Vaccinating wild animals can protect human health, and spare animals from extinction and suffering.
The Coyote Getter, invented in the 1930s, was a hunting device that spewed cyanide into the mouth of any coyote that bit its scented wool bait. Thirty years later, researchers revisited the device. But rather than revamping it to kill more efficiently, they wanted to replace the cyanide payload with something wholly different: a coyote vaccine.
Wild animal vaccines are remarkable for many reasons, but the most remarkable might be that they exist at all. Vaccines are usually tools civilization reserves to defend the humans and domesticated animals within its bounds. The wild, by contrast, is a place from which we extract resources or defend ourselves, or where we simply leave things untouched.
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But defense doesn’t have to be adversarial. Around 60 percent of infectious diseases are zoonotic in origin, meaning they are transmitted from animals to humans, and the majority of them originate from wildlife rather than livestock or pets. Ebola came from fruit bats; HIV from chimpanzees; SARS from horseshoe bats and civets; Lyme disease lurks in deer and mice. In theory, preventing disease at its source in wild populations could protect people better than simply reacting to spillovers when they occur.
Preventing human illness is not the only reason to vaccinate wild animals. Many recent programs have been motivated by conservation, such as efforts to protect bats from white-nose syndrome or koalas from chlamydia. There is also budding recognition that these programs are valuable on welfare grounds, sparing animals from pain and suffering.
Nevertheless, wild animal vaccination first emerged as a form of defense. In the mid-twentieth century, laws mandating the vaccination of dogs pushed down the number of rabies cases in the United States, from 74 reported human deaths across the country in 1921 to single digits per year by the 1960s. The remaining cases occurred overwhelmingly through contact with wildlife: bats, foxes, skunks, and raccoons. But worryingly, the prevalence of rabies in wild animals seemed to be growing, both in the United States and in Europe. To keep rabies contained, researchers had to figure out how to immunize these animals, too.
Sick as a dog
Rabies is a terrifying disease. It is transmitted to humans through bites or scratches from an infected animal, such as a dog, bat, or coyote. The virus travels silently through the peripheral nervous system, taking a month or two to creep up into the brain and spinal cord. Once it infects the central nervous system, an array of alarming symptoms emerge. The ancient Greek physician Hippocrates is thought to have been describing rabies when he wrote of ‘persons in a frenzy [who] drink very little, are disturbed and frightened, tremble at the least noise, or are seized by convulsions’. And when these appear, death is virtually guaranteed within days.
Since rabies doesn’t spread between humans, infecting us only incidentally, it’s far more cost-effective to wipe out the disease reservoir in animals than to vaccinate humans. So developed countries have long implemented public health programs to control its spread from animals to humans: vaccinating pets and regulating their movement across borders, neutering or euthanizing strays, surveilling and investigating cases, and rapidly administering treatment after potential exposure. These early efforts worked. By the 1960s, the US had largely brought dog-mediated rabies under control, reducing the number of cases affecting humans almost twentyfold. In 2007, the canine variant of the rabies virus was officially declared eradicated from the United States, with the last recorded case occurring in 2004. Many European countries had achieved this milestone earlier. The United Kingdom had been free of canine rabies since 1922; France, 1960; and Italy, 1973. Human deaths from rabies are now almost unheard of in rich countries, though it continues to kill tens of thousands of people per year in the developing world.
But as canine rabies subsided in the West, another problem arose: wildlife rabies. Between 1938 and 1958, the annual number of rabies cases reported in wild animals grew from 44 to 2,075. Part of the reason for this was increased detection, but there also seemed to be a genuine rise in the number of cases. Rabies was spreading in raccoons, skunks, and foxes across the Americas; in Europe, too, a growing number of rabies cases were identified in red foxes, beginning in Eastern Europe in the 1940s and expanding westward. Genetic analysis of rabies strains indicates that outbreaks on both sides of the Atlantic occurred independently of one another. In both cases, the virus is thought to have jumped from dogs into wildlife.
These infected animals endanger any person who comes into contact with them. Every year, around 100,000 Americans are injected with a precautionary course of post-exposure rabies treatment after wild animal bites or scratches. This treatment, first developed in the late-nineteenth century, is thankfully highly effective, but expensive. Post-exposure treatment also works only if administered before the onset of symptoms, and the prospect of needing it is terrifying. The better solution is to control the disease at its source, in the wild.
