Consider two pandemics: the white-nose syndrome now devastating North American bats and the Black Death that killed a third or more of Europeans in the 14th century. Lethality aside, they may not seem to have much in common. But recent studies suggest they both offer important lessons about understanding that the deadliness of disease organisms is very much a product of the circumstances in which they appear.
Two weeks ago in Nature, a multi-institutional team of U.S. Geological Survey scientists presented conclusive evidence the parasitic fungus that lends white-nose syndrome its name is indeed the cause of the mysterious bat epidemic. The illness came to light in New York in 2006, when cave explorers started finding thousands of little brown bats (and later, other species) dead together in the caves where they spent the winter months, their bodies covered with a white fungus, Geomyces destructans. It has since spread throughout the northeastern U.S., where bat populations have declined on average by 73 percent—which may make it one of the most rapid declines in wildlife populations ever observed. Worse, white-nose syndrome is still on the move, with documented cases in four Canadian provinces and states as far south and west as Tennessee, Missouri, and Oklahoma.
This sharp decline in bats carries serious human consequences. Without bats to prey on them, insect populations explode, which can mean more crop losses and insect-transmitted disease or, conversely, more expenses and risks from additional pesticide use (or both). Last April, a team of researchers estimated in Science that the value of bats to U.S. agriculture alone is very roughly $22.9 billion annually—with a swing as low as $3.7 billion but maybe as high as $53 billion.
A harmless killer?
What makes the bats’ deaths so mystifying is that G. destructans infection doesn’t seem as though it should be lethal. The fungus can (and does) damage delicate skin on bats’ wings but it doesn’t grow exceptionally fast and it doesn’t produce toxic byproducts that could poison the animals. Kept in check by bats’ immune systems and normal grooming habit, the fungus shouldn’t be much more than a nuisance—the chiropteran equivalent of athlete’s foot. Until recently, the fungus was largely confined to Europe (scientists suspect the North American outbreak was caused by spores carried on a caver’s shoe). Yet European bats seem to handle white-nose infections without difficulty, even during their own overwinter hibernations in a state of torpor, when their metabolisms and immune functions drop almost to nil.
But then how does G. destructans kill the bats? Several possibilities are still debated, but the evidence might point toward an indirect mechanism championed by Craig K.R. Willis of the University of Winnipeg and others: the itchy nuisance may disturb the bats’ torpor too much and cause them to starve or dehydrate to death.
Bats can survive without feeding for the winter months only because they may consume energy while in torpor at about 1 percent of their normal rate. But torpor poses its own challenges. The bats need to periodically rouse to groom themselves and to sleep normally. (Strange as it may seem, torpor isn’t sleep, and bats in torpor for too long suffer memory problems like sleepless humans do.) While awake or sleeping, however, the bats start consuming energy at the normal feverish pace of small mammals. As a result, bats’ fat reserves often last just barely long enough to see them through to spring, with the animals using up 70 percent or more of that energy during the short interruptions of their torpor.
So if the white fungus infection does anything to make the bats groom themselves more, the bats may run out of energy too soon. As they starve, moreover, the strength of their immune responses decline, too, which probably leaves them even more vulnerable to skin damage and dehydration from the fungus, and their health may spiral downward rapidly.
Yet then why isn’t G. destructans as deadly to European bats? They have had much longer to co-evolve with the fungus, and perhaps to reduce its impact on torpor. Evolutionary biologists will no doubt be watching North American bat populations very closely for evidence of rapid co-evolution: given the high selection pressure that white-nose syndrome is exerting, any bats with heritable traits or behaviors that reduce the problem will be highly favored.
Not exactly the “bubonic inconvenience,” but …
So the ecological and environmental context in which G. destructans appears may change it from a relatively benign parasite into a genocidal pathogen—even though the organism itself is no different. That insight can apply to diseases of any species, and a particularly striking human example presents itself in some recent findings about bubonic plague, the cause of the medieval Black Death.
Historical records suggest that mortality rates among those infected with the plague may have been around 40 percent. That figure is higher than modern authorities have seen during the rare, isolated outbreaks of bubonic plague more recently, however. Some scientists have therefore wondered whether the identification of Black Death as bubonic plague might be mistaken, or whether mutations might have reduced the lethality of the plague bacterium Yersinia pestis.
Now those questions can be put to bed. As they recently described in Nature, geneticists were able to extract and analyze bacterial DNA from the disinterred teeth of 14th-century London plague victims. Analysis of the DNA sequences confirmed that the bacteria were indeed Y. pestis, so those people were felled by bubonic plague and not some other kind of hemorrhagic illness. (Some earlier studies that had isolated Y. pestis from Black Death victims’ remains had reached similar conclusions, but disputes over technical details of those papers had left the matter unsettled.) Moreover, gene sequence comparisons indicate that Y. pestis has mutated remarkably little over the past six and a half centuries, and not in ways that made it less pathogenic.
Why, then, is bubonic plague now so much less deadly? Again, the answer seems to be the environmental context. The difference is not in the bacterium but in the human society in which it spreads. Apparently, the vast improvements in personal hygiene (more bathing! fewer fleas!), nutrition, and access to effective medical care that improve public health in endless ways also make bubonic plaque less virulent; people infected with it don’t die as quickly and don’t pass it along as easily.
At one level, that realization may seem underwhelming: of course those health improvements reduce the severity of plague. But it should also serve as a reminder that every disease needs to be understood as the result of organisms interacting with one another and with many external factors. The severity of an illness is not intrinsic to the pathogen that causes it; it is the reflection of qualities within the pathogen, the host, and their setting. And with that expanded understanding should come recognition of more ways to think about thwarting disease and improving health. Y. pestis and G. destructans show that even for the most devastating illnesses, the prescription isn’t always black or white.
Little brown bat with white nose fungus: Marvin Moriarty/USFWS
Woodcut from “Dance of Death,” by Michael Wolgernut (1493)