Welcome to Bioblog
Dedicated to biology and music
On biotunes.org

Thursday, July 12, 2007

We need biological control agents that work

Biological control of pest species has come under a lot of criticism in recent years. Employed by governments and private businesses since the late 1800's, the practice was largely unregulated until the 1980's, and regulation remains varied and complicated among different countries, and different states within the U.S.

Classical biological control specifically refers to the importation of an alien species to control pests that are usually aliens themselves. Traditionally, it has been employed in agricultural systems, in which the alien pest arrived in its new location accidentally. More recently, classical biocontrol has been undertaken to control pests in natural systems, which in the case of plants, were usually intentionally introduced through horticulture trade of botanical gardens. It is currently viewed by many ecologists as a critical tool in the battle against invasive alien species, which are growing into an ever larger economic and ecological problem.

The recent criticism of biocontrol has focused on the likelihood of "non-target" attacks, which occur when the introduced agent feeds on unintended prey or plant species, including natives. This is an especially important problem in areas with many endemic species - in the U.S., the states most affected are Hawai`i, California, and Florida because of their high native species diversity. The concern about non-target attacks is excessive, in the opinion of most biocontrol practitioners, including Messing and Wright (2006), who describe a scenario in which the peril to Hawai`i's agriculture and ecosystems is being increased by a bureaucracy that will not allow alien biocontrol agents to be imported, even to combat serious economic and ecological pests in Hawai`i that are contributing to the destruction of native ecosystems.

Certainly their concern for the native species of Hawaii is not misplaced. Invasive alien plants such as thorny blackberry crowd out natives and are less likely to be eaten by foraging alien herbivores such as pigs and goats. Generalist insects such as the two-spotted leafhopper consume hundreds of native plant species which have no natural defenses against the aliens feeding on them. So it does seem unreasonable that Hawai`i is so stingy with its species importation permits, when researchers do their best to show that their biological control agents will not feed on any native species. (I know both of the authors personally, and can verify that they are stringent in their criteria for potential non-target interactions.)

The problem with Messing and Wright's paper is the same problem with most discussions debating the use of biological control in the scientific literature, at conferences, and in online discussions. While we are focusing much energy and attention on predicting non-target interactions, which in many biocontrol programs has thus been adequately addressed, there is almost no discussion about doing a better job of predicting whether or not the introduced agent will actually be effective once introduced.

Messing and Wright themselves toss out that only 16% of effective biological control programs have been effective at controlling the target, and yet later in the paper complain about their inability to introduce agents, which is based on the assumption that the introduced agents will actually work. The high probability that (based on current practices) they will not work is never addressed in their paper. Twice the number of effective biocontrol agents, or around 33% actually establish -- probably an underestimate, since follow-up generally does not extend for years, and those that are not actively controlling the target could be missed early in monitoring -- and rarely has any follow-up been done to understand their role in the native ecosystems. If they are not attacking non-targets, and they are not controlling the pest, how are they interacting with native species?

It is true, as Messing and Wright point out, that in the current modern age of regulation, non-target effects have greatly decreased. But it is also true that even in the case where a known specialist was introduced, there can be indirect food web effects discovered when people have taken the trouble to look, which they rarely do. In one case (Willis and Memmott 2005), a native parasitoid attacking an specialist insect herbivore introduced to control an alien weed increased greatly in numbers and thus made native herbivores much more susceptible to attack, upsetting the food web in the system.

Effective biological control programs are indeed cost-effective, but a lot of money is spent for many years on the assessment of a single agent, and are we getting our money's worth if only 1 in 6 actually work? A whole new science may need to be developed to further our ability to predict the effectiveness of biological control agents. Those who are generally against biocontrol find the balance of effective agents vs. the risk of non-target effects, which while getting lower, will never be zero, to be unacceptable. What if biological programs could predict effectiveness 50% of the time? That would alter the equation, and make these programs more palatable to many ecologists such as myself.

How can something as notoriously unpredictable as species interactions be better assessed before release? One method which would give researchers much better data about the role of species in both native and alien habitats is the construction of quantitative food webs. Normally when biocontrol workers go the country of the target pest's origin, they observe only the two-species interactions between the target species an its natural predators or herbivores. This provides no predictive value because plants and animals do not interact in 2- or 3-species bubbles, they interact complexly both directly and indirectly with many species. Why don't we construct food webs of biocontrol agents in their native habitat and figure out why they seem to be effective there? We can also do retrospective studies on established biocontrol agents that are ineffective and use food webs in both the new and native habitats to try and understand why.

