Threat to both ferals and indoor/outdoor pets
by Merritt Clifton
Asked one of the most dedicated of the multitude of “cat ladies” of my acquaintance, “Do you know if there’s truth to the idea that if cats eat rats who have been into bait stations, the cats will also get the effects of the warfarin?”
The short answer is yes, absolutely.
But a long answer is appropriate to adequately respond to all aspects of the question.
Urban cat ecology
This particular “cat lady,” a serious observer of urban wildlife ecology who has written scientific papers about her findings, monitors her neuter/return colonies with “wildcams,” hidden cameras that transmit real-time images of her feeding stations to her laptop.
Thus the “cat lady” sees exactly how many cats are visiting, which cats they are, and can respond promptly to any illnesses, injuries, or arrivals of unsterilized newcomers among her colonies.
Many years ago now, I pointed out to this “cat lady” that feeding feral cats in neuter/return colonies is usually a bad idea, because the cats would not be present in the first place without an adequate food source to sustain them, and that feeding some feral cats tends to attract more.
Also, feeding feral cats may attract cat predators, such as coyotes, foxes, fishers, hawks, owls, and eagles, who may take over the food resource by killing the cats.
Almost certainly, feeding feral cats at a location where the cats are already making a living by hunting rats and mice will turn out to be feeding the rats and mice too.
Instead of prowling to find the rats and mice wherever they are, the cats will learn to just wait in ambush near their dish.
Exceptions to rules
But sometimes there are exceptions to almost every rule. The “cat lady” who asked about warfarin inherited several of her colonies from other neuter/return practitioners who no longer live nearby. Longtime feeding had already habituated some of the cats to being fed––but not to being handled––that at their already relatively advanced ages, they would probably not fare well without feeding.
The “cat lady” in question recognized in each situation the opportunity to confirm theory with verified observations, collected and documented on video.
At one colony the last of the now elderly cats and the local rats––who are also mouse predators, preying chiefly on pinkies in their nests––appear to have become friendly rivals. The cats and the rats share dishes of catfood. Because the cats at that particular feeding station do not kill and eat the rats, and are not doing much mouse-hunting either, those cats are probably safe.
This is not the case for other colonies, where both rats and mice remain on the cats’ menu, and are abundant enough that local shopkeepers, homeowners, and birders concerned with birds’ nest predation by rodents are setting out poison, principally warfarin.
Disneyland for cats
The “cat lady” whose question occasioned this discussion does not allow her own household cats to roam beyond her own yard. Instead, her cats have an elaborate system of tunnels and climbing tubes that allows them to meander through treetops, look over fences, and pretend to be wild, without ever actually coming into contact with wildlife.
The yard could be described as Disneyland for cats, with only catnip incarnations of Mickey Mouse.
But many other people do allow their household cats to roam––about half of all U.S. and Canadian cat-keepers, to be precise, who have only about a third of the owned pet cats because of the much higher mortality rate among cats who go outdoors.
Frequent, deadly, insidious
Outdoor cats are vulnerable to many hazards, including cars, predators, traps set for furbearing and “nuisance” wildlife, and irate birders with deadly weapons.
Secondary poisoning from consuming poisoned rats, mice, birds, and other animals, though, should be recognized as one of the most frequently deadly and insidious threats to outdoor cats––even if most cat caretakers do not recognize the symptoms when they see it occur.
Learned the hard way
Secondary poisoning could kill the cats you care about.
I know because more than 30 years ago secondary poisoning killed two of my cats, back when I lived in a remote corner of Quebec where I let my sterilized, vaccinated, but still quasi-feral cats roam because they always had.
This was a big part of how I learned to keep my cats home in a yard with fences that cats cannot get over, as I now recommend that household cats should be kept.
Lest anyone imagine that my experience was so long ago and far away that “It can’t happen to our cats, here,” let me point out immediately that a set of secondary poisoning cases almost identical to mine killed four bobcats on the University of California at Santa Cruz campus in 2014 and 2015, before the symptoms were recognized by Duane Titus of Wildlife Emergency Services, a Moss Landing-based nonprofit organization.
“Tests revealed three kinds of rat poison” in the remains of one of the bocats, reported Nala Rogers of the Santa Cruz Sentinel, “two of which were ‘second-generation anticoagulants’ — poisons recently deemed too dangerous for public sale by the state of California and the U.S. Environmental Protection Agency,” but still licensed for use by professional applicators and other government agencies.
“Hardly an isolated case”
The U.C. Santa Cruz bobcat “was hardly an isolated case,” continued Rogers.
“About 73% of 492 wild animals tested in California from 1995 to 2011 had second-generation anticoagulants in their bodies, according to the California Department of Pesticide Regulation. The animals included mountain lions, hawks, owls and endangered San Joaquin kit foxes. Some animals had up to five different kinds of rat poison in their livers,” WildCare animal hospital director of wildlife solutions Kelle Kacmarcik, told Rogers.
