by Darryl Jones
Frank signed up in 1988 and has been sending in his records without fail ever since, but he began making detailed notes long before. Nothing feathered escapes his notice, and he has often been the first to see rare and unusual species passing through. “I recorded an Eastern Phoebe and a pair of Golden-crowned Kinglets in ’65, and even a Swamp Sparrow in ’75. And I can tell you for certain that there weren’t any House Finches in these parts earlier than 1977, March to be exact,” Franks states confidently. “I was trying to attract Goldfinches with the new nyger seed at the time and was amazed to see a flock of unfamiliar finches at the feeder. At first I thought they must be slightly different Purple Finches, but the color was just not right. I had never seen them here before, but from then on we had swarms of them. And spunky! The goldies and the purples had a real hard time getting to the feeders once the House Finches moved in.”
Frank had experienced the early stages of a most unusual and dramatic invasion of the eastern United States by an otherwise “native” species. His-torically, House Finches were mainly dryland birds of the western region of North America. It is believed that the massive population that eventually enveloped the eastern side of the continent originated from a handful of cage birds released on Long Island in 1940. For about two decades a tiny flock managed to just hang on before mysteriously exploding in abundance around the early 1960s. House Finches spread in all directions, with the introduced birds reaching the natural range of the species in the west, evidently completing a full cross-continental distribution. Although apparently identical, the eastern-introduced finches are much more likely to be associated with humans, preferring urban areas and spending a lot of their time in gardens and back yards. These eastern House Finches love feeders, where they often aggregate in large flocks. Unsurprisingly, they are among the most common species recorded by Project FeederWatch participants; about 75% of all reports include House Finches.2
It was during one of his routine counts of the birds on his main feeder in January 1994 that Frank first noticed something seriously amiss with several of House Finches. Two within a small group were uncharacteris-tically quiet, sitting to one side, listless and immobile. When he looked more closely through his binoculars, Frank could see immediately that both birds had grossly swollen eyes that were oozing some sort of nasty secretion. “They looked to be blind and very sick,” says Frank. “In fact, it was obvious that they could hardly find the seed on the platform.” When he approached, the birds fluttered weakly away. He quickly rang a neighbor, Rich, also a keen FeederWatcher, and was alarmed to learn that Rich had also been seeing House Finches with crusty, weeping eyes. A few days later, Rich arrived at Frank’s place with a small plastic bag and a worried expression. “It was two dead finches that Rich had found on the ground near his feeder. After some discussion, we decided to take it to our local vet. He didn’t really know what was wrong with the birds but said he would send it to the university. I also let the Cornell Lab people know straightaway. But the way the birds looked, it reminded me of the sore eyes my children used to get sometimes. Conjunctivitis, the nurse called it.”
These actions by Frank and Rich—and about a dozen other people from various places in the mid-Atlantic region—were instrumental in alerting wildlife agencies to the start of a significant wildlife disease outbreak.3 Perhaps even more remarkable was that decisive action was under way very promptly. Microorganisms extracted from the tissues of the infected birds were found to be Mycoplasma gallisepticum, a pathogen known to affect poultry but which had never previously been associated with wild birds. And Frank’s hunch was right: the disease was classified as mycoplasmal conjunctivitis, though more commonly known as the House Finch disease.4
Because of the efforts of Frank Wilston and other FeederWatchers, key people at the Cornell Lab of Ornithology quickly became aware of the outbreak. They soon realized that this was a highly unusual and extremely worrying situation: the pathogen appeared to have moved from domestic birds to wild species, and sick birds were using feeders and could be spreading the infection, potentially to any other species mixing with House Finches. Alarm bells were ringing. André Dhondt, who had arrived at the Lab only a few years earlier, immediately saw an opportunity for monitoring this disease using the network of existing Project FeederWatch participants.5 Within a few months of the initial outbreak, the Lab launched the “House Finch Disease Survey,” inviting FeederWatchers to keep a sharp eye out for birds showing signs of the disease. Usefully, these signs were all-too obvious and could be detected from a distance, and with House Finches being abundant, reporting was reliable and rapid. So was the spread of the disease. Within a year it had reached Ontario, West Virginia, and Ohio; by the fall of 1996, Wisconsin and Iowa. The rate of movement was astonishing and extremely alarming, a perception possible only because of the unprecedented geographical and temporal detail being provided by the huge number of reports flood-ing in. By 2004, over 10,000 participants had submitted almost 90,000 monthly reports; ten of these people (yes, Frank was one of them) had even sent in more than a hundred.6
This level of detail provided the framework for a broad suite of sophisticated modeling and epidemiological studies of the House Finch disease, making it one of the most intensively researched wildlife diseases in wild birds. Although much remains unclear about aspects of the disease (such as how it infiltrated into wild House Finches), André Dhondt and his colleagues continued to sieve through the data trying to discern patterns and lessons. They were able to show that the disease had a rapid and dramatic impact on House Finch abundance as it moved through an area. Within only a couple of years, overall numbers decreased by around 60% and the average group size recorded at feeders dropped from more than twelve to only about four or five.7 This was clearly a disease that was spread easily and effectively among House Finches, though the mechanism of transmission had yet to be confirmed.
