TNR Opponents’ Reaction(?) to the Recovery of the California Sea Otter

Photo: Wikipedia/Michael L. Baird

For several years now, TNR opponents have blamed Toxoplasma gondii infection in California sea otters on outdoor cats, the idea being that the parasite is spread from cat feces into the soil and then flushed into the Pacific by way of runoff. From the start, it’s been a dubious argument—requiring believers to focus narrowly on specific data while ignoring a great deal more.

And the argument has only grown increasingly weak in recent years, as additional research findings have further questioned the role of domestic cats in sea otter infection. Perhaps most compelling of all are the results of the 2016 sea otter census, which estimates that the population along the California coast might be greater than it’s been in more than 100 years.

So how do TNR opponents reconcile these findings with their claims that outdoor cats pose a grave threat to the sea otters?

They don’t, of course.

Instead, they simply ignore the research—all the while telling anybody who will listen that they have science on their side. Read more

Hawaiian Monk Seals: The Latest Excuse for Toxo Hysteria?

Hawaiian monk seal at Five Fathom Pinnacle, Hawaii. Courtesy of Wikimedia Commons and N3kt0n.

The latest “black mark against domestic cats,” explained a headline in yesterday’s Washington Post: “They’re killing Hawaii’s rare monk seals.” As is so often the case, though, in the age of click-bait journalism, the story is considerably more complicated than the misleading headline suggests. Read more

Conservation Biology, Outdoor Cats, and the Magic 8-Ball

For too many in Hawaii’s conservation community, the answer is always the same—regardless of the question being asked.

Examining the ongoing campaign to eradicate Hawaii’s outdoor cats, one soon discovers a familiar pattern: the rationale is often based on flawed science (often produced by government agencies). But, perhaps because of conservation concerns more desperate than those on the mainland, there’s an unsettling tendency to “interpret” scientific evidence in a way that will implicate cats regardless of a study’s actual results.

No matter what the research question, it seems the answer is invariably “cats.”

Witness, for example, a paper published earlier this year in the Journal of Wildlife Diseases, in which the authors suggest that outdoor cats pose a threat to Hawaii’s state bird, the Nene (or Hawaiian goose), by spreading the parasite Toxoplasma gondii. One problem: the island where the researchers found the greatest seroprevalence of T. gondii infection among the birds, Molokai, just so happens to be home to perhaps the most dramatic increase in their numbers in recent years. Read more

Toxo “Hype Train” Running Out of Steam?

Recent research is challenging the “conventional wisdom” that infection with the Toxoplasma gondii parasite can alter human behavior, lead to mental illness (especially schizophrenia). As a recent post on Discover magazine’s Neuroskeptic blog notes, “The idea of ‘behavioral’ toxoplasmosis has driven a huge amount of research and media interest.”

Of course, it’s also driven the witch-hunt against outdoor cats—used by the American Bird Conservancy and others in their ongoing campaign of misinformation and scaremongering. Read more

“The Science Points to Cats”? Not so Fast!

Mother sea otter with pup, photographed at Morro Rock, CA. Photo courtesy of Wikimedia Commons and “Mike” Michael L. Baird.

“The science points to cats,” proclaimed David Jessup (long-time opponent of TNR) and Melissa Miller in their contribution to the Spring 2011 Issue of The Wildlife Professional, in a special section called “The Impact of Free Ranging Cats” (available free via issuu.com). As I explained at the time, it wasn’t science so much as certain scientists pointing to cats as the primary cause of California sea otter mortalities associated with Toxoplasma gondii infection.

And now, a study recently published in the International Journal for Parasitology: Parasites and Wildlife goes much further in challenging the scapegoating. Read more

10 Most Important Community Cat News Stories of 2013

It’s that time of year again—time to take stock of the year’s milestones. Check out Rolling Stone’s 50 Best Albums of 2013, for example, or Fresh Air’s book, TV, movie, and music picks.