“Second-generation anticoagulants prevent blood clotting and cause animals to hemorrhage internally,” Rogers wrote, summarizing information from California Department of Fish and Wildlife pesticide effects coordinator Stella McMillin. “They take up to a week to kill, so rodents can ingest many times the lethal dose. The sick rodents are then vulnerable to predators. And when predators eat poisoned rodents, the poisons can build up in their bodies and persist for months.”
My cats worked for a living
My Quebec cats worked for a living in nearby fields and barns. They visited my home every day for kibble treats and to sleep on a soft warm bed, especially during the bitter winters, but even in winter they mostly chose to enjoy a lot of outdoor time.
As McMillin told Rogers, secondary poisoning occurs when an animal eats another animal who was crippled by pesticides.
All predators run the risk of secondary poisoning.
Cats at greatest risk
Cats who hunt tend to be much more at risk than most predators, however, because the species whom cats most often hunt––rats, mice, voles, and sometimes small ground-feeding birds such as starlings and English house sparrows––also tend to be the species whom humans most often try to poison.
Even when humans are not deliberately trying to poison the species whom cats prey upon, seed-eating rodents and birds may ingest poison residues which might in turn harm cats.
Crops & lawns
Back when field crops were sprayed more heavily with more deadly pesticides than today, before lawn sprays for home use came into vogue, rural and semi-rural cats were probably more vulnerable to secondary poisoning than urban cats. These days suburban cats may be at equal risk.
In general, the more concentrated the pesticide that the cat may encounter through a prey species, the greater the danger.
The cats at most risk tend to be those living anywhere that neighbors perceive a rat or pigeon problem, and put out lethal baits which will typically kill smaller rodents and birds within minutes.
Most frightening, as McMillan pointed out, the symptoms of secondary poisoning may not appear for weeks or even months after the cat or other predator eats the poisoned animal.
The initial poisoning may occur at any time of the year in urban habitats. In rural and suburban areas it is most likely to occur in late spring, when farmers and gardeners apply pesticides most heavily.
When my two cats suffered secondary poisoning, I was already something of a pesticides expert. As a longtime environmental journalist in an agricultural district, I knew enough to look out for pesticide exposure, and I knew what each local farmer used and when.
I was even the guy some local doctors called for quick advice when they got a case of human pesticide intoxication or poisoning.
But I still learned most of what I know about secondary poisoning and cats the hard, painful way. The process was, of course, even harder and more painful for the two cats involved.
In the spring of 1980, I lost Smudge, a young black male. He had apparently eaten a mouse who had just eaten warfarin, both then and now the world’s most widely used anticoagulant rodenticide. The mouse may have been his first and last.
I saw Smudge pounce the mouse, from about 50 feet away, but I thought the mouse was hobbling because Smudge had already attacked him once before I noticed, not because the mouse had been poisoned.
Neither cat nor mouse had a chance
Knowing that an injured mouse would have next to no chance of survival even if rescued, and that Smudge could effect the kill more quickly than I could perform any sort of field euthanasia, I let Smudge finish the job and then enjoy his hard-earned meal.
That was a big mistake. Within 15 minutes Smudge hemorrhaged. He died of internal bleeding two hours later while undergoing emergency surgery.
Smudge probably never had a chance. Warfarin kills rats and mice in very small doses by causing them to hemorrhage to death. The neighboring farmer was using warfarin bait to protect his seed corn. Since warfarin is advertised as dangerous only to rodents, neither he nor I realized before Smudge died that it can kill cats — and dogs — as well.
Lethal dose same for cat as for mouse
The OSHA/EPA Registry of Toxic Effects of Chemical Substances says an ingested warfarin dose of only 800 milligrams per kilogram of body weight is fatal to dogs.
Similar information is not available for cats, but since cats have a more delicate digestive system, the lethal dose could well be lower.
What I knew right away was this: The lethal dose for Smudge was approximately equal to the lethal dose for the one mouse he ate, the only one found in his stomach.
Corky seemed to be much luckier in early September of 1986. I called her Corky because, when healthy, she bobbed around like a furry cork in a stream. She was a little cat, a poor candidate to survive poisoning because, at eight years old, she was still only the size of a three-quarters-grown kitten.
She was an avid, skilled hunter, who unlike most cats, preferred birds or flies to mice — anything on the wing, no matter how hard I tried to discourage her.
On Labor Day morning she abruptly became paralyzed. As usual, she had eaten her breakfast, licked the leftovers out of my oatmeal bowl, and went upstairs for a nap, all without giving the least indication of illness or injury.
