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Biodiversity May Not Protect us from Disease, After All

Posted by Richard Conniff on March 20, 2013

The theory put forward a couple of years back was that biodiversity  prevents emerging diseases from actually emerging.  But now researchers at Stanford University say, “Hold on a minute.”

First, by way of background, here’s how I described the “dilution effect” at the time:

A diversity of species can also help prevent the emergence of new diseases, though we tend to blame, rather than credit, nature for this particular ecosystem service. We sometimes respond to Lyme disease, for instance, by trying to kill the major players, blacklegged ticks and white-footed mice. But the “dilution effect,” proposed by Rick Ostfeld at the Cary Institute of Ecosystem Studies, suggests counterintuitively that having the broadest variety of host species in a habitat is a better way to limit disease. Some of those hosts will be ineffective, or even dead ends, at transmitting the infectious organism. So they dilute the effect and keep the disease organism from building up and spilling over to humans. But when we reduce biodiversity by breaking up the forest for our backyards, we accidentally favor the most effective host — in this case, the white-footed mouse. And we free the undiluted disease organism to operate at full strength.

The implications go well beyond Lyme disease. Around the world over the past half-century, researchers have tracked about 150 emerging infectious diseases, from Ebola to HIV, with 60 to 70 percent being zoonotic — that is, transmitted from animals to humans. “The question,” says Aaron Bernstein, a Harvard pediatrician and co-editor of the 2008 book Sustaining Life: How Human Health Depends on Biodiversity, “is whether humans are doing something to make these zoonotic diseases come out of the woodwork.” Clearly, we are doing a lot of one particular thing — knocking down forests and creating species-poor habitats with no “dilution effect” in their place. Thus the fear is that many more such epidemics may lie ahead.

Now here’s the discouraging word from Stanford University:

More than three quarters of new, emerging or re-emerging human diseases are caused by pathogens from animals, according to the World Health Organization.

But a widely accepted theory of risk reduction for these pathogens – one of the most important ideas in disease ecology – is likely wrong, according to a new study co-authored by Stanford Woods Institute for the Environment Senior Fellow James Holland Jones and former Woods-affiliated ecologist Dan Salkeld.

The dilution effect theorizes that disease risk for humans decreases as the variety of species in an area increases. For example, it postulates that a tick has a higher chance of infecting a human with Lyme disease if the tick has previously had few animal host options beyond white-footed mice, which are carriers of Lyme disease-causing bacteria.

If many other animal hosts had been available to the tick, the tick’s likelihood of being infected and spreading that infection to a human host would go down, according to the theory.

If true, the dilution effect would mean that conservation and public health agendas could be united in a common purpose: to protect biodiversity and guard against disease risk. “However, its importance to the field or the beauty of the idea do not guarantee that it is actually scientifically correct,” Jones said.

In the first study to formally assess the dilution effect, Jones, Salkeld and California Department of Public Health researcher Kerry Padgett tested the hypothesis through a meta-analysis of studies that evaluate links between host biodiversity and disease risk for disease agents that infect humans.

The analysis, published in the journal Ecology Letters, allowed the researchers to pool estimates from studies and test for any bias against publishing studies with “negative results” that contradict the dilution effect.

The analysis found “very weak support, at best” for the dilution effect. Instead, the researchers found that the links between biodiversity and disease prevalence are variable and dependent on the disease system, local ecology and probably human social context.

The role of individual host species and their interactions with other hosts, vectors and pathogens are more influential in determining local disease risk, the analysis found.

“Lyme disease biology in the Northeast is obviously going to differ in its ecology from Lyme disease in California,” Salkeld said. “In the Northeast, they have longer winters and abundant tick hosts. In California, we have milder weather and lots of Western fence lizards (a favored tick host) that harbor ticks but do not transmit the Lyme disease bacterium.”

So, these lizards should be considered unique in any study of disease risk within their habitat. Or, as Salked put it, “All animals are equal, but some animals are more equal than others.”

Broadly advocating for the preservation of biodiversity and natural ecosystems to reduce disease risk is “an oversimplification of disease ecology and epidemiology,” the study’s authors write, adding that more effective control of “zoonotic diseases” (those transmitted from animals to humans) may require more detailed understanding of how pathogens are transmitted.

Specifically, Jones, Salkeld and Padgett recommend that researchers focus more on how disease risk relates to species characteristics and ecological mechanisms. They also urge scientists to report data on both prevalence and density of infection in host animals, and to better establish specific causal links between measures of disease risk (such as infection rates in host animals) and rates of infection in local human populations.

For their meta-analysis, the researchers were able to find only 13 published studies and three unpublished data sets examining relationships between biodiversity and animal-to-human disease risk. This kind of investigation is “still in its infancy,” the authors note. “Given the limited data available, conclusions regarding the biodiversity-disease relationship should be regarded with caution.”

Still, Jones said, “I am very confident in saying that real progress in this field will come from understanding ecological mechanisms. We need to turn to elucidating these rather than wasting time arguing that simple species richness will always save the day for zoonotic disease risk.”

Bear in mind that a meta-analysis based on only 13 published studies does not constitute the last word on what could be a life-or-death question.

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