Captive cheetahs are being besieged by amyloid deposits and fibrils (bottom panels, respectively) in their livers.
Credit: Yumi Une/National Academy of Sciences, PNAS (2008)
Although famously speedy, cheetahs can't seem to outrun a deadly disease called amyloid A (AA) amyloidosis. The illness kills up to 70% of the cats in captivity and has frustrated breeding efforts. In a new study, researchers provide the first compelling evidence that may explain how the disease is transmitted.
AA amyloidosis resembles mad cow disease. Like mad cow disease, a misfolded version of a protein--in this case amyloid A--converts normal proteins into abnormal ones, a process that snowballs into large deposits of damaging protein in tissues such as the spleen and liver. (The mad cow protein does most of its damage in the brain and central nervous system.) Animals often die of kidney failure, and the incidence of AA amyloidosis has spiked from 20% to 70% of captive cheetahs since the 1980s.
AA amyloidosis is not caused by a bacteria or virus, yet there's reason to suspect that it can spread from animal to animal like an infectious disease. Both mad cow disease and scrapie--a related disease in sheep--appear to be contagious. And when captive cheetahs are kept in small enclosures close together, AA amyloidosis strikes younger animals and with more severity, a finding that supports the contagion hypothesis. Yet biologists have been hard-pressed to figure out how the disease moves from cat to cat.
To examine potential routes of transmission, Keiichi Higuchi, a biologist at Shinshu University in Matsumoto, Japan, and colleagues isolated the AA protein from diseased animals' livers. From the protein, the researchers were able to develop a fluorescent tag that, in further experiments, picked up the AA protein in feces of diseased cheetahs. The find supports previous studies that had flagged feces as a possible infection route for similar diseases in deer and mice. What's more, the AA protein in the feces was more transmissible and more effective in inducing the disease in mice than the protein isolated from the liver, possibly due to its smaller size and greater instability, the researchers report online today in the Proceedings of the National Academy of Sciences.
It's still unclear how captive cheetahs come into contact with each other's feces. Higuchi's team suspects that this may happen when the cats lick their fur while grooming or when they eat food that has touched contaminated soil. Based on their finding, the researchers suggest that zoos or captive-breeding colonies can limit the spread of AA amyloidosis by removing feces as soon as possible or by keeping the animals' food separated from areas that have come into contact with feces. "These results provide possible measures for rescuing cheetahs from extinction," says Higuchi. There are only about 12,500 cheetahs alive on the planet today, he notes, so any cheetah death is a blow to the species' chance of survival.
Sarah Durant, a conservation biologist at the Zoological Society of London and the U.S.–based Wildlife Conservation Society, says limiting the spread of AA amyloidosis among captive animals is a good strategy. Although the disease is unlikely to affect free-roaming cheetahs, she says that conquering it in captivity could raise awareness of the plight of wild cheetahs.