In poultry, the pathogen seems to be transmitted through direct contact between birds. Given the highly social nature of House Finches and their habit of aggregating—and agitating—in tight groups at feeders, this seemed to be the obvious explanation: cross-contamination through direct contact between birds. Direct contact would seem to be an important condition of transmission because this type of bacteria has no cell wall, meaning that it cannot survive for long outside a suitable protected environment, usually the cells of another animal. Mycoplasma does appear to be able to remain viable, however, if it is attached to certain substances that are moist and organic (objects or substrates that potentially harbor disease are known as “fomites”). Unfortunately, some feeders provide fomites in abundance: droppings, decaying seeds, moist dust, and detritus. Thus, the pathogen could be transferred directly between birds or indirectly through fomites at the feeders.
Perhaps unexpectedly, careful study of video recordings of interactions between House Finches at feeders showed that physical contact between birds was actually quite rare. All that jostling and squabbling seemed to be birds avoiding a jab from sharp beaks; direct bird-to-bird exchange of infectious material was less likely than simple contact with the feeders themselves.8 However, there is much more to the busy social life of House Finches than fighting for feeder space; in the cold months especially, these birds live in flocks, providing plenty of time for transmission of the disease away from the feeder. These three components of the finch-disease story—the type of flock, level of aggression at feeders, and time spent at feeders—were carefully considered in an important study conducted in Virginia.9 By capturing House Finches at their study site and attaching minute electronic tags to leg bands, the researchers were able to track the movements and interaction of almost 200 House Finches as they visited a series of feeders fitted with tag readers. It was by far the most detailed study of feeder visits ever undertaken.
The Virginia researchers made some fairly obvious and logical predictions: the House Finches most likely to pick up the disease are those that belong to larger flocks with more stable membership, ar
e involved in more aggression at feeders, and spend more time at feeders. Given the many possible influences and variables that were considered, these results were unexpectedly straightforward: the risk of acquiring the disease was almost entirely associated with how long they remain at the feeder. The significance of flocking and aggression was effectively trivial. In other words, the transmission of House Finch disease is clearly indirect: the pathogen is spread by the feeding structure rather than bird to bird.10
The Virginia study did not, however, actually examine the feeders themselves. But others have done so.11 Swabs from a large number of feeders used by infected House Finches showed that the pathogen did indeed remain viable and infectious for up to 12 hours, plenty of time for other birds to be exposed. Once infected, the signs of conjunctivitis take a few days to develop and peak in severity at about 10 days. As the disease progresses, infected birds become inactive, often remaining on the feeder for extended periods throughout the day. This, of course, only adds to the level of contamination at the feeder. However, experimental studies found that although large proportions of infected birds develop the disease, the number of birds that died was actually fairly low, with many birds eventually recovering. Nonetheless, affected birds could remain infectious for several months.12
These findings indicated that House Finches visiting contaminated feeders readily picked up the pathogen before moving on to other feeders, at least for the next few days. When the disease kicked in, their lack of vigor and difficulty in seeing made remaining near or even on a feeder a sensible survival strategy. Being rendered effectively blind made the predictable location and supply of food associated with a feeder an obvious place for a sick bird to stay. On recovery, however, revitalized but still infectious House Finches were able to move on. Indeed, unlike the much more sedentary western House Finches, the eastern birds have a pronounced north–south and seasonal movement pattern, aggregating at feeders in winter—where infections are more likely—and then migrating northward, back to their spring breeding grounds, bringing the disease with them.13
Like almost all wildlife diseases that bring pathogens and host species together, House Finch conjunctivitis is extremely complex and difficult to understand, predict, and control. Its progression over almost an entire continent has been, however, unusually easy to track thanks entirely to the existence of an army of ideal and dedicated observers. Observers who carefully watch their feeders. Feeders where sick birds may gather. Thereby increasing the likelihood of passing the disease on to other birds. There is no escaping this conundrum: the feeders are at the epicenter of the epidemic yet are essential to the monitoring process. It is actually highly probable that the disease would not have spread if feeders had not been present, but it is also certain that we would know almost nothing about it without them.
Such quandaries are, however, somewhat vacuous: the feeders are here to stay. They may in fact provide the most effective means of future control of the disease. With infected birds apparently staying close to feeders rather than disappearing into the landscape, potential treatments (though not yet available) could possibly be administered directly to these localized birds. More immediately, the realization that feeder structures themselves may be key vectors of transmission means than feeder owners can interrupt this process simply by careful attention to hygiene (more details to come). There are extremely important responsibilities associated with bird feeding beyond the provisioning of food.