Of course, ecological research is conducted at the whim of funding agencies, largely NSF in the U.S. Politics and inertia often determine what is funded more than science does. Perhaps someday, however, people will realize that for both economic and political reasons, research into the prediction of the effectiveness of biocontrol agents makes clear economic, ecological, and political sense. We do need biocontrol as an option for saving some ecosystems. But we particularly need biocontrol that works.


References


Messing, R.H. and Wright, M.G., 2006. Biological control of invasive species: solution or pollution? Frontiers in Ecology and Evolution 4:132-140.

Willis, A.J. and Memmott, J. 2005. The potential for indirect effects between a weed, one of its biocontrol agents and native herbivores: A food web approach. Biological Control 35:299-306.

Labels: , , ,


Wednesday, April 11, 2007

Is BSE risk a legitimate concern?

I used to give blood regularly, but am now forbidden because I lived for months at a time in England from 1998-2001, where BSE (Mad Cow disease) emerged in the mid-1990's. I have scoffed at this rule; from everything that I understood, Britain has far greater monitoring of beef than the U.S. True, BSE has been found in thousands of British cattle and very few North American cattle, but then again one is unlikely to find such a sneaky pathogen if one is not looking for it. Unfortunately, the U.S.D.A., which exists to serve agribusiness interests, rather than those the American public which pays for its existence, has at best dragged its feet on increased testing of cattle, and at worst actively has prevented those who would test on their own initiative from doing so.

The U.S.D.A. itself has drastically curtailed its BSE testing in the last few months. The agency presents no data on BSE testing on its website after August, 2006. However, the new policy is spelled out based on the detection rate from the previous sampling:

Since the enhanced surveillance program began, USDA has sampled more than 759,000 animals and, to date, only 2 animals have tested positive for BSE under the program. Both cases were in animals born before the United States banned the practice of feeding recycled ruminant protein to other ruminants. In line with USDA policies, neither of the affected animals detected under the enhanced surveillance program nor the imported cow detected in 2003 entered the human food or animal feed chains.

Based on the wealth of information gained during both the enhanced surveillance program and BSE surveillance conducted in the United States in the 5 years prior, USDA recently concluded that the prevalence of the disease in this country is extremely low, less than 1 case per million adult cattle, and that the most likely number of cases is between 4 and 7 infected animals out of 42 million adult cattle. Our analysis was submitted to the scrutiny of a peer review process, and the expert panel agreed with the appropriateness of our assumptions and the factors we considered, as well as with our estimate of BSE prevalence.


The new testing protocol is as follows:

The ongoing BSE surveillance program, which will sample approximately 40,000 animals each year, will continue to sample the cattle populations where the disease is most likely to be found. The statistically valid surveillance level of 40,000 is consistent with science-based internationally accepted standards. This level allows USDA to detect BSE at the very low level of less than 1 case per million adult cattle, assess any change in the BSE status of U.S. cattle, and identify any rise in BSE prevalence in this country.

The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as nonambulatory animals.


As they say, the methodology is based on standard science. But does that really protect our food supply? The unknowns about BSE are disturbing, and unfortunately the testing protocol is based on assumptions that may not be true because we still know so little about this disease.

Britain's beef supply is not currently as safe as I thought, as this 2002 report spells out in detail:

BSE: risk and regulation
A case study paper commissioned by the National Consumer Council
Prepared by Patrick van Zwanenberg & Erik Millstone
Science and Technology Policy Research, Sussex University

It turns out there are still many questions out there about how animals are contracting BSE and how to prevent it:

Indeed, to date, there have been 14 cases of BSE in animals born after August 1996; they constitute an anomaly which remains inexplicable. The mechanisms by which those animals were infected are unknown... It is therefore likely that some animals under 30 months will be sub-clinically infected with BSE and will be entering the human food chain. We cannot know how many animals under 30 months might be incubating the disease, however, because the existing short-term tests can only detect infected animals shortly before clinical symptoms appear, and the UK government has chosen not to conduct any sort of test for BSE on animals entering the human food chain. In 2001 there were 761 reported cases of BSE in the UK... A further 335 cases were also reported in that year from the, as yet uncompleted, active surveillance programme;... but in the summer of 2001, the European Commission's Food and Veterinary Office noted that "[a]s active surveillance is practically not performed [in the UK], it has to be assumed that the BSE incidence for GB has to be seen with a considerable degree of uncertainty."


