conservation

This week's Nature has a news article by Emma Marris about bison conservation and genomics. I've been very interested in cattle and bison as an example of introgression in large mammals; in this case between two genera separated by over a million years of divergence. Possibly all, and certainly most of the bison left today have cattle genes in them. The article profiles geneticist James Derr, who sees these cattle genes as a conservation problem:

Wildlife managers have considered the genetic diversity of animals for some time, and animals in captivity have often been bred to preserve genetic diversity. But those were blunt approaches. Now, armed with genomic tools, researchers are starting to look at specific sequences in the genome, and are raising questions about what the fundamental unit of conservation should be. Most people see preserving wildlife as a matter of saving individuals; if all the individuals die out, the species becomes extinct. But that reasoning looks simplistic when considered at the genomic level. If the genes of a species change enough — through interbreeding, for example — that species will cease to exist even if individuals that look something like the original continue to thrive.

This issue is quite threatening to the entire idea of endangered species preservation. One argument for extending protection to multiple populations of species like chimpanzees is that you are preserving gene pools that have unique evolutionary histories. You can't just preserve one tiny corner of a species and expect to retain the genetic diversity that was present in the whole species' range.

But if your species' genetic diversity is already compromised by introgression, either from within the same species or from other more distant lineages, this argument is weakened. And if it's OK to preserve a fragment of diversity in an interbred population, then why not simply introgress the endangered species' genes into a more common, cosmopolitan relative. That is, why save the wolf, if you've already got lots of dogs with wolf genes in them? Why save the polar bear, when its genes will continue to exist in brown bears?

As the article notes, this question is really academic for most threatened species, whose population histories may not lend themselves to such promiscuous gene mixing. But bison are an interesting case nonetheless --

In 1905, then US President Theodore Roosevelt and William Hornaday, head of the New York Zoological Society (now known as the Wildlife Conservation Society), founded the American Bison Society, which collected bison and established herds in a few reserves in Montana, Oklahoma and South Dakota. A small herd, perhaps 30 in number, was still roaming Yellowstone National Park. According to Derr, all the bison in the United States today — there are now up to a million of them, mostly on private ranches — can probably be traced back to fewer than 200 bison.

Other scientists argue that the most important thing may not be unique genes, but instead unique cultural inheritance and status within ecological communities:

"There are more important things than genes," says Rurik List, an ecologist at the National Autonomous University of Mexico, who works with a herd that spans the US–Mexico border. These bison have some cattle genes, but they also have institutional memory. If List were to remove them and replace them with pure animals, would the bison still be able to find the water holes that the current herd knows so well? "They have been behaving like bison for 80 years," says List. "They have been fulfilling an ecological role."

So far all the genetic estimates of introgression are based on only 14 markers -- probably good enough as a test for the fraction of introgression dating back within the last 150 years, but it's not going to give any information about the dynamics or even the identity of genes that have moved into bison. Many more markers are going to be necessary in this and other cases of reintroductions and hybridization with domesticated varieties.

References:

Marris E. 2009. Conservation: The genome of the American West. Nature 457:950-952. doi:10.1038/457950a

Scientific American reports on a taxonomic auction by Purdue University:

Naming your kid after you is one thing. But imagine if an entire species were named for you.

This week, Purdue University is auctioning off the rights to name seven newly discovered bats and two turtles, the Associated Press is reporting. The winners — who will shell out a minimum of $250,000 for at least one of the bats, a Purdue spokesman told ScientificAmerican.com — can link their own name or that of a pal to the animal’s scientific name.

"Unlike naming a building or something like that, this is much more permanent. This will last as long as we have our society," John Bickham, who co-discovered the nine species, told the AP.

I don't think there's anything wrong in principle with selling the naming rights to your new species. Heck, I'd be happy to name a new species after a donor, if I had either. I don't even think there's anything wrong with consistently adopting a splitter's viewpoint on new species, keeping in mind that you have many donors and other people that you might honor with your work.

But it seems to me there is a truth-in-advertising problem here. Species names are not eternal. They are hypotheses. We re-evaluate the relations between living populations and fossil populations all the time. The scientific community ignores ("sinks") taxonomic names that they come to believe are synonymous with existing taxa. So there is an obvious question: what are you really paying for, if you bid on naming rights for a species?

Naturally, it will depend on the investigators. Are they credible? Do they have a good record in the practice of taxonomy?

In the end, you're taking a bet: A bet against future discoveries. A bet that today's knowledge is the best there will be, at least where taxonomy is concerned. A bet that today's fashion won't reverse itself -- where the fashion is to recognize lots and lots of species, which helps to promote conservation goals tied to Endangered Species status.