By the 1960s, crude methods like culling and sterilizing rabies-carrying wild animal species had shown limited success, despite hundreds of thousands of foxes, coyotes and other animals being killed. These efforts may even have been counterproductive, as they increase contact between humans and animals, and could spread disease between animals in different areas. With elimination impracticable, prevention was the only solution. In 1962, early research into wildlife vaccination began, led by veterinarian and virologist George Baer at the CDC (at the time the Communicable Disease Center; now the Center for Disease Control).
Animal vaccines work in the same way as many human vaccines: killed or attenuated (weakened) pathogens trigger immune responses, teaching the immune system how to recognize a real infection. What’s different, and more difficult, is delivering those vaccines. Foxes don’t check themselves into clinics, and attempting to capture thousands of feral animals living over vast swaths of wilderness would be a logistical nightmare. Delivery methods would have to be designed differently.
Throughout the 1960s, Baer and his colleagues attempted to solve the distribution problem with imaginative gadgets. The Coyote Getter, as mentioned, was modified to shoot out inactivated rabies vaccine instead of poison. But in field trials, the forceful device often injured animals’ mouths and was unreliable at producing immunity. Another early prototype was CDC veterinarian William Winkler’s Vac-Trap, a spring-loaded needle trap that injected a syringe full of vaccine when stepped on. However, it was expensive, inaccurate, and hazardous. Any animal, or unlucky hiker, could trigger the needle.
The breakthrough came when Baer’s group pivoted to oral vaccination. The rabies vaccine variant used in human post-exposure treatment, where the virus is fully inactivated, must be injected: otherwise, it would be destroyed by the digestive system. But in 1971, Baer’s team discovered that pipetting an attenuated rabies virusvaccine, where the virus has been rendered harmless without being killed, into the mouths of foxes produces immunity. The next step was to package the oral vaccine into something an animal would want to chew.
This concept – live, attenuated virus tucked into a tasty bait – was first field-trialed in Europe. Fox rabies had been advancing westwards across the continent since the 1940s, reaching Switzerland by March 1967. In response, Swiss veterinarian Franz Steck and colleagues built on Baer’s work and began testing a range of vaccine baits, from sausages to dog biscuits to eggs, in the mid-1970s.
Eggs were rejected, as foxes would often save them for later. Sausages and dog biscuits fared better, but the ultimate winner was chicken heads. On 17 October 1978, Steck’s team scattered over 4,000 vaccine-laden chicken heads along the eastern shore of Lake Geneva, creating a barrier against the advancing epizootic. The heads also contained tetracycline, an antibiotic that incorporates into bone and teeth and glows fluorescent yellow under ultraviolet light, allowing researchers to track which foxes had consumed the bait. Within a few years, fox rabies was cleared from the area.
Following this success, Switzerland scaled up its efforts dramatically. Millions of vaccine baits were distributed nationwide over the next two decades, with individual chicken heads flung onto roadsides and airdropped over the Swiss Alps by helicopter. By 1999, fox-mediated rabies was eliminated from Switzerland entirely.
In the meantime, the US was hit by multiple rabies crises. A raccoon rabies variant had emerged near Virginia in 1977, and spread across the Eastern seaboard over the following decades. To the south, two large epizootics infecting coyotes and gray foxes had spread along the Texas–Mexico border, beginning in 1988. Hundreds of canine rabies cases popped up, and, given rabies’s near-certain fatality, thousands of people faced with potential exposure needed preventive treatment at a cost of around $3,500 per person. Alarmingly, the disease was spreading north towards San Antonio and other major cities. By 1994, the animal outbreaks had become severe enough that Texas Governor Ann Richards formally declared a state health emergency.
Several affected states launched oral rabies vaccination (ORV) programs in response, though with a less grisly bait than deployed in Switzerland. Rather than chicken heads, researchers employed fishmeal blocks covered in fish oil or vanilla. Despite their manufactured, brick-like appearance, these baits proved attractive to hungry animals.
The programs were remarkably successful. The raccoon ORV program halted the westward spread of raccoon rabies, creating a barrier at the Appalachian Mountains that has held for decades. In Texas, every dollar spent on the coyote ORV program saved an estimated $4 to $13 in human treatment – not to mention reducing the risk to human life. By 2008, the state had eliminated the dog-coyote rabies variant. By 2009, the gray fox variant followed. Today, the USDA National Rabies Management Program distributes eight to ten million vaccine baits annually across the US, placed next to dumpsters or in other places raccoons and foxes are likely to frequent, or dropped over large rural areas by plane. The rabies vaccine demonstrated that wild animals could be immunized at scale.
