Category Archives: Conservation

Always a Bridesmaid, Never a Bride

Well, it’s happened again.  My work has been written up in Science but I am not mentioned.  I’m actually not that concerned this time — we’re going to submit the paper for publication soon. I’ve been telling myself (and other people) that this thing we’ve ben working on (all the while being very cryptic about what this thing exactly is) is important.  Every once in a while, I wonder if I’ve just been fooling myself.  The fact that this work has been written up in Science the day after the paper was presented at the Montreal Conference on Retroviruses and Opportunistic Infections suggests to me that it is, indeed, important.

Press on our PNAS Paper

Our new paper at PNAS has been out a day now and Wired Magazine has already done a story on it.  It’s a nice piece but it gets several things hilariously wrong. It says:

Bird’s team recently published a study on “fire stick farming,” a traditional method of ecosystem management still used by aborigines in Australia’s Western Desert. By burning wooded areas, lizards are driven towards hunters; cookpot-friendly kangaroos and emus fatten themselves on grasses flourishing on newly cleared lands.

The thing is that (1) Martu don’t use fire to drive game, and (2) Murtu don’t burn woodland — only spinifex grassland.  That’s really what drives the process.  Spinifex may be bullet-proof.  It may puncture the tires on your Land Rover. It may eat other plant species for breakfast.   But, boy, does it burn!  By burning spinifex, Martu hunters open the grasslands up for colonization by early successional species that couldn’t otherwise compete.  From a hunter’s perspective, burning increases access to goanna burrows and therefore  increases foraging returns.

Science reporting is hard.  You have to turn around comprehensible — and compelling — stories on tight deadlines.  It’s nonetheless a shame that this piece gets such a fundamental piece of the story wrong.  One thing that is very nice, however, is that there is a link to the actual paper.

Aboriginal Burning Promotes Grassland Biodiversity in Australia’s Desert

We have a new paper out in this week’s Proceedings of the National Academy of Sciences Early Edition.  The paper suggests that subsistence related burning increases local landscape heterogeneity and may promote biodiversity in Australia’s Western Desert.  What’s really interesting about this is that promoting biodiversity is not the goal of individual hunters – they are really just trying to maximize their foraging returns.  My Stanford Anthropology colleagues Rebecca Bliege Bird and Doug Bird have been working with Martu foragers in Western Australia since 2000.  They gather amazingly detailed quantitative ethnographic and ecological data, focusing on such classic problems as understanding subsistence economy in a foraging population and the ecological factors favoring a sexual division of labor.

Martu foragers burn the climax spinifex grass in search of goanna lizards and in so-doing, promote the growth of plant species that cannot compete with adult spinifex, which is a nasty grass with high-silica content:

Spinifex is extremely flammable and once a fire is started in a patch, it will race through until it is pretty much all burned.  The vegetation that characterizes other successional stages is far less flammable.  Previous work by Doug and Rebecca has shown that burning increases hunters’ encounter rates and probability of capturing goanna lizards and other prey species. 

Using their detailed information on hunting and burning, we correlated foraging activity with measures of habitat heterogeneity derived from satellite imagery.  We compared local habitat heterogeneity in areas where Martu were actively foraging (and burning) to areas where there was no foraging and the fire regime was instead driven by lightning ignitions.  What we found was that the heterogeneity in the foraging localities was greater than in the “natural” burn regimes.  In particular, foraged localities had remarkably uniform distributions of successional stage.  The non-foraging localities would show peaks at different successional stages — depending on the age of the last burn — but the frequency of whatever stage was present would typically fall off from whatever the characteristic mean was.  In contrast, the successional stage distribution we observed in the foraged localities looked like a mixture of several different smaller “natural” localities.  This is because that’s essentially what they are!

When people burn for subsistence needs, they tend to start lots of small fires at many different times.  What results is a mosaic of successional stages. But this is really a local re-arrangement.  When we looked at the landscape level, the diversity of habitats looks very much like that of the smaller foraging localities.

One interesting implication of this work is that the human impact on the Australian environment — grassland engineering, if you like — was likely to only be substantial following the establishment of more intensified aboriginal economies (approximately 1500 years ago).