Well, I suppose we can say that the people who would splurge for more than $250,000 for a name don't really care if the name sticks. They probably want something else -- let's say, a story. That might include a motive to fund research on bats (in this case) or some other group of organisms, or just to fund conservation work generally. Or it might just be a line at a cocktail party -- hey, my wife has a species named after her. Or in the case of a recent taxon sale, good advertising for a casino.

But maybe the people who bid on species naming rights ought to be made aware that it is a bet. Not eternal glory, just a chance at it.

(via Sandwalk)

In last week's Science, Stanislas Dehaene and colleagues describe the relation of cultural invention to "universal intuition" about mathematical logic:

The mapping of numbers onto space is fundamental to measurement and to mathematics. Is this mapping a cultural invention or a universal intuition shared by all humans regardless of culture and education? We probed number-space mappings in the Mundurucu, an Amazonian indigene group with a reduced numerical lexicon and little or no formal education. At all ages, the Mundurucu mapped symbolic and nonsymbolic numbers onto a logarithmic scale, whereas Western adults used linear mapping with small or symbolic numbers and logarithmic mapping when numbers were presented nonsymbolically under conditions that discouraged counting. This indicates that the mapping of numbers onto space is a universal intuition and that this initial intuition of number is logarithmic. The concept of a linear number line appears to be a cultural invention that fails to develop in the absence of formal education (Dehaene et al. 2008:1217).

The idea is that children in Western societies have to learn that a number line is a linear representation; they begin by compressing the space devoted to large numbers:

When asked to point toward the correct location for a spoken number word onto a line segment labeled with 0 at left and 100 at right, even kindergarteners understand the task and behave nonrandomly, systematically placing smaller numbers at left and larger numbers at right. They do not distribute the numbers evenly, however, and instead devote more space to small numbers, imposing a compressed logarithmic mapping. For instance, they might place number 10 near the middle of the 0-to-100 segment. This compressive response fits nicely with animal and infant studies that demonstrate that numerical perception obeys Weber's law, a ubiquitous psychophysical law whereby increasingly larger quantities are represented with proportionally greater imprecision, compatible with a logarithmic internal representation with fixed noise (7, 20, 21). A shift from logarithmic to linear mapping occurs later in development, between first and fourth grade, depending on experience and the range of numbers tested (17-19).

They note that there's a problem testing these ideas in Western children, who are surrounded throughout their development by numbers -- in books, "elevators" and other places. Most of these numbers are small ones -- especially one through ten -- so they might naturally accentuate the ones they know.

They found when testing the Mundurucu that both adults and children tended to compress the high end of the number scale, even testing numbers between one and ten. This compression is logarithmic -- they accentuate contrasts between small numbers disproportionately. It makes sense logically -- we care more about detailed contrasts between small numbers than large numbers. They don't give an idea of which logarithm people are using; and in fact it may be different ones for different people. The important fact is the small number/large number contrast.

Dehaene and colleagues attribute this scaling to mapping at the neural level:

What are the sources of this universal logarithmic mapping? Research on the brain mechanisms of numerosity perception have revealed a compressed numerosity code, whereby individual neurons in the parietal and prefrontal cortex exhibit a Gaussian tuning curve on a logarithmic axis of number (27). As first noted by Gustav Fechner, such a constant imprecision on a logarithmic scale can explain Weber's law -- the fact that larger numbers require a proportional larger difference in order to remain equally discriminable. Indeed, a recent model suggests that the tuning properties of number neurons can account for many details of elementary mental arithmetic in humans and animals (21). In the final analysis, the logarithmic code may have been selected during evolution for its compactness: Like an engineer's slide rule, a log scale provides a compact neural representation of several orders of magnitude with fixed relative precision.

From that perspective, the Western conception of the number line appears as a very distinctive invention, capable of adjusting the logarithmic encoding to arrive at faster and more accurate mathematical conclusions about large numbers. The authors speculate that addition and subtraction (which display invariance between large and small numbers) and experience with measurement underlay the development of the linear concept in Western children.

References:

Dehaene S, Izard V, Spelke E, Pica P. 2008. Log or linear? Distinct intuitions of the number scale in Western and Amazonian indigene cultures. Science 320:1217-1220. doi:10.1126/science.1156540

That's a quote from the International Union for Conservation of Nature, in this Elizabeth Rosenthal article. This spring has seen a backlash against biofuel generation based on its apparent impact on food prices. Among the most promising alternatives to starch or sugar-based ethanol production is cellulosic production from wild grasses or reeds.