Yet soon afterward I found her lying halfway down the stairs, paralyzed in the hind quarters and losing feeling in her front feet, which were cold to the touch. She knew something terrible had happened. She struggled hard to tell me what. Mystified, I looked her over and found no bruises, no swelling and no broken bones. Her alert green eyes pleaded for help I couldn’t give because I did not know what had happened.
Plainly Corky did not want to be put out of her misery. She wanted to go racing up and down the stairs playing tag with me as usual. She wanted to sneak out and grab one of the birds she heard singing. She wasn’t in evident pain — just unable to move.
It is not easy to find a veterinarian on Labor Day, especially in a remote rural area, but I managed.
Two hours after paralysis set in, the vet examined Corky and offered a diagnosis: pesticide intoxication. Her mouth was inflamed. Her extremities were numb, except for her tail. She could still control her tail, so the vet ruled out the possibility of spinal injury.
It was clear that this was another case of secondary poisoning. But Corky’s problem was not as simple to solve as Smudge’s had been. Symptoms of warfarin poisoning are unmistakable. Symptoms of poisoning by most other pesticides are easily confused, but the vet and I had to identify the source of the poisoning to know if Corky could recover.
Our detective work indicated just how widespread and commonplace secondary poisoning of cats can be, even though it is not well documented. We began without a single clue. I didn’t use pesticides of any sort. Neither did the organic farmers at the two nearest farms, one of whom bought out the warfarin user and raised healthy corn without applying anything more toxic than pig manure.
Further, despite her hunting habits, Corky was not inclined to wander far afield. She had been in the house for the whole morning preceding her paralysis.
I inspected each room of the house, searching for chemical hazards I might not have noticed before. I found none, so investigated possible toxic properties of our houseplants, using the EPA/NIOSHRegistry of Toxic Effects of Chemical Substances.
I had tracked down a lot of pesticide-related problems over the years, including cases involving school children and chemicals that had been banned 10 years before they were used, but the case of the poisoned kitty had me stumped, and also stumped others I called for help.
Twelve hours after my investigation started, a kernel of seed corn was discovered in the middle of the basement floor.
Seed corn should not have been around anywhere at that time of year. Farmers sow corn in late spring or early summer. No seed corn had ever been used where I lived. Yet there the kernel lay, about a foot from where an unidentified cat had tossed up a hairball.
On the chance the same cat had tossed up the seed corn, and that the cat had been Corky, I picked it up and checked it out.
Red or pink corn
Chemically treated seed corn is usually bright red or fluorescent pink, as a warning that it should not be confused with corn for human or animal consumption. Unfortunately, small children sometimes mistake the dyed corn kernels for candy, with occasionally fatal consequences.
This kernel was pink, all right.
Returning to the EPA/NIOSH Registry of Toxic Effects of Chemical Substances, I ran down every chemical seed treatment I knew about. I cleared the fungicide captan; it is carcinogenic, but doesn’t produce short-term paralysis. I cleared atrazine, which usually isn’t directly applied to the seed, and paraquat, which also is not directly applied to the seed and would have affected Corky’s breathing.
I couldn’t clear methyl mercury. Most of the symptoms didn’t match up, but a few did.
Cats, I knew, are more susceptible to methyl mercury than people, as established by the “Dancing Cats Syndrome” noted in Japan just before the “Minimata Syndrome” attacked people who had eaten mercury-tainted fish. People, in turn, are so susceptible that methyl mercury seed treatments had been banned for 20 years or more, but that did not necessarily mean some old treated seed corn was not still around.
If the culprit was methyl mercury, Corky would not recover.
I sought help. I called an old acquaintance, Judith Hollebone, Ph.D., of Agriculture Canada’s pesticides division in Ottawa.
“That fluorescent pink color is the key,” Hollebone told me. “That’s a tipoff that your seed has been treated with one of the carbamate pesticides, probably captan or diazanon. In your area, you might get a captan, diazanon and lindane combination.”
“Lindane is used in flea collars,” I noted. “I can’t see that paralyzing a full-grown house cat.”
“It’s the concentration,” Hollebone explained. “On seed corn, the concentration of the coatings can be as high as 20%.”
She listed other pesticides for me to investigate: methoxichlor, thiran, carbathion. One by one, I ran them down in my registry, eliminating symptoms.
And then I found the culprit: malathion — one of the mildest of insect sprays.
Concentrated up to 20 percent, however, the malathion coating on that single piece of seed corn had been enough to partially paralyze a bird Corky might have eaten three or four months earlier. For some reason the kernel remained in her stomach, perhaps lodged in a hairball. The hairball might have protected the malathion coating from stomach acids. Suddenly, however, something caused the coating to begin dissolving. Within minutes, Corky lay paralyzed herself.
Other known symptoms of malathion poisoning include panting, nausea, listlessness and insomnia, all of which Corky developed during the next 12 hours. She did not die only because she threw up the kernel while still mobile, before all the malathion coating entered her bloodstream.
