinations of those genes. Recombination like this can re-mix the genes of species that reproduce mostly without sex; and the Red Queen implies that coevolution should favor higher rates of recombination even in sexual species.
That’s the case for the red flour beetle, the subject of a study just released online by the open-access journal BMC Evolutionary Biology. In an coevolutionary experiment that pits this worldwide household pest against deadly parasites, the authors show that parasites prompt higher rates of recombination in the beetles, just as the Red Queen predicts.