Disease Is Easy to Miss
Coming to a feeder to pick at a tightly packed volume of seed is a most unnatural way for birds to obtain food. Apart from species that feed on large animal bodies, either as predators or scavengers, almost all food sought by birds is scattered, dispersed, and spatially separated. Even when seasonal bonanzas become available, such as a tree full of berries or a hedge laden with caterpillars, there is usually room for plenty of takers. Sure, really assertive individuals may try to control access to the best bits, but such monopolies are rather difficult to maintain for long. For birds that forage largely on seeds, grain, or fruit—the majority of species visiting our feeders—their typical foraging places are characteristically in fields, woodlands, and forests. Plenty of room to avoid the crowds or prickly neighbors.
Feeders attract birds because they offer plenty of food in abundance and typically in a highly predictable location. But there are often plenty of recipients in such a deal and competition can be stiff. Still, apart from difficult times when natural foods or other feeders are scarce, picking up a snack is usually possible, even if you have to be quick. What feeders do is bring together lots of birds, of a variety of species, to the same specific spot, repeatedly and continuously. Many of these species would normally have nothing to do with one another and most of these individuals would usually avoid contact with others of the same species. Feeders can change all that, with a range of potential consequences, including the possibility of exchanging diseases.
The House Finch disease is just one example, its spectacular spread apparently directly associated with the aggregating of large numbers of birds at feeders. At a feeder the possibility of another picking up something nasty is greatly increased. Minimizing the spread of avian diseases at feeders should most definitely be one of the primary concerns of anyone engaged in wild bird feeding. This is why maintaining the cleanliness of all feeders, including the ground beneath, must always be a top priority. But illustrating this point by describing the House Finch disease story may actually be counterproductive. A key reason for the success of the House Finch disease survey was the fact that this particular ailment was so conspicuous: the birds drew attention to themselves by behaving differently, remaining at the feeder for long periods that allowed them to be scrutinized, their physical symptoms clearly visible. These features attracted attention and generated concern. Unfortunately, such visibly distinct evidence of disease is extremely unusual. Sick birds do not necessarily display their condition and, being typically lethargic, are less able to compete and are easily driven away. They are also much more susceptible to predators and are more likely to die away from the garden. This means that even feeders that are significant disease transmission sites, steadily infecting visiting birds, may not appear to be so, at least to human eyes. Only rarely do birds linger at feeders or die nearby; as well will see, the disease would need to be exceptionally virulent for birds to succumb so quickly. The problem is that the absence of overt indications of disease does not mean that none exists. We all tend to assume that because we have never seen things of obvious concern—like a sick bird—our feeders must be safe. As is becoming increasingly clear, this can be a dangerous assumption.
The Tricho-Catastrophe
The Woodpigeon is a bird usually found in rural areas of Europe though it is increasingly seen in urban areas, even on suburban feeding tables. It is also one of the most important game birds in continental Europe, with around 10 million shot annually. A significant proportion of the populations from northern and eastern Europe overwinter in Portugal and Spain, often roosting in huge numbers. Although these birds usually find plenty of natural food in the oak woodlands of the region, many also take advantage of the supplementary grain provided for other game species, such as partridges and pheasants. During late 2000, gamekeepers in a large hunting preserve in southern Spain began to notice dead Woodpigeons lying in their fields. When they started to systematically search, they found about twenty birds each day over the following 2 years.14 By the end of the outbreak, over 2,600 dead Woodpigeons had been collected, though almost certainly many more were missed. This was of great concern because, as well as affecting future pigeon hunts, several endangered raptors occurred in the area and were known to eat pigeons, including dead ones. Subsequent analysis confirmed the pathogen to be Trichomonas gallinae, a protozoan parasite responsible for the disease trichomoniasis.15 This horrifying ailment causes necrosis of the oral cavity and digestive tract, usually leading to starvation as the birds are unable to ingest their food
properly. Although the disease is also found in birds of prey, it is more commonly associated with pigeons, with the main reservoir of the infection worldwide being the ubiquitous feral pigeon. Indeed, the disease has been linked to the extinction of the Passenger Pigeon in North America following the introduction of domesticated Rock Doves by the European colonists in the 1700s.16
A detailed review of what was the largest outbreak of trichomoniasis in wild pigeons ever witnessed concluded that the most likely vector of transmission were the feeders supplying grain for the various game species.17 The period of pronounced pigeon mortality—2000–2001—coincided with a failure of the local acorn supply, leading many Woodpigeons to visit the feeding stations supplied for the pheasants and partridges. Of course, plenty of feral pigeons were using these places as well. Although the ultimate source of the infection was not identified conclusively, the most likely culprits were these feral pigeons, who may have contaminated the grain as they fed. Fortunately in this case—and unlike the House Finch disease—a highly effective treatment (dimetridazole) for trichomoniasis was readily available. This was subsequently added to the grain in the same feeding stations with almost immediate effect; no further dead Woodpigeons—or any other species—were detected after just two treatments. The crisis appeared to have been averted, in Spain at least. A year later, however, in the autumn of 2002, an almost identical outbreak occurred in southern England, again among Woodpigeons, but this time also among Collared Doves.18 “Trich” was confirmed quickly, and the treatment administered. But, if indeed there were sighs of relief, they were to be short lived.