This means that testing only sick and downer cattle doesn't necessarily cover the possible infected animals. Clearly we have done some things that have helped reduce the risk considerably, for example not allowing cattle to be fed mammal by-products any more. Yet there are loopholes; from the FDA itself: "In August 1997, FDA established a regulation that prohibits the use of most mammalian protein in the manufacture of animal feeds for ruminants." Apparently though it is still legal to feed chickens mammalian protein. BSE may not pass this way, but we know so little about it we cannot say for sure.

And some rules put in place in the 1990s have already been relaxed:
The U.S. Food and Drug Administration today published several amendments to the July 2004 interim final rule, "Use of Materials Derived from Cattle in Human Food and Cosmetics," that will allow the use of certain cattle-derived material in human foods and cosmetics...

As a result, FDA is amending the rule to allow use of the small intestine in human food and cosmetics, provided that the distal ileum has been removed. The U.S. Department of Agriculture is publishing today a similar amendment to its interim final rule on BSE.

The amendments also clarify that milk and milk products, hides and hide-derived products, and tallow derivatives are not prohibited for use in human food and cosmetics.


Is there any other reason for this than pressure from industry? Shouldn't the U.S. government be erring on the side of caution in the case of such a potentially devastating health issue? Those infected with BSE take decades to show their symptoms. This is not a situation where a couple people will drop dead and the FDA will say "whoops, better change that rule" as a result.

As a final note, among the real unknowns about spongiform encephalopathies is that despite what is reported in the popular press, it is clear from official and scientific documents that it is not known without doubt that prion proteins are the proximate cause. It is certainly the currently most popular idea, and most scientists are studying prion proteins based on this assumption, but there are still peer-reviewed papers in respected journals which assert alternative hypotheses, for example:

Manuelidis, L. 2007. A 25 nm virion is the likely cause of transmissible spongiform encephalopathies. Journal of Cellular Biochemistry 100:4.

The transmissible spongiform encephalopathies (TSEs) such as endemic sheep scrapie, sporadic human Creutzfeldt-jakob disease (CJD), and epidemic bovine spongiform encephalopathy (BSE) may all be caused by a unique class of "slow" viruses. This concept remains the most parsimonious explanation of the evidence to date, and correctly predicted the spread of the BSE agent to vastly divergent species. With the popularization of the prion (infectious protein) hypothesis, Substantial data pointing to a TSE virus have been largely ignored. Yet no form of prion protein (PrP) fulfills Koch's postulates for infection. Pathologic PrP is not proportional to, or necessary for infection, and recombinant and "amplified" prions have failed to produce significant infectivity. Moreover, the "wealth of data" claimed to support the existence of infectious PrP are increasingly contradicted by experimental observations, and cumbersome speculative notions, Such as spontaneous PrP mutations and invisible strain-specific forms of "infectious PrP" are proposed to explain the incompatible data. The ability of many "slow" viruses to survive harsh environmental conditions and enzymatic assaults, their stealth invasion through protective host-immune defenses, and their ability to hide in the host and persist for many years, all fit nicely with the characteristics of TSE agents. Highly infectious preparations with negligible PrP contain nucleic acids of 1-5 kb, even after exhaustive nuclease digestion. Sedimentation as well as electron microscopic data also reveal spherical infectious particles of 25-35 nm in diameter. This particle size can accommodate a viral genome of 1-4 kb, sufficient to encode a protective nucleocapsid and/or an enzyme required for its replication. Host PrP acts as a cellular facilitator for infectious particles, and ultimately accrues pathological amyloid features. A most significant advance has been the development Of tissue Culture models that support the replication of many different strains of agent and can produce high levels of infectivity. These models provide new ways to rapidly identify intrinsic viral and strain-specific molecules so important for diagnosis, prevention, and fundamental understanding.


I am not advocating a specific position on this at all; clearly, the current scientific consensus does not support this view, and I do not have the expertise in this area to judge. But I recommend that anyone who believes this is an important issue read up on it at the U.S.D.A. site and the British consumer report. In the meantime, I will be continuing my policy of avoiding factory feedlot beef (and not only because of the risk of BSE). I will also continue to update current research here because of my own interest in the topic.

Labels: , , ,


Friday, March 2, 2007

Bees to their knees

Although Walking the Berkshires beat me to it, I'm still going to put in my two cents about the latest problems plaguing beekeepers these days. After all, I am a hymenopterist (lover and researcher of the order containing ants, wasps, and bees), and I hobnobbed with scientists at the U.S.D.A. Bee Lab in Tucson when I lived there.

