Prior to 1994, house finch numbers were estimated to be in the billions in North America. Then came an unknown but unfortunate event that somehow resulted in a parasitic bacterium found in chickens to jump to finches. Finch numbers crashed by about 50 per cent, and have never rebounded.
The disease in finches, called Mycoplasma gallisepticum (or conjunctivitis), causes the birds to develop swollen, red, crusty, and watery eyes. This interferes with their ability to see—which in turn impacts their ability to find food or escape from predators. Either scenario is more deadly than the bacterium itself.
“We’ve proven the DNA of the pathogen traces back to one single source: chickens,” said Wesley Hochachka, a senior research associate at the Cornell Lab of Ornithology and the lead author of the recent study “Host Population Dynamics in the Face of an Evolving Pathogen.” And it only took one successful chicken-to-finch transfer to put the pathogen on its destructive path.
So, if the pathogen was so rampant, why did even 50 per cent of the birds survive? The answer to that question also likely explains why they’ve never recovered to their peak numbers of the 90s: the birds have developed an “imperfect immunity.” This also enables the bacterium to evolve just as fast, or at an even faster rate, in response. Hochachka’s research concludes that this partial, or imperfect, immunity likely enables selective mutations and more severe disease.
“The house finch is a moving target and the goal post keeps changing every time there is a genetic change to the bacterium,” he says. “Developed immunities make the population stronger as a whole, as they’ve out-competed each other and are still alive…but genetically they can’t adapt fast enough.” And there are endless opportunities for the pathogen to create variations. “Mutations are made by cell copying errors when they divide, which could happen with every single bacterial cell,” says Hochachka. Those mutations can happen in hours, compared to the years it takes for the birds to adapt genetically.
But on the finch’s side, many of the birds seem to get just the right amount of exposure to the disease to develop immunity to an existing strain, and then, if they’re lucky, do it again once the bacterium mutates. “They don’t quite wipe it out, but not every exposure leads to severe disease,” says Hochachka.
Today, at their new population numbers, finches are holding their own in the fight against the disease. But Hochachka doesn’t believe it’s ever likely that they’ll return to the record highs of the 90s. “They’re not climbing back to the same density, but they’re still here, and still one of the top ten birds we see.”
Although Hochachka calls bird feeding a “double edged sword,” there’s no definitive proof it’s been a prime cause of the spread of this particular finch bacteria. “We don’t know for sure. Sometimes feeders are good in some climates, especially if the birds have the disease and can’t see well to find food.” But feeders have been known to spread other pathogens, like salmonella. So if you do want to feed birds, keep the feeder and the areas beneath them clean, says Hochachka. If you’ve attracted large numbers of birds, consider putting out another feeder. And if you notice birds with red, crusty eyes, take down the feeder for a week or so.
Radio tracking has shown that finches aren’t socially cohesive, which means the ones you see at your feeder today may not be the same ones you’ll see tomorrow. But that also means the birds are likely spreading the disease quite efficiently, says Hochachka. And that “feeders could also be responsible for a large percentage of the population developing immunity.”
Want to help house finches and other bird species? Visit Project FeederWatch.