ANIMALS: Why Indoor Cats Live Much Longer

Secondary poisoning could kill your cat. I know because it killed two of mine.

Secondary poisoning occurs when an animal eats another animal who was crippled by pesticides. All cats who hunt run the risk of secondary poisoning.

Rural and semi-rural cats were more vulnerable than urban cats, back when field crops were sprayed more heavily with more deadly pesticides, and before lawn sprays for home use came into vogue, but 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 are most risk are probably those living anywhere that neighbors perceive a rat or pigeon problem, and put out lethal baits which will typically kill any rodent or bird within a matter of minutes.

Any cat can become a victim.

Most frightening, the symptoms of secondary poisoning may not appear for weeks or even months after the cat eats the poisoned animal, depending on how the animal was poisoned. 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.

As a longtime environmental journalist in an agricultural district when my two cats suffered secondary poisoning, I was already something of a pesticides expert. I knew enough to look out for pesticide exposure, and I knew what the farmers were using 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, the world’s most widely used rodent poison. It may have been his first and last mouse. We saw the mouse when he attacked it, but thought it was hobbling because he had already attacked it once, not because it had been poisoned. Therefore, we let Smudge finish it off instead of rescuing it. That was a big mistake. Within 15 minutes, Smudge had hemorrhaged. He died of internal bleeding two hours later while undergoing emergency surgery.

Smudge probably never had a chance. Warfarin is an anticoagulant. It 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. 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 isn’t available for cats, but since cats have a more delicate digestive system, the lethal dose could well be lower.

We know this much: 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. We 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 8 years old, she was still only the size of a three-quarters-grown kitten. But she was mostly Russian Blue, and Russian Blues don’t run large. Typical of Russian Blues, she was an avid, skilled hunter, who preferred birds or flies to mice — anything on the wing, no matter how hard we tried to discourage her.

On Labor Day morning she abruptly became paralyzed. As usual, she had eaten her breakfast, licked the leftover milk out of my oatmeal bowl, and went upstairs for a nap, all without giving the least indication of illness or injury.

Yet soon afterward we 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 us what. Mystified, we looked her over and found no bruises, no swelling and no broken bones. Her alert green eyes darted from one of us to the next, pleading for help we couldn’t give because we didn’t know what had happened.

Plainly Corky didn’t want to be put out of her misery. She wanted to go racing up and down the stairs playing tag with us as usual. She wanted to sneak out and grab one of the birds she heard singing. She wasn’t in pain — just unable to move.

It isn’t easy to find a veterinarian on Labor Day, but we 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 we had 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 we 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. We didn’t use pesticides of any sort on our farm. Neither did the new farmer next door, who bought out the warfarin user and was unusual in that he 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.

We inspected each room of our house, searching for chemical hazards we might not have noticed before. We found none. So we investigated possible toxic properties of our house plants, using the Registry of Toxic Effects of Chemical Substances. I have 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 us all stumped.

Twelve hours after our detective work started, my mother-in-law wondered where a kernel of seed corn came from that she found lying 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. We don’t ever have any seed corn at all. Yet there the kernel lay, about a foot from where some unidentified cat had tossed up a hairball. On the chance the cat had tossed up the seed corn, too, I picked it up and checked it out.

Chemically treated seed corn is usually bright red or fluorescent pink. This kernel was pink, all right. Returning to the 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 have 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, Dr. Judith Hollebone, 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 percent.”

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.

Of course, more malathion-treated kernels might have remained in her stomach. We 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 by the time we confirmed the diagnosis, 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 suggests that it might actually be quite common, occurring anywhere cats can hunt animals that might be eating poisoned grain or lawn seed.

Since a cat will wander half a mile or more to hunt, that’s 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.
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’s eaten a poison is intelligent: it is easier than catching a healthy one.

However, secondary poisonings 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 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, or great horned owls around–because grain-eating birds roost after dark. They 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 may still 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.

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. I suspect many cats with secondary poisoning are treated for other ailments or put down as supposed victims of stroke.

Yet, as Corky’s case showed, cats indirectly poisoned by mild pesticides can seem to make full recoveries, no matter how ill they seemed to be.

But again, there can be nasty surprises later. After the initial publication of this article in 1987, Corky 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 long-term complications, she 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 we 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, I suppose, is that secondary poisoning can kill a cat long after the ingestion as well as immediately following. This makes it doubly dangerous.

ABOUT THE AUTHOR

-Merritt Clifton serves as Editor in Chief for ANIMAL PEOPLE, the world’s leading independent newsmagazine on animal issues.