Appeared to recover
Of course, more malathion-treated kernels might have remained in her stomach. The vet could have administered an atropine antidote, but Hollebone recommended against it. Atropine has toxic effects in itself. Rather than expose Corky to a second poison, even in a controlled dosage, Hollebone suggested we gamble that Corky had already survived the worst of her attack. If paralysis was the worst of it, she would recover.
Indeed, she had begun improving, managing to drag herself to her food, water and litter box. After 48 hours she could climb a few steps. In three days she was almost well again, even arching her back when petted.
Freak accidents? Once, possibly. Twice, probably not.
Two cats suffering secondary poisoning within six years suggested to me that it might actually be quite common, occurring anywhere cats can hunt animals who might be eating poisoned grain or lawn seed.
I began collecting case accounts. Within months I had accumulated enough confirmed cases of secondary poisoning in cats to feel certain––since the confirmed cases were and are almost certainly rare compared to the total number––that secondary poisoning kills more cats than even curiosity.
Since a cat will wander half a mile or more to hunt, that would be anywhere within half a mile of a carefully tended lawn or grain field of any kind, including backyard garden corn patches.
This in turn is almost anywhere. The larger the scale of grain-planting or lawn-growing, the greater the likelihood of birds and rodents being affected, and therefore the greater the likelihood of secondary poisoning.
Cats who hunt birds are more endangered simply because a poisoned bird can travel farther than a poisoned rodent before dropping dead.
What can be done?
Is it possible to develop safer seed coatings? Probably. Yet seed-coating is already the safest form of pesticide used. Unlike sprays, which tend to drift and endanger anything nearby, seed coatings protect specific crops for a specific (usually short) period.
It is not likely that developing more intelligent cats will prevent secondary poisonings, either. It is a cat’s nature to hunt, and the nature of all hunting animals to pick on weakened prey animals. To a cat, eating a bird or mouse who has eaten a poison is intelligent: it is easier than catching a healthy one.
However, secondary poisonings of pet cats can be held to a minimum. If you live anywhere near grain fields or lawns or rats or an urban pigeon-poisoning program, be extra careful to keep your cat away from hunting opportunities. Make sure that the cat cannot go beyond your own secure fences.
If near grain fields, keep your cat indoors during daylight hours at planting time, usually no more than a day or two. That is when birds are most likely to eat treated seed grain.
You can let your cat out after dark with relative safety––if there are no coyotes, foxes, fishers, or great horned owls around––because grain-eating birds roost after dark. Grain-eating bird species are most vulnerable to cat attack when down on the ground, either eating grain or suffering from having eaten it. After dark, poisoned birds may still be on the ground, but will be dead, no longer moving in a manner that attracts cat attention.
Your cat will hunt rodents after dark, but unless you live right beside a grain field, a sprayed lawn, or someone battling against rodents, the danger is reduced.
Not much can be done to protect feral cats from secondary poisoning, for which reason I would not consider any location where rats, mice, or birds are poisoned, or seed grain is stored, to be a suitable site for neuter/return.
Be alert to symptoms of secondary poisoning. Some veterinarians may recognize pesticide intoxication; many will not. The most common symptoms are labored breathing, numbness and paralysis, listlessness, loss of appetite and nausea — all symptoms of other ailments as well.
Most likely many cats suffering from secondary poisoning are treated for other ailments, or are put down as supposed victims of stroke.
As Corky’s case showed, cats who have been indirectly poisoned by mild pesticides can seem to make full recoveries, no matter how ill they seemed to be.
But there can be nasty surprises later, for which reason prompt euthanasia, rather than treatment, can be the most humane response when a cat is known to be suffering from secondary poisoning.
Corky, unfortunately, died of a fast-forming cancer almost certainly related to her secondary pesticide poisoning.
Within six weeks of having seemingly made a full recovery from her paralysis, with X-rays showing no sign of longterm complications, Corky became unable to digest solid food. She survived in good health, good spirits and apparently without pain on a diet of milk and raw eggs, while the vet and I treated her for more common causes of chronic vomiting such as worms and impacted hairballs.
When her vitality failed, it failed abruptly. This time, X-rays revealed numerous tumors throughout her body, including an egg-sized tumor in her liver that hadn’t been there 10 weeks before. Exploratory surgery showed dozens more tumors throughout her digestive system.
There is rarely any way to conclusively relate a cancer to a specific cause. However, pesticide residues tend to accumulate in the liver first, and the malathion/captan seed coating Corky had ingested via the bird is known to cause similar cancers — the captan, a fungicide, being the suspected carcinogen.
The lesson is that secondary poisoning can kill a cat long after the ingestion, as well as immediately afterward.
This makes it doubly dangerous.
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