The problem is that the perfect biofuel species -- one that grows easily in a variety of habitats, with little care, and possibly perennial so that it can be harvested year after year without repeated planting -- pretty much is the textbook definition of an invasive plant species.

The European Union is funding a project to introduce the "giant reed, a high-yielding, non-food plant into Europe Union agriculture," according to its proposal. The reed is environmentally friendly and a cost-effective crop, poised to become the "champion of biomass crops," the proposal says.

A proposed Florida biofuel plantation and plant, also using giant reed, has been greeted with enthusiasm by investors, its energy sold even before it is built.

But the project has been opposed by the Florida Native Plants Society and a number of scientists because of its proximity to the Everglades, where giant reed overgrowth could be dangerous, they said. The giant reed, previously used mostly in decorations and in making musical instruments -- is a fast-growing, thirsty species that has drained wetlands and clogged drainage systems in other places where it has been planted. It is also highly flammable and increases the risk of fires.

Well, burning the stuff certainly defeats the purpose. It seems to me that most of these drawbacks come from insisting on a monoculture, which -- if you have an efficient cellulose processing capacity -- I don't see why you care about. A real natural marsh or tallgrass ecosystem can't stand much mowing, but if you could tune a multispecies ecology for biofuel production, that would pose much less risk of invasive potential, and would be less trouble to look after. The tallgrass ecosystem was based on burning, anyway, so you should be able to maintain the soil while taking out hydrocarbons with minimal fertilizing.

A new paper in Current Biology documents the mortality suffered by Taï Forest chimpanzees as a result of common human respiratory ailments during the last ten years. Tissue samples of deceased animals provided information about the pathogens that caused the outbreaks:

Necropsy samples were screened for respiratory pathogens by using different PCR methods. As for most human respiratory cases, a mix of bacterial and viral respiratory pathogens was found in the lungs. The most common bacterium was Streptococcus pneumoniae, which was found in all respiratory outbreaks. In addition, Pasteurella multocida played a role in the 2004 outbreak [10]. All available samples tested positive for one of two paramyxoviruses: human respiratory syncytial virus (HRSV) was diagnosed in two individuals that died in the 1999 north group outbreak and in one adult female (east group) and one infant (south group) who died in the 2006 outbreak, which occurred simultaneously in both groups. The second virus identified was human metapneumovirus (HMPV), detected in three animals that died in the 2004 south group outbreak (Table 1).

Humans have suffered from these respiratory ailments for a long time. The number of human respiratory pathogens almost certainly proliferated greatly during the last 10,000 years, after the advent of agriculture and village life brought the potential of "crowd diseases." For example, human respiratory syncytal virus (HRSV) is closely related to the bovine BRSV and pneumonia virus of mice (PVM). It seems plausible that the human pathogen descended from the mouse or cattle (or sheep) virus, but no one has yet demonstrated this -- and it is after all possible that they got it from us. HRSV is an important cause of lower respiratory tract infections in humans worldwide, especially in children. In an ironic twist, HRSV was first identified in captive chimpanzees as the cause of a respiratory infection with runny nose and sneezing (called coryza) (Blount et al. 1956). It was actually the human RSV virus contracted by the chimpanzees that had caused the infections.

Much the same thing has happened to the wild chimpanzees, but with a high death toll. A 1999 outbreak of HRSV, compounded by Streptococcus pneumoniae, killed 6 out of 32 animals in the affected group, including 5 adults. A 2004 outbreak killed 8 out of 44 animals. These two outbreaks each killed nearly a fifth of the chimpanzees in these groups, and demographic records show that several "multiple mortality events" in the last 24 years are not attributable to poaching or other diseases such as ebola or anthrax (each of which had least one outbreak).

Easily spread respiratory ailments are among the main causes of sickness in contemporary hunter-gatherers, partly because they are able to persist and spread effectively in low-density populations, and partly because they are so common in neighboring groups. Today, respiratory diseases are an important cause of death in these groups -- including adults -- although they count for fewer deaths than gastrointestinal pathogens and parasites. Their ability to infect low-density populations suggests that some human respiratory pathogens surely date to much earlier periods of human evolution.

One thing is certain: humans have undergone thousands of years of selection, in which susceptible individuals have disproportionately been killed by human-infecting respiratory viruses and bacterial strains. Many of these pathogens have adapted very well to humans, including a substantial time or fraction of the population in which they may be present without causing noticeable symptoms.

