Just warm enough

Mammals' body temperatures may represent balance between warding off fungi and limiting food needs

Fungi may be to thank for mammals’ warm blood, a new theory suggests. But exactly how hot-blooded an animal is may depend on balancing fungal protection with food consumption. 

IN THE RANGE Mammals have a range of body temperatures, but most hover around 37° Celsius. Such warm bodies help protect against fungal infections, but being hotter means eating a lot more. A new study finds that 36.7°C is the optimal body temperature for striking a balance between the two. SOURCE: C. Ladd Prosser, ed. Environmental and Metabolic Animal Physiology, 4th ed. Wiley-Liss, 1991

NOT TOO HOT Researchers calculated an organism’s fitness as a function of body temperature, revealing 36.7°C as the ideal body temperature. Fitness — designated W(T) above — represents the balance between the benefit of fighting of fungal pathogens and the energy costs of maintaining a higher body temperature. A. Bergman & A. Casadevall/mBio 2010

The optimum body temperature for organisms to ward off fungal infections without burning too much energy is 36.7Ë Celsius — close to the core body temperatures of mammals, including humans, researchers at Albert Einstein College of Medicine in New York City reported online November 9 in mBio. The finding is the latest piece of evidence for a theory that fungi may have been a driving force in the evolution of mammalian body temperatures. The new mathematical analysis also helps explain why mammals aren’t even hotter.

“Mammals don’t make any sense,” says Arturo Casadevall, a microbiologist at Einstein who devised the theory. “We have to eat all the time. Our reproduction rate is low.” In fact, until catastrophic events caused the extinction of the dinosaurs, “mammals were an experiment that wasn’t going anywhere,” he says.

Casadevall wondered why reptiles didn’t retake control of the Earth once environmental conditions had stabilized again.

A couple of pieces of evidence led him to develop the new theory. First, a massive fungal bloom swept the Earth about the time of the dinosaur extinction. “The world became a huge a compost pile,” he says.

Second, fungi plague plants, insects and other cold-blooded creatures far more often than they do mammals or birds. Putting two and two together, he formulated a theory that the warm body temperatures of mammals and birds might have protected them from fungal pathogens, while diseases caused by fungi might have been a factor keeping the reptiles from rising again.

“We are cautiously suggesting that fungi may have been responsible for the success of the mammals,” he says.

To test the theory, Casadevall and Vincent Robert of the CBS Fungal Biodiversity Center in Utrecht, the Netherlands, measured the thermal tolerance of 4,802 types of fungi. For every degree Celsius the researchers raised the temperature above 30Ë C, 6 percent fewer fungal species could grow, the team reported last year in the Journal of Infectious Diseases.

Most mammals have body temperatures of about 37Ë C (98.6Ë Fahrenheit). But if higher temperatures ward off more fungi, why don’t mammals run even hotter?

In the new paper, Casadevall and coauthor Aviv Bergman, an evolutionary systems biologist also at Einstein, attempted to answer the question with a mathematical model. Mammalian body temperature is a trade-off between fighting fungi and burning too much fuel, they found.

“If you were to go higher, you’d have more protection, but then you’d have to eat a lot more,” Casadevall says.

Their model doesn’t address all the biological questions related to mammalian body temperature, says Bergman, but it does suggest that threats from fungi could impose constraints on some aspects of mammalian evolution.

“I think it’s a really cool idea,” says Leah Cowen, a medical mycologist at the University of Toronto. What’s striking about the new study is that the model is simple, “but the vision is large,” potentially answering a huge question in evolutionary biology. “This is a big picture question addressed by a simple mathematical model.”

The real mark of a good model is whether it can make predictions, says Joseph Heitman, a microbiologist and geneticist at Duke University. This model is “really creative and a bit out there,” he says, but “one of the beauties of it is that it is fairly straightforward.”

One might predict from this model that raising an animal’s temperature would lead to greater resistance to fungi. Lowering body temperature would then be expected to make animals more vulnerable to fungal infections.

Frogs and other amphibians in decline around the world — in part because of infections with a chytrid fungus — may provide some evidence that the theory is correct. Warming up infected frogs can help clear them of the fungus, Heitman says.

Reducing a mammal’s temperature in the laboratory to find out whether lower body temperatures lead to fungal disease is difficult because messing with body temperature can affect many other biological processes. But hibernating bats may provide a clue that Casadevall is onto something, says David Blehert, a microbiologist with the U.S. Geological Survey’s National Wildlife Health Center in Madison, Wis.

Blehert studies white-nose syndrome, a fungal disease that is killing bats in large numbers in the eastern United States. A fungus called Geomyces destructans infects bats while they are hibernating — a time when body temperatures drop from 40Ë C to about 7Ë. “They’re not warm-blooded when they get infected,” Blehert says. When bats are up and around and at their normal body temperature, they seem impervious to the infection, he says.

In a report published November 11 in BMC Biology, Blehert and others described how the fungus, which erodes and replaces the bat’s skin, damages wings and leads to death. Casadevall’s idea has “become important in our thinking about this disease,” Blehert says.

The idea of a link between fungal disease and body temperature is not controversial among scientists, Blehert says. “It’s very logical.”

Tina Hesman Saey is the senior staff writer and reports on molecular biology. She has a Ph.D. in molecular genetics from Washington University in St. Louis and a master’s degree in science journalism from Boston University.

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