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.
--Merritt
Clifton, Editor, ANIMAL PEOPLE |