Chimpanzees lack this history. Relatively minor diseases in humans may have major effects on chimpanzees, and diseases like RSV that cause measurable mortality among human infants may have devastating effects on chimpanzee communities. Together, respiratory illnesses, ebola, and anthrax are having a death toll in the studied chimpanzee groups almost as great as smallpox in post-contact American Indians.

The shocking thing is that this enormous death toll seems likely to have been caused by the researchers themselves, along with ecotourists:

It has long been recognized that respiratory disease is the most important cause of morbidity and mortality among wild great apes habituated to human presence for research or tourism [4], [24], [25], [26] and [27]. However, the etiological agents of such disease have not been documented. Possibly as a consequence of respiratory disease, about half of the long-term chimpanzee research populations have shown major declines [4] and [28]. Our results suggest that the close approach of humans to apes, which is central to both research and tourism programs, represents a serious threat to wild apes (Köndgen et al. 2008:262).

The authors temper this conclusion in two ways. First, they show that the presence of the research station and the tourist site both have significantly decreased the incidence of poaching at and around these areas. Both areas have lots of chimpanzees, but little sign of poachers in contrast to the rest of the protected forest, where poacher sign is common. Poaching accounts for nearly as many documented deaths in the study population as respiratory infection, so this protective effect may be very important.

On the other hand, communicable diseases may well spread beyond a single group, so much of the forest may be at high risk from both poaching and human pathogens. And needless to say, poachers may spend less time around the research and tourist areas, but that hasn't stopped them from killing lots of chimpanzees there. So the protective effect may not be much of a shield.

Second, they provide recommendations that may decrease the risk to the chimpanzees while permitting continued human presence:

In order to reduce the negative effects of research and tourism, strict hygiene protocols, including vaccination requirements for tourists, tourism personnel, park staff, and research personnel against all potentially dangerous diseases for which vaccines are available (e.g., measles, mumps, and rubella), should be implemented [5], [6], [29] and [30]. Only nonsymptomatic visitors and staff should have access to habituated apes. Feces, vomit, and other human debris or wastes should be removed from areas where chimpanzees may come in contact with it or buried at a depth where other animals will not uncover it [29]. Because carriers of human respiratory pathogens are often nonsymptomatic, wearing of masks (e.g., N95 masks as recommended for avian flu) [31] should be mandatory. Human populations living around the parks and reserves should be vaccinated, thereby decreasing the chances of human-pathogen introduction into chimpanzee populations. As in the Taï project, demographic, clinical, and diagnostic monitoring systems should be implemented to objectively document the negative effects of research or tourism. Furthermore, we urge an intensification of research on ways to prevent disease transmission, as well as the development of new methods for vaccine and treatment delivery, to wild apes (e.g., oral baiting) (Köndgen et al. 2008:262-263).

These are necessary precautions, but they are unlikely to be enough. There is no effective or widely available for RSV, or HMPV. S. pneumoniae normally exists in the respiratory tract of 10 percent of healthy adults. There is no way that chimpanzees can hold off these diseases if they are in recurrent contact with people.

References:

Blount RE Jr, Morris JA, Savage RE. 1956. Recovery of cytopathogenic agent from chimpanzees with coryza. Proc Soc Exp Biol Med 92:544-549.

Köndgen S and 17 others. 2008. Pandemic human viruses cause decline of endangered great apes. Curr Biol 18:260-264. doi:10.1016/j.cub.2008.01.012

A Cornelia Dean article explores a theme that concerns many primatologists, indeed anyone who studies threatened animals: When you confine a small set of animals to a tiny patch of forest, they can't move when their patch starts to degrade. Climate change will certainly pose such a threat over the long term -- today's climate being vastly different from the Pleistocene -- and many are worried that local climate changes may significantly impact habitat patches within the next 100 years.

This kind of uncertainty is widespread. For example, Dr. Hamilton said that on the Northern California coast, fog has an influence on natural systems. But "none of our climate models can tell us what is going to happen with fog," she said. "So we are facing profound uncertainties about how our coastal ecosystems are going to look."

"It's a real dilemma," said David S. Wilcove, a conservation biologist at Princeton. "What you are trying to do is balance the urgent needs of the present -- the ongoing destruction of habitats that species need now -- with the urgent needs of the future -- places where they may end up if they are able to move in response to changing climate."