Shielding nature
As the conservation movement grew, the technology found a second application: preserving biodiversity. Wild species have always been threatened by disease, but human activity has exacerbated this. Habitat destruction and climate change have increased crowding in animal habitats and put stress on animals’ immune systems, amping up disease transmission. Humans and livestock also spread disease directly to wildlife, a phenomenon known as spillback.
The scale of destruction can be enormous. Chytridiomycosis, a fungal disease that infects amphibians’ skin and often fatally disrupts their vital functions, has affected at least 501 amphibian species over the past fifty years, with 90 species going extinct and another 124 declining in population by over 90 percent. In 2015, 200,000 saiga antelopes – 60 percent of the global saiga antelope population – were killed in three weeks by an outbreak of hemorrhagic septicemia, a bacterial infection that triggers sudden internal bleeding. White-nose syndrome is caused by a fungus that invades bats’ skin and disrupts their hibernation, often leading to fatal starvation and dehydration. It has killed over six million North American bats since 2007, with three bat species declining by over 90 percent. Outbreaks like these illustrate how diseases of wildlife, amplified by human activity, can push species toward extinction faster than they can recover or adapt.
Wild animal vaccines are emerging as a promising tool to fight this devastation. In September 2025, Australia approved the world’s first chlamydia vaccine for koalas. While plenty painful and embarrassing for humans, chlamydia is a far more serious threat to koalas, with infections much more likely to cause infertility and often resulting in blindness and death. Disease outbreaks account for upwards of half of all deaths in koalas and are pushing some colonies towards extinction. Alarmed by the threat posed to Australia’s iconic marsupials, Peter Timms, a microbiologist and chlamydia expert at the University of the Sunshine Coast, has spent over a decade leading development of the vaccine.
Distribution, as always, poses a challenge. Since koalas exclusively eat eucalyptus leaves, bait vaccines, like those used for rabies, don’t work. It is feasible, though, to capture koalas. Simply surround a tree with cages, and sooner or later, they will climb down and wander into the harmless traps.
After completing the largest and longest ever study conducted on wild koalas, Timms’s team found that the vaccine decreased mortality by around 65 percent and reduced the likelihood of developing chlamydia symptoms. With vaccines now available for wildlife hospitals, veterinary clinics, and field use, there’s new hope for preventing koala populations from vanishing.
Vaccines for other diseases are still in the pipeline, including vaccines for bats threatened by white-nose syndrome, which wakes them up repeatedly during winter hibernation, draining their stored energy and water until they die from starvation or dehydration. The fungal disease has already killed millions of North American bats, but the stakes extend even beyond their extinction. Many of these bat species are insectivores; without their voracious consumption of agricultural pests and mosquitoes, crop yields could fall and insect-borne disease transmission could rise. For reasons like these, the USGS estimates that bats contribute billions of dollars to the US agricultural economy annually.
But their insect-based diet also makes vaccine distribution complicated. Bats, like koalas, aren’t tempted by food baits. But they won’t leisurely wander into cages either. So researchers are experimenting with novel delivery methods instead, such as a vaccine gel or paste that could be applied onto roosting bats, which they would spread as they groom themselves and other colony members. Since September 2025, epidemiologists have been actively conducting field trials at a key site in Wyoming, racing to protect bat populations before the disease wipes them out.
Human kind
From airdropped chicken heads to anti-fungal bat gel, scientists have used ingenious methods to adapt human vaccines for animal use. Some of these efforts have already brought impressive successes, protecting humans and preserving animal species. Peculiarly, in all cases, animal welfare itself is considered incidental – a positive side effect. Even with conservation-driven programs, the concern is for populations, not individuals. A species can be considered safe while millions of its members suffer painful diseases and die, as long as the population remains stable.
There’s a growing group of researchers and activists who seek to go further. Disease isn’t bad solely because it threatens a species’s survival but because it causes suffering. Every koala or raccoon that contracts a fatal illness spends days or weeks vomiting, seizing, blind, feverish, or paralyzed. None can hope for treatment. Then, alone and in pain, they die.
Wild animal vaccines could mitigate such suffering. Vaccines like the oral rabies bait show that it’s possible to effectively improve wild animal welfare, and there are other painful diseases we could prevent, too.
In 1936, the Coyote Getter was invented to kill coyotes with cyanide. Thirty years later, it was retrofitted to administer medicine. The same ingenuity that made us effective predators could also make us effective protectors. Perhaps wild animal vaccines hint at what we’ll ultimately choose to become.