It may seem counter-intuitive that hunting with fire promotes biodiversity, but that really seems to be what is happening here.  The results have clear conservation and management implications. Excessive fire suppression in highly flammable grasslands is probably not a good idea.  Now we need to measure the actual species diversity rather than simply the diversity of habitat types.

See Rebecca’s fire ecology website for more on this research and reprints of various papers.  The full text of our paper can be found here.

 

Devastating Virus in Tasmanian Abalone Fishery

A news story reports the outbreak of abalone viral ganglioneuritis in Tasmania.  This is the first report of the disease in Tasmanian fisheries.  In fact, the disease appears to be quite newly emergent since, according to the Department of Primary Industries for the State of Victoria, the virus was previously not described in Australia prior to 2005.  Since 2005, it has been devastating abalone fisheries in Victoria.  Now it’s in Tasmania.  One theory for the emergence of this herpes-like virus is that it is actually endemic in abalone populations and usually harmless. Environmental stress (e.g., via warming or polluted water) could induce increased virulence, leading to the high observed mortality rates.  This is an outbreak to keep an eye on. The PROMED-mail moderator writes this about the virus:

Ganglioneuritis is an interesting condition causing inflammation in the nervous tissue, which swells. The result is curling of the abalone foot and swelling of the mouth. Thus, the organism cannot eat and looses its grip on the rocks it so depends on.

Abalone viral ganglioneuritis (AVG) is a highly virulent herpes-like virus, undescribed in Australia before 2005, and still not well characterized. The virus affects the nervous tissue of abalone and rapidly causes death. The virus can be spread through direct contact, through the water column without contact, and in mucus that infected abalone produce before dying. The virus is thought to survive only a short time when out of a moist environment.

TB in Captive Elephants

A new study of tuberculosis (TB) prevalence in captive elephants (presumably Elephas maximus) in India, reported in the Times of India, shows that approximately 15% of southern India’s captive elephants test positive for TB.  This is a big problem for the health and well-being elephants.  The study makes me wonder (1) what TB prevalence in free-ranging elephants is, and (2) how frequently TB is transmitted from elephant to humans, and (3) what the infectious organism is (M. tuberculosis vs. M. bovis), (4) where do the infections of captive elephants come from: cattle, humans, other elephants?

The PROMED-mail moderator wrote the following on the topic of TB epidemiology in elephants.  Elephants are known to be susceptible to infection by both Mycobacterium tuberculosis and M. bovis. The above article does not specify the bacteria identified in the Indian elephants. A short review on tuberculosis in elephants, by Susan Mikota, was published by ProMED-mail in July 2007 (see ProMED archive 20070702.2111). It included, among other things, the following: “While most cases in the U.S. have been due to M. tuberculosis, we may find more cases of M. bovis in Asia, where elephants often share grazing land with domestic livestock.” The review, to which subscribers are referred, also covered data on the sampling and laboratory techniques applicable in elephants.

Elephant Deaths From Anthrax in Namibia

A very sad story appeared on PROMED-mail recently about a die-off of elephants around Nakabolelwa, Namibia.  While still not completely investigated, the most likely cause seems to be anthrax.  Bad news for elephant conservation. If anthrax infection turns out truly to be the cause of mortality, then it raises all sorts of problems.  Chief among these is the possibility that people will eat meat from the carcasses, leading to almost certain infection and death if anthrax is indeed the culprit.  But even if people don’t eat meat from the carcasses, scavengers might and could then spread the anthrax spores around the landscape.  Bad news for anthrax control.  Anthrax spores in the ground remain infectious for a potentially very long time — potentially decades. One can just imagine what a control nightmare having a checkerboard of cryptic anthrax hotspots across a landscape is.

Burning the elephant carcasses, which might be done for other types of animal infections, is impractical because it would take so much fuel in this xeric region with few woodlands and chronic shortages of cooking fuel. The PROMED moderator writes:

Dealing with elephant carcasses is difficult, as one would imagine. The prescribed technique is to pile the carcass with thorn brush to discourage scavengers while the carcass decomposes. The drop in pH will kill the vegetative cells quickly in the unopened carcass. Burning takes a significant volume of wood, and it is hard to get proper ventilation of the underside of the carcass.