Clearly, even though governments and others have been setting aside patches of habitat for 100 years, that is nothing compared to the geological time over which species originated. A true conservation plan will require contingencies for climate change, in some cases extending to relocation plans. But as the article points out, much of the activity of conservationists is mere triage -- trying to stabilize threatened populations. It doesn't help that the natural world can be as unstable as the human world. Species have adapted to natural instability, but being penned in by humans is entirely new.

Rex Dalton reports on Charles Musiba's efforts to preserve the Laetoli footprints with a new museum:

[The weathering to the trackways] prompted Tanzanian anthropologist, Charles Musiba, now at the University of Colorado in Denver, to call for the creation of a new museum to reveal and display the historic prints. But other anthropologists question this idea -- as they did when the tracks were covered -- because Laetoli is several hours' drive into Ngorongoro National Park, making guarding and maintaining any facility extremely difficult. Musiba presented his proposal for the museum last month at the International Symposium on the Conservation and Application of Hominid Footprints, in South Korea. He says that Tanzania now has the scientific capacity and the funds to construct and monitor a museum.

Dalton quotes Tim White and Terry Harrison as skeptics, citing them as

among a group that favours cutting the entire track out of the hillside, then installing it in a museum in a Tanzanian city

The article weighs pros and cons. Dalton also gives a good description of the problems that arose with previous attempts to preserve the trackways. Initially covered with dirt, the trackways were endangered when acacia trees sprouted and started breaking up the ash layer. The current setup, constructed in 1995, involves a mat overlain by fill, but this is eroding out.

I tend to think they should be managed in a way that maximizes their benefit to local people. It's hard for me to believe that chunking the whole thing out and moving it in trucks halfway across Tanzania would be better than whatever might happen in a poorly-guarded museum. But clearly there are no perfect choices. It is a real challenge to start and build continuing interest in a museum like this without very strong support -- but I would like to see it succeed.

References:

Dalton R. 2008. Fears for oldest human footprints. Nature doi:10.1038/451118a

Julien Riel-Salvatore has been following the fungus problems at Lascaux. His earlier post discusses a December NY Times article on the problem. That article is a really good one, it explains why this fungus problem is different from the white fusarium fungus that preservationists battled in the cave in 2001.

Whatever the reason for the problems at Lascaux, the white mold outbreak in 2001 led the government to close it to all nonessential visitors.

It was so serious that, to stop the invasion, the floor was covered with quicklime and scientists began treating the problem chemically, said Marc Gauthier, president of the International Scientific Committee for Lascaux, which was created as a result of the crisis.

The new problem at Lascaux, however, does not appear to be linked to the fusarium fungus. Described by experts as black stains, the blemishes are in fact both gray and black. "They vary from a few millimeters to 4 centimeters," said Mr. Geneste, noting that most are found in the passages where the rocks are most porous and paintings had faded the most long before modern man entered. While only a few stains have affected the paintings, they have now been found in some 70 different spots.

Now, Julien links to a more recent story from the CBC, which describes the political pettifog between the International Scientific Committee and the French government:

[The team of specialists] put pressure on the French government by alerting UNESCO, which classifies the caverns as a World Heritage Site, about the conditions.

Laurence Leaute-Beasley, president of the International Committee for the Preservation of Lascaux, called for the management of the caves to be taken out of the hands of the French government, saying someone who understands the science involved should take over.

The French government, not wanting such an an important site to be seen as neglected, has decided to accept the committee's advice and act now against the fungus.

So they were threatening to bring the UN into France to fight an invasive subterranean fungus. Don't tell the "black helicopter" believers!

The experts disagreed on the cause of the problem. Some say global warming is to blame, others that human activity in the caves is exacerbating the problems.

Global warming is not to blame. It's not a totally silly idea -- the Times article discusses an increase in the average soil temperature around several caves, and Lascaux is a relatively shallow one that might be influenced by increasing soil temperatures. But the climate around these caves has fluctuated a whole lot more during the last 20,000 years than in the last 20. The important recent changes have been caused by people -- walking into the cave, lighting the cave, ventilating the cave.

But now that the changes have been initiated, they can't be solved by people just leaving the cave alone. It seems like such a curious contrast -- archaeologists know they must destroy the sites to learn from them; art historians must preserve their objects to learn from them. Lascaux is both site and object, and has faced both pressures.

Good news for bonobos:

Congo has announced the establishment of a rain-forest preserve intended to shield the bonobo, one of human beings' two closest ape relations, from wildlife poachers and deforestation.

The Sankuru Nature Reserve -- at 11,803 square miles, it is larger than the state of Massachusetts -- is being created through a partnership involving American and Congolese conservation groups and government agencies.