Not to be outdone, I’ve compiled a list of what I see as the year’s 10 most important community cat news stories—a number of which even the most avid readers may have missed. (Indeed, I’ve blogged about only a handful.)

Suffice it to say, others will disagree with my choices. In fact, I’d be very surprised if anybody agreed with the entire list.

That’s fine. Better than fine, actually—if it means my selections will spark a conversation, or even a debate. Maybe even inspire others to set to work on their own list for 2014.

Without further ado, then, my picks for the 10 most important community cat news stories of 2013… Read more

Free-Roaming Cats, Infectious Diseases, and the Zombie Apocalypse

A recently published paper describing free-roaming cats as “a significant public health threat” fails to deliver convincing evidence. In fact, the very work the authors cite undermines, time and time again, their claims.

“Domestic cats are a potential source of numerous infectious disease agents,” write Rick Gerhold and David Jessup, in their paper, “Zoonotic Diseases Associated with Free-Roaming Cats,” published online in July by the journal Zoonoses Public Health (and to be included in an upcoming print edition).

“However, many of these diseases are controlled in cats belonging to responsible owners through routine veterinary care, proper vaccination regimens and parasite chemotherapy. Free-roaming cats often lack the necessary preventative care to control these diseases and consequently pose a potential health threat to other domestic animals, wildlife and humans.” [1]

Just how much of a threat do these cats pose?

Gerhold and Jessup would have us believe that the risks are high and the consequences dire. A careful reading of their paper, however, reveals the authors’ tendency to cherry-pick some studies and misrepresent others. And, occasionally, simply get their facts wrong.*

All of which raises serious questions about Gerhold and Jessup’s case against free-roaming cats. Read more

HAHF-Truths, HAHF-Measures, Full Price (Part 3)

Complaining of the impacts of free-roaming cats on wildlife and the environment, along with a range of public health threats, dozens of veterinarians in Hillsborough County, Florida, have banded together to fight TNR. Evidence suggests, however, that their real concern has nothing to do with the community, native wildlife, or, indeed, with cats. What the Hillsborough Animal Health Foundation is most interested in protecting, it seems, is the business interests of its members.

In Part 3 of this five-part series, I discuss some of the science surrounding Toxoplasma gondii, and challenge HAHF’s claim that TNR increases the exposure risk for toxoplasmosis.

Cats and Toxoplasma gondii
As recently as last week, the Hillsborough Animal Health Foundation was insisting that cats are the only source of Toxoplasma gondii—essentially that without cats, there’s no toxoplasmosis. It looks like they’ve done some editing in the past few days, and the particular statement I’m recalling has been removed.

In any case, it’s not quite that simple. Read more

Tune In to Animal Wise Radio Sunday!

Tune in tomorrow to Animal Wise Radio, when I’ll be catching up with hosts Mike Fry and Beth Nelson. (It’s been more than seven months!) Among the topics up for discussion: toxoplasmosis, rabies, and typhus (oh, my!).

Listen online—and while you’re at it, why not show your support by “Liking” their Facebook page.

Toxoplasmosis Linked to Suicide Attempts?

“There’s fresh evidence that cats can be a threat to your mental health,” according to a post on yesterday’s NPR health blog, Shots. The threat, reporter Jon Hamilton explains, is not the cats themselves by the Toxoplasma gondii parasite that some cats pass in their feces.*

“A study of more than 45,000 Danish women found that those infected with [Toxoplasma gondii] were 1.5 times more likely to attempt suicide than women who weren’t infected.” [1]

“Still,” Hamilton continues, “the absolute risk of suicide remains very small. Fewer than 1,000 of the women attempted any sort of self-directed violence during the 30-year study span. And just seven committed suicide.” [1]

In fact, it may well be that T. gondii infection has no bearing on the risk of suicide at all.

As the researchers themselves point out in a paper published in this month’s issue of the Archives of General Psychiatry, “we cannot say with certainty whether the observed association between T. gondii infection and self-directed violence is causal.”