Wayne Getz and his collaborators have a relatively new project to study the ecology of episodic anthrax transmission around Etosha Park, Namibia.  I await the results from this project eagerly since, as far as I can tell, just about everything that comes out of his lab is great, and if not great, at least interesting.

More Crocodile Pansteatitis

About a month ago, I posted on the mysterious deaths of crocodiles in the Olifants river system in Kruger National Park, South Africa.  A recent update indicates that the cause of the fatal pansteatitis outbreak is still unknown despite intensive study.  An interdisciplinary research captured 11 live crocodiles and found that seven of them were afflicted by pansteatitis.  This is a scary prevalence rate.  The media release strangely refers to these cases as “infections,” but this is probably not correct as pansteatitis is typically caused by environmental poisons (e.g., rancid fat from spoiled fish).  The current theory is that the crocs are acquiring the poisoning from eating the carcasses of other afflicted crocs.  The intervention park managers are attempting now is to burn the bodies of dead crocs recovered by rangers.  So far, rangers have counted 130 crocodile carcasses in the park.

Update on Salmonellosis Saintpaul

The Centers for Disease Control and Prevention have just issued a new report on the ongoing outbreak of Salmonella serotype Saintpaul infection. Since April, 1237 people have been infected.  The investigation has continued to focus on raw tomatoes but also jalepeño (and serrano) chiles and cilantro.  This further supports my previous speculation, based on the age profile of the cases, that salsa consumed while drinking alcoholic beverages might be implicated in this outbreak.  Epidemiological investigations are greatly complicated when multiple vehicles that are typically consumed together are implicated.

There is an interesting caution that accompanies the epidemic curve:

Salmonellosis Saintpaul Epidemic Curve

This has to do with the fact that it can be very misleading to read too much into an epidemic curve for an ongoing outbreak. Consider the epidemic curve for the 2003 SARS outbreak in Singapore:

Singapore 2003 SARS Epidemic Curve

Now imagine we were looking at the curve as it evolved on 12 March.  We might have be tempted to say that the epidemic was coming to an end and, man, would we ever have been wrong! There are a couple of things at work here.  First, epidemics often have multiple introductions and while theory tells us that an epidemic curve will be more or less bell shaped, this is based on the assumption of a single introduction.  If you look at the SARS epidemic curve hard enough, you can see several more-or-less bell-shaped components added together.  The second issue with SARS is that there is extreme heterogeneity in transmission.  Patient #1 probably infected 21 other cases, patient #4 probably infected 62.  The great majority of others infected none.  Individuals who infect more than 10 others are what is known as “superspreaders.”  There were five in the Singapore outbreak out of a total of 201 probable cases of SARS and 722 suspect cases.  Finally, there is often a delay between when people get sick and when their cases are reported.  This means that the trailing edge of the epidemic curve always looks like it’s closing off its bell shape. The full case report for the Singapore outbreak can be found here

So, is the current Salmonellosis outbreak on the wane?  Let’s hope so, but as CDC warns:

It can be difficult to say when the outbreak is over, because of the reporting delay.   The delay means that the curve for the most recent three weeks always looks like the outbreak could be ending even during an active outbreak. The full shape of the curve is only clear after the outbreak is over.

With a vehicle-borne disease, we don’t have to worry about superspreaders, but the fact that we still don’t know the source of the infection or the ultimate cause of the contamination is troubling.  Who knows how much contaminated (presumably) produce is lurking out there?  I, for one, will make sure to wash my produce well! 

Pansteatitis and Questions about Affected Species

Here is a review of pansteatitis (and other diseases) in farm raised crocodiles (and ostriches), including a picture of the hardened yellow fat in crocodile tails.  This hardening of the fatty tissue in crocodile tails impairs their mobility and therefore their ability to hunt.  Crocs with pansteatitis therefore waste away and die of starvation.  There is no specific indication in the articles of the state of the crocs bodies.  Are they emaciated? Another posting on ProMedmail, including some details of the dam that may be a source of pollutants is here.  The moderator asks the important question: Is anything else affected?  No mention is made in any of the news articles.  What about other aquatic organisms in the Olifants River? For example, what about Cape Clawless Otters (Aonyx capensis)?