This is just a fascinating story from the international Der Spiegel:

Knut Should Be Killed, Say Some Animal Activists

Berlin's polar bear cub Knut is more famous than ever. Even star photographer Annie Leibovitz has been to take his picture. But not everyone loves the little bear. Animal rights activists want him put to sleep because he has been raised on a bottle.

It is such a contrast -- the photography is toward the aim of making the polar bear a symbol against climate change; the "animal rights activists" decry the fact that the cub is being raised by people.

Berlin Zoo is allowing Knut to be raised in such a way that the bear will have a behavioral disorder for the rest of his life, Albrecht believes. "In actual fact, the zoo needs to kill the bear cub," he adds.

He's not alone. Wolfram Graf-Rudolf, director of the Aachen Zoo, told the newspaper, "I don't consider it appropriate for the species that the little polar bear is being raised on a bottle." The animal will be fixated on his keeper and not be a "real" polar bear, he says. However he feels it is now too late to put Knut out of his supposed misery. "The mistake has been made. One should have had the courage to put him to sleep much earlier."

Of course, some "animal rights activists" are simply anti-zoo, and this case seems like quite the publicity-driver. The really surprising part of this to me is that it has happened before:

The idea isn't as outlandish as it may at first seem. Although giving Knut a death sentence would likely bring his many fans out on to the streets, baby zoo animals have been killed for the same reason in the past. Two-day-old baby sloth Hugo was put down by lethal injection in Leipzig Zoo at the end of last year, sparking emotional protests.

I couldn't find any other story confirming "emotional protests" after the death of a sloth named Hugo, so I have my doubts. But this certainly seems a different context than discussions about American zoo animals.

Like pandas. Those little guys can't feed themselves!

(via Volokh Conspiracy)

Jim Robbins of the NYT has written a long article about genetic introgression of cattle genes into bison populations. The article is mainly concerned about management, and wildlife managers are trying to minimize the proportion of cattle genes in their conserved herds:

Over time, cattle genes have spread into many of the remaining herds of American bison. Since the late 1990s, Dr. Derr and his graduate students have traveled to public and private bison herds around the country, taking blood samples. They have concluded that the vast majority of the 300,000 or so bison in the United States are hybrids, though they look like pure bison. Fewer than 10,000 bison are genetically uncontaminated.

The whole idea of "genetic contamination" implies that there is something bad about this genetic introgression. But we can guess that the cattle genes don't intrinsically reduce fitness, since bison with cattle genes have been greatly increasing in numbers. And these introgressed herds are unlikely to be fixed for any cattle genes, so the original bison alleles still have every chance to compete with the cattle alleles. In other words, the cattle introgression has introduced variation into bison, some of which might be adaptive.

As you can tell, I'm not very sympathetic to the idea that we should prevent "genomic extinction" by insisting on some kind of genetic purity. It seems to me that we want to retain as much variation in our conserved populations as possible, so that they can adapt to changing climatic conditions in the future. We can't predict which alleles will be adaptive.

The geneticists in the article worry that cattle genes will make the bison susceptible to cattle-borne diseases like Texas fever. But making a large herd of genetically uniform bison is hardly the way to prevent disease!

Now, a history of selection for docility on ranches is of more concern:

"Ranchers might get rid of a cantankerous bull, for example," said Curt Freese, a biologist who directs Great Plains bison restoration for the World Wildlife Fund. "Breeding bison to be docile and meaty are the kinds of things that affect the wildness of the bison."

But it's unpredictable what behavioral traits will adapt bison to a conserved herd, which after all must be smaller and occupy a lot less space than many of the ancestral bison herds. They may end up more docile anyway, or just the opposite. I tend to think that selection will sort all this out.

Managers of these herds must also keep a wary eye on hybridized invaders. In Yellowstone, officials found a domestic bison that had wandered into the wild population from a neighboring ranch. And Wind Cave National Park is adjacent to Custer State Park, where the animals are hybridized.

The new approach may change other aspects of management, as agencies move from managing the species to managing the genetics. Dr. Derr is involved in a study, for instance, of whether the hunting of the bison that leave Yellowstone might be selecting certain behaviors from the population because animals that migrate are targeted.

This kind of selection is unavoidable in conserved populations, and might even be desirable -- they do, after all, want to stop the bison roaming out of the park. Roaming out of the park is one of the more noticeable bison phenotypes. I'm more worried about all the selection that is happening but doesn't have obvious effects.

This seems like a good doctoral project for somebody: how do the introgressed bison compare behaviorally with "genetically pure" bison? And the all-important question: how does mean fertility compare between these herds? They've both historically grown very rapidly, but does one maintain higher mean fitness than the other? Are there more animals in the Custer herd that fail to reproduce?

Anyway, there was no way to quantify the introgression until recent molecular techniques made it possible, and Ted Turner and others were happy to breed large bison herds that contained introgressed cattle genes. The only difference now is that wildlife managers know that some herds are "more pure" than others. But making conservation decisions on "purity" seems less relevant than fitness, which they still don't know much about because it's harder to measure. There is a presumption that the originally bison alleles will be more fit, but today's conserved situations are very different from those faced by ancient bison. And the historic bison -- the ones shot up by Buffalo Bill -- were facing a very novel environment compared with their ancestors.

The best we can hope for is a capacity for adaptation, which will maximize the chance of survival. In that context "genetic purity" is less important than genetic variability.

Here's a happy AP article:

BRISTOL, England - A western lowland gorilla has given birth at a zoo in southwest England after being given a fertility drug that is normally used on humans, zoo officials said Friday.

She's been trying for 20 years, after having a first baby young.

After consulting gynecologist David Hill, a senior lecturer at the University of Bristol, zoo veterinarians gave Salome a fertility drug called clomifene to stimulate ovulation, Carroll said.

Salome became pregnant three months after first receiving the treatments, he said.

We're running completely irony- and snark-free here on Christmas. Nothing more than a touching story of gorilla motherhood.

"Female gorillas, like their human counterparts, find conceiving more difficult as they get older, so zoos may now be able to give some of their important breeders a helping hand," Caroll said. "Being able to treat female gorillas with human fertility drugs is potentially a very important breakthrough."

Carroll said the treatment was likely to be replicated worldwide.

OK, I guess that was a little bit too Handmaid's Tale-like...

The title of the one-page paper by Magdalena Bermejo and colleagues tells most of the story: "Ebola oubreak killed 5000 gorillas."

Over the past decade, the Zaire strain of Ebola virus (ZEBOV) has emerged repeatedly in Gabon and Congo. During each human outbreak, carcasses of western gorillas (Gorilla gorilla) and chimpanzees (Pan troglodytes) have been found in neighboring forests (1). Opinions have differed as to the conservation implications. Were these isolated mortality events of limited impact (2)? Was ZEBOV even the cause (3)? Or, were they part of a massive die-off that threatens the very survival of these species (4)? Here, we report observations made at the Lossi Sanctuary in northwest Republic of Congo, where ZEBOV was the confirmed cause of ape die-offs in 2002 and 2003 (5). Our results strongly support the massive die-off scenario, with gorilla mortality rates of 90 to 95% indicated both by observations on 238 gorillas in known social groups and by nest surveys covering almost 5000 km². ZEBOV killed about 5000 gorillas in our study area alone.

Gorillas aren't alone; the authors estimate that ca. 85 percent of chimpanzees also died, but don't have detailed observations on their initial numbers, so they can't give a census number.

The paper doesn't answer an important question -- how do these apes get Ebola? There is a Timesarticle that tries to address this:

Precisely how gorillas contract the disease is a mystery. Scientists assume they must catch it somehow from another animal that acts as a natural reservoir host and carries the virus without being harmed by it. Fruit-eating bats are suspected, but none has been confirmed as the reservoir, Dr. Nichol said.

Whatever the host, it could infect western gorillas by defecating on their food, which is mostly fruit. The gorillas could then infect one another, both inside their own social groups and between groups. The virus is spread by bodily fluids and by touching sick or dead animals. Dr. Walsh said that gorillas commonly eat one another's dung, which could also transmit the virus.

Scientists have debated about whether gorillas' infecting each other plays much of a role in spreading the disease, or whether the reservoir host is really the main culprit. The new report says the gorillas themselves do play an important part: it shows that the spread of the disease and the timing of outbreaks match the pattern that would occur if the animals were infecting one another, both within and between groups.

It's hard for me to imagine it isn't spreading directly from individual to individual. Still, it seems to be jumping between groups very quickly -- certainly faster than individuals transfer between social groups. Which suggests it may spread more easily between these apes than between humans. Which is scary, since it suggests it might evolve to spread more readily between people than it does now.

Yikes.

References:

Bermajo M, Rodríguez-Teijeiro JD, Illera G, Barroso A, Vilà C, Walsh PD. 2006. Ebola oubreak killed 5000 gorillas. Science 314:1564. DOI link

I ran across this story about unusual disease affecting hybrids of Asiatic and African lions in Indian zoos:

NEW DELHI - Nearly two dozen crossbred lions are slowly dying in northern India from a mysterious disease afflicting the hybrid offspring of Asiatic and African cats paired in a discontinued experimental program.

Zookeepers are mournfully watching the results of the program, which began in the late 1980s at the Chhatbir Zoo and was ended in 2002 after many of the nearly 80 crossbred lions were struck by a mysterious disease linked to inbreeding and a weakened gene pool, said Kuldip Kumar, Punjab state's conservator of forests and wildlife.

This is very curious. I did a little search to see if anything more detailed had been written. The best I could find was an article from 1990 that mentioned possible problems related to inbreeding Asiatic lions in American zoos, which turned out to be genetic hybrids:

Meanwhile, Paul Joslin was not quite sure whether the "Asiatic lions" in US zoos were really Asiatic lions. Joslin, then assistant director of Chicago's Brookfield Zoo and now an independent zoo consultant, had noticed that many of the lion males lacked a telltale belly fold, a flap of loose skin on their undersides that distinguishes Asiatic from African lions. He was also worried that increased infant mortality among "Asiatic lions" in US zoos signaled inbreeding problems.

...

O'Brien and Martenson eventually found that almost all Asiatic lions in US zoos and some in Asian ones as well were hybrids. As a result, US zoos agreed to suspend mating Asiatic lions and allow the hybrid animals to die off naturally (Cohn 1990:168).

So I wonder if this is some infectious disease that has been affecting their chronic health, or if -- as the reports seem to suggest -- there is some postzygotic incompatibility between the lion subspecies.

References:

Cohn JP. 1990. Genetics for wildlife conservation. BioScience 40:167-171.

Either this continues today's Kansas theme, or this week's genetics theme. In either case, it's nice to see some attention to agricultural genetics and its growing connection to energy economics, in this Times article:

Like his father and grandfather before him, Mr. Kepley grows wheat. But energy costs that have quadrupled in three years, along with one of the worst droughts to grip the region in a century, have made it too expensive for him to irrigate. So today Mr. Kepley grows wheat under dry-land conditions, capturing rainfall for two years to make one year's crop.

"These are called semi-dwarfs," he said while surveying his burnt-looking wheat stalks one recent afternoon. “Our geneticist started developing this. Generally our wheat will be about knee-high when it is harvested. It doesn’t use much energy in developing the stalks.”

The theme is that pumping water has become more and more expensive with increasing energy costs, and farmers are looking for improved draught-tolerant breeds to help compensate. It's not a cure, since productivity and diversification both are improved with irrigation, but it can be a more economical solution as irrigation becomes more expensive.

In contrast to the terrible white buffalo stories, there is a fairly genetically enlightening story about Argentine ants, by Jeanna Bryner.

The problem is that these ants are invasive in California, and succeed so well because -- being descended from a single founder -- their limited genetic variation makes them all behave as if they were in a single colony. All the ants across California acting as a single colony. This is like the real worst-case ant scenario -- much worse than Them, where you can just sort of find the big ants and hit them with artillery. These aren't fire ants, but fire ants also pose a similar problem -- adjacent colonies that would have competed and fought if they were genetically variable, instead just help each other out.

Eventually this situation will degrade, as ants will slowly gain genetic variation. This is a really interesting question about intergroup selection, though -- because an ant colony that expresses a "foreign-looking" pheromone will be set upon by every other colony it ever encounters. It's hard to see that as being advantageous unless population structure reinforces it. For instance, a large and successful colony might hold off repeated attacks from lots of small itinerant colonies around it, and being able to recognize them and attack them helps to police its territory.

But until this gets sorted out, scientists want to do something to help the poor native ants, who are all getting annihilated. They're coming up with pheromone formulas, smearing them on the ants, and seeing if they get attacked:

Getting the chemical treatment was dizzying. First, Tsutsui and his team coated the inside of a vial with the chemical. They plopped an ant into the tube and spun it in a machine for 90 seconds to make the chemical stick.

"After all that shaking it's a little bit wobbly, but usually it's still alive," Sulc said. "Then, we put it back into the Petri dish with 10 of its friends from the same colony and then we observe how aggressive they are toward him."

The other ants immediately attacked, using their large mandibles, or jaws, to bite and tear off its legs, Sulc said.

Nice. Pummel them around the face and jaw, and then send them in for the kill.

Still, it's hard to figure how they are going to get this pheromone onto bajillions of ants in the field. Maybe they can engineer a virus to do it. An ant body odor virus.