One scientist at the lab (no longer there) was Steve Buchmann, who advocated tirelessly for the study of the use of native bees as pollinators. Clearly one reason why this idea hasn't taken off is that native bees probably can't ever be big business, because they are (as far as I know) all solitary rather than social. This means you can't keep several thousand in a box and lug them around.

But even hardworking honeybees are not just a bunch of equipment. They are living organisms that have basic biological needs. The idea that we are just pushing the colonies we have left too far is an intriguing one. The reason bees are overextended is that there are too many disease pressures on them now, especially the notorious varroa mite. Certainly being trucked around the country to work isn't something bees' evolutionary history prepared them for.

Here's one site that claims we aren't as dependent on honey bees as we think. Note that it is from a vegan site advocating that vegans avoid honey, but it makes some valid points about problems with having a large dependence on a single alien species.

Perhaps an answer to the problem would be the use of "Africanized" (a.k.a. "killer") bees. Beekeepers from South America to Mexico have had no choice but to use these, because they always take over as they spread. Africanized bees were introduced to the Americas in the 1950's when researchers in Brazil hybridized African and European honeybees, hoping to create a super pollinator. Not only did they actually create a super agressive hybrid that is hard to handle, but of course the bees escaped and have been making their way north ever since. They have created problems for many native American bees along the way, able to outcompete them for resources in some areas. They are moving northward in California, so perhaps there will be enough wild colonies there soon to do the job.

Bottom line: when domesticated honeybees are around in droves, they may push competitors out. I'm betting the void will be filled, if not by wild Africanized bees, than by all the natives out there that just want a chance at their slice of the pollen pie.

Labels: , ,


Wednesday, February 14, 2007

The U.S.D.A. loves G.M.O's - but does the environment?

An article in today's NY Times about a Monsanto product exemplifies the shortsightedness of government policy with regard to genetically modified organisms (GMOs). Here's a snippet:

A federal judge in Washington said last week that the Agriculture Department had not done adequate assessments before approving field trials of genetically engineered grass. And last August a federal judge in Hawaii, in a case involving field trials of crops engineered to produce pharmaceuticals, ruled that the Agriculture Department had not adequately assessed the possible impact on endangered species.


No, I am not a rabid anti-GMO type at all. I'm just tired of the USDA existing to serve corporate interests. As a biologist studying ecological issues related to biological control of pests, I have a lot of experience with the U.S.D.A. and know many U.S.D.A. scientists, and so I know about a lot of stupid U.S.D.A. policy. Assuming the case was in Hawai`i because the crops were, it's a double whammy that they were introducing such an organism into a state with such a fragile environment.

U.S. government agencies have always had policies destructive to the environment, and often with questionable societal benefit - for example, until (I believe) 1979, your tax dollars were hard at work on the quest to introduce alien game animals from around the world. You'd honestly think, though, in this new century of increased environmental knowledge and general public awareness, that policies would make a little more sense. And undoubtedly the case is more complicated than presented in the article. But apparently the U.S.D.A. decided that the alfalfa in question was "harmless to people and livestock" and called it good. Huh? I'm certainly not assuming that all GMOs are harmful to the environment, and I think human health is not likely to be a problem with the great majority, but plants do commonly hybridize. To have no data on the conditions under which this plant might cross breed with un-modified alfalfa or (worse in my opinion) native legumes, and approve it anyway, is just another one of seemingly endless examples of government at least appearing to prioritize corporate interests ahead of long-term environmental stability.

Fortunately, even Monsanto seems to know when they have made a really bad decision. This article reminded me of when years ago, there was a lot of hype about Roundup-ready turfgrass being made available for use in those facilities of compelling national interest, golf courses. In the face of serious protest of their attempt to create a super weed (these grasses spread and hybridize with related species, albeit at low frequency), they actually backed off:


Superweed No Superstar
gone from hero to zero, as biotech firm Monsanto withdrew its proposal to commercially market the genetically engineered turfgrass. Turns out the product is resistant to the top-selling weedkiller Roundup, a brand also owned by Monsanto. The problem, according to the International Center for Technology, is that commercialization of the genetically engineered creeping bentgrass would be "an environmental nightmare." The CTA has petitioned the United States Department of Agriculture to federally prohibit the use of the grass and label it a "noxious weed." (Albright Seed Company, November 2002 newsletter)

Labels: , ,