T. gondii infection is likely not a random event and it is conceivable that the results could be alternatively explained by people with psychiatric disturbances having a higher risk of becoming T. gondii infected prior to contact with the health system.” [2]

In other words, it’s possible that mental illness is a risk factor for T. gondii infection, rather than the other way around. Read more

Less Toxo, More Hype

“As human populations continue to expand farther out into natural areas,” warns The Wildlife Society in a February 17 blog post, “domesticated animals will continue to be at risk for exposure to diseases carried by their wild relatives.” Considering the domesticated animals in question are cats, the organization’s apparent concern is almost touching. Almost.

Actually, TWS is, not surprisingly, much more concerned about cats transferring disease from “their wild relatives” to humans. Results of a recent study, published a month ago in the online, open-access journal PLoS ONE, suggests TWS blogger “policyintern,” illustrate “the importance of keeping domesticated cats close to home to prevent disease transmission among cats and to humans.”

Among those diseases is one that’s been getting lots of attention recently in the mainstream media: toxoplasmosis.

And just how likely is it that your cat will give you toxoplasmosis?

Not very—at least according to this latest research. (The study also looked at bartonellosis and Feline Immunodeficiency Virus, but I’ll save those for another post.) To begin with, “feral, free ranging domestic cats were targeted in this study” [1, emphasis mine], not pets. And, despite what TWS and others would have us believe, contact with these cats is relatively uncommon.

Then there’s the unexpectedly low infection rate reported by the authors of the study: just 1 percent for domestic cats, as compared to 75 percent for pumas and 43 percent for bobcats. Based on previous studies, one would expect seroprevalence rates of 62–80 percent for feral cats. [2] (Even “owned” cats* were found to have rates of 34–36 percent. Interestingly, the highest rate of seroprevalence was found among cats living on farms: 41.9–100 percent.)

Seroprevalence, with bars representing 95 percent confidence intervals, of T. gondii IgG,** for domestic cats, bobcats, and pumas at all study locations (FR = Front Range, CO; WS = Western Slope, CO; OC = Orange County, CA; SDRC = San Diego/Riverside Counties, CA; VC = Ventura County, CA). Sample sizes are listed above columns.

This should be big news for TWS.

At the very least, the low infection rates found in feral cats—combined with the much higher rates in bobcats and pumas—raise serious questions about domestic cats’ role in environmental contamination of T. gondii. Just a year ago, an article published in a special section of The Wildlife Professional called “The Impact of Free Ranging Cats,” was unambiguous: “the science points to [domestic] cats.” [3]

“Based on proximity and sheer numbers, outdoor pet and feral domestic cats may be the most important source of T. gondii oocysts in near-shore marine waters. Mountain lions and bobcats rarely dwell near the ocean or in areas of high human population density, where sea otter infections are more common.” [3]

And, over the past several months, TWS Executive Director/CEO Michael Hutchins has used the TWS blog to hammer the point home, arguing (and twisting the facts along the way), for example, that a 2011 NIH study provided “further evidence that feral cats are a menace to our native wildlife and should be controlled.

In July, it was the grave threat to humans:

T. gondii infection has recently been correlated with the incidence of Parkinson’s disease, autism, and schizophrenia in humans, and it has long been known to cause fetal deformities and spontaneous abortions in pregnant women… Let’s hope that public health officials, including the CDC, begin to take note of these growing concerns about cats and their implications for human health.”

In fact, this latest study suggests that such concerns may not be growing at all, at least where toxoplasmosis is concerned. On the other hand, the simpler, scarier story—cats as a menace to both wildlife and humans—is certainly an easier sell for TWS.

* I assume this refers to indoor/outdoor cats, but have not chased down the individual studies to confirm this.

** Refers to immunoglobulin, or antibody, G (IgG), “which is detectable for ≥52 weeks after infection,” as compared to immunoglobulin M (IgM), “which indicates recent infections and is usually detectable ≤16 weeks after initial exposure.” [1]

Literature Cited
1. Bevins, S.N., et al., “Three Pathogens in Sympatric Populations of Pumas, Bobcats, and Domestic Cats: Implications for Infectious Disease Transmission.” PLoS ONE. 2012. 7(2): p. e31403. http://dx.doi.org/10.1371%2Fjournal.pone.0031403

2. Dubey, J.P. and Jones, J.L., “Toxoplasma gondii infection in humans and animals in the United States.” International Journal for Parasitology. 2008. 38(11): p. 1257–1278. http://www.sciencedirect.com/science/article/B6T7F-4S85DPK-1/2/2a1f9e590e7c7ec35d1072e06b2fa99d

3. Jessup, D.A. and Miller, M.A., “The Trickle-Down Effect.” The Wildlife Professional. 2011. 5(1): p. 62–64.

Crazy Is As Crazy Does

An article in The Atlantic describes fascinating research into the effects of Toxoplasma gondii infection, but what role do domestic cats really play?

Although we’re not even halfway through February, an article in the March issue of The Atlantic is already getting a lot of attention. But with a title like “How Your Cat Is Making You Crazy,” that’s no surprise. (Don’t get me wrong: the article is a great read.)

What is surprising is that the story hasn’t been picked up by the American Bird Conservancy or, more likely, The Wildlife Society.

Not yet, anyhow. Surely, it’s only a matter of days before ABC, TWS, and others (mis)use the article to stir up their witch-hunt against free-roaming cats. A careful read, however, suggests such a move would be both premature and misguided (as if that makes any difference).

Excerpts
At the center of “How Your Cat Is Making You Crazy” is the intriguing research* of Jaroslav Flegr, an evolutionary biologist at Charles University in Prague, who’s spent the past 20 years or so exploring the possible connections between infection with Toxoplasma gondii, a parasite cats can pass in their feces, and human behavior.

“Healthy children and adults,” explains writer Kathleen McAuliffe, “usually experience nothing worse than brief flu-like symptoms before quickly fighting off the protozoan, which thereafter lies dormant inside brain cells—or at least that’s the standard medical wisdom.”

But if Flegr is right, the ‘latent’ parasite may be quietly tweaking the connections between our neurons, changing our response to frightening situations, our trust in others, how outgoing we are, and even our preference for certain scents. And that’s not all. He also believes that the organism contributes to car crashes, suicides, and mental disorders such as schizophrenia.

As I say, it’s just a matter of time—and not much of it, I suspect—before TNR opponents jump all over this, shaping it to fit their (tired) message.

I expect to see the lengthy quote from Joanne Webster, a parasitologist at Imperial College London, parsed very carefully, for example. Webster and her colleagues discovered that Toxo-infected rats are actually attracted to cat urine, a phenomenon they dubbed “fatal feline attraction.” Commenting on Flegr’s research, Webster is, in McAuliffe’s words, “more circumspect, if not downright troubled.”

I don’t want to cause any panic. In the vast majority of people, there will be no ill effects, and those who are affected will mostly demonstrate subtle shifts of behavior. But in a small number of cases, [Toxo infection] may be linked to schizophrenia and other disturbances associated with altered dopamine levels—for example, obsessive-compulsive disorder, attention-deficit hyperactivity disorder, and mood disorders. The rat may live two or three years, while humans can be infected for many decades, which is why we may be seeing these severe side effects in people. We should be cautious of dismissing such a prevalent parasite.

I imagine those first two sentences will be among the first to be dropped from any ABC or TWS reference to the article. As will this response from Robert Sapolsky, a professor of biology and neurology at Stanford:

…I’m not too worried, in that the effects on humans are not gigantic. If you want to reduce serious car accidents, and you had to choose between curing people of Toxo infections versus getting people not to drive drunk or while texting, go for the latter in terms of impact.

Infection in Humans
“Humans,” explains McAuliffe, “are exposed not only by coming into contact with litter boxes, but also, he found, by drinking water contaminated with cat feces, eating unwashed vegetables, or, especially in Europe, by consuming raw or undercooked meat. According to the Centers for Disease Control and Prevention, the infection rate in the U.S. among those 12 and older is estimated to be 22.5 percent.

And while Toxoplasmosis “can come from cats,” the CDC points out that “people are more likely to get it from eating raw meat or from gardening.”

Nowhere in McAuliffe’s article does she mention the proportion of people infected through contact with cat feces, as compared to those infected from eating raw or undercooked meat. For the purposes of Flegr’s work, the source is largely immaterial. (And, virtually impossible to know, I gather—which would explain why I’ve never seen so much a guess.)

Infection in Cats
In the infamous “University of Nebraska-Lincoln paper,” published in 2010, the authors report—correctly, according to their source—that “most feral cats (62 percent to 80 percent) tested positive for toxoplasmosis.” [1] Trouble is, testing positive—seroprevalence—is simply not a useful measure of their ability to infect other animals or people.

“Most cats only shed oocysts for about one week in their life” (Note: The Atlantic suggests a three-week duration, as noted below) and seroconvert afterward. [2] “Thus, it is a reasonable assumption that most seropositive cats have already shed oocysts.” [2] “Testing positive,” in this case, is nothing more than the detection of antibodies resulting from seroconversion. Furthermore, because “most seronegative cats shed millions of oocysts after exposure to T. gondii… seropositive cats are likely to be less of a public health risk than seronegative cats.” [3]

Environmental Contamination
Because Flegr’s work doesn’t involve environmental contamination, McAuliffe only touched on the subject (“the parasite is typically picked up from the soil by scavenging or grazing animals—notably rodents, pigs, and cattle…”). For many TNR opponents, however, this is a hot topic—as some have suggested a direct connection between the presence of domestic cats and toxo-related infections in other animals, primarily land and marine mammals. (See, for example, my post from May 17 of last year.)

As a recent paper reports, bluntly: “Cats are the definitive host: the disease only occurs when cats are present.” [4] In fact, this claim is contradicted by a number of studies:

  • High levels (75 percent) of congenital transmission of T. gondii, for example, in a “wild population of mice,” led UK researchers to conclude “that this phenomenon might be more widespread than previously thought.” [5] Infections in sheep also point to congenital transmission, which “may be more important than previously considered.” [6]
  • The “high incidence of T. gondii found, among others, in free-living ruminants suggests a possibility of other, so far unknown, paths of transmission of this protozoan.” [7] “Due to the fact that they are widespread, and tick-bites occur frequently both in humans and in animals, ticks might play an important role in toxoplasmosis transmission.” [7]
  • Of particular interest are studies in the Arctic, where the prevalence of T. gondii infection in arctic foxes, Svalbard reindeer, sibling voles, walruses, kittiwakes, barnacle geese, and glaucous gulls “indicates that infection by oocysts is not an important mode of transmission on Svalbard.” [8] “T. gondii most likely is brought to Svalbard by migratory birds that become infected in temperate agricultural areas in the winter. However, marine sources of infection may exist. The high seroprevalence of T. gondii in the arctic fox population on Svalbard may be due to: (1) infection from migratory bird species through predation; (2) vertical transmission; and (3) tissue cyst transmission within the Svalbard ecosystem through scavenging and cannibalism. Together, these transmission routes cause a surprisingly high seroprevalence of T. gondii in a top predator living in an ecosystem with very few cats.” [8] Researchers studying infection rates in polar bears concluded: “It would… be inconceivable to assume that the few cats would play a major role in the epidemiology of T. gondii in the vast high Arctic. This is apparently the case in East Greenland as well.” [9]

In the Spring 2011 issue of The Wildlife Professional’s special section, “The Impact of Free Ranging Cats,” the authors argue: “Based on proximity and sheer numbers, outdoor pet and feral domestic cats may be the most important source of T. gondii oocysts in near-shore marine waters. Mountain lions and bobcats rarely dwell near the ocean or in areas of high human population density, where sea otter infections are more common.” [10] What the fail to acknowledge is that the most common type of T. gondii found to be infecting sea otters is the Type X strain, [11] which has yet to be traced to domestic cats, [12] or that “dual infections of T. gondii and S. neurona were more frequently associated with mortality and protozoal encephalitis than single infections, indicating a role for polyparasitism in disease severity.” [13]

Now What?
So, what are we to make of all this?

Or, as McAuliffe poses the question: “Given all the nasty science swirling around this parasite, is it time for cat lovers to switch their allegiance to other animals?”

Even Flegr would advise against that. Indoor cats pose no threat, he says, because they don’t carry the parasite. As for outdoor cats, they shed the parasite for only three weeks of their life, typically when they’re young and have just begun hunting. During that brief period, Flegr simply recommends taking care to keep kitchen counters and tables wiped clean. (He practices what he preaches: he and his wife have two school-age children, and two outdoor cats that have free roam of their home.)

Certainly, there’s still plenty we don’t know about T. gondii. A May 2011 article in Scientific American, for example, concedes simply: “The exact link between T. gondii and psychiatric diseases is tantalizing but remains murky.” [14]

Most telling of all may be the reaction of the pharmaceutical industry. Or, lack of a reaction, to be more precise. “Until solid proof exists that Toxo is as dangerous as some scientists now fear,” observes McAuliffe, “pharmaceutical companies don’t have much incentive to develop anti-Toxo drugs.” And if Big Pharma doesn’t think there’s money to be made here, how worried should we really be?

•     •     •

If history is any indication, “How Your Cat Is Making You Crazy” will be badly misrepresented by some TNR opponents, used to further vilify free-roaming cats as a public health threat. Not that they’ll offer anything in the way of a solution, of course—just more fear-mongering.

Now, if ABC, TWS, and all the rest are really concerned about toxo, why not propose a meat-free diet? OK, now that’s crazy.

*As opposed to, say, the unconvincing claims attempting to link T. gondii to brain cancer, published in a paper last summer. As expected, TWS took the bait.

Literature Cited
1. Hildreth, A.M., Vantassel, S.M., and Hygnstrom, S.E., Feral Cats and Their Management. 2010, University of Nebraska-Lincoln Extension: Lincoln, NE. elkhorn.unl.edu/epublic/live/ec1781/build/ec1781.pdf

2. Dubey, J.P. and Jones, J.L., “Toxoplasma gondii infection in humans and animals in the United States.” International Journal for Parasitology. 2008. 38(11): p. 1257–1278. http://www.sciencedirect.com/science/article/B6T7F-4S85DPK-1/2/2a1f9e590e7c7ec35d1072e06b2fa99d

3. Vollaire, M.R., Radecki, S.V., and Lappin, M.R., “Seroprevalence of Toxoplasma gondii antibodies in clinically ill cats in the United States.” American Journal of Veterinary Research. 2005. 66(5): p. 874–877. http://dx.doi.org/10.2460/ajvr.2005.66.874

4. Duffy, D.C. and Capece, P., “Biology and Impacts of Pacific Island Invasive Species 7. The Domestic Cat (Felis catus).” Pacific Science. 2011. 66(2 (Early View)): p. 000–000. http://pacificscience.files.wordpress.com/2011/09/pac-sci-early-view-66-2-6.pdf

5. Marshall, P.A., et al., “Detection of high levels of congenital transmission of Toxoplasma gondii in natural urban populations of Mus domesticus.” Parasitology. 2004. 128(01): p. 39–42. http://dx.doi.org/10.1017/S0031182003004189

6. Hide, G., et al., “Evidence for high levels of vertical transmission in Toxoplasma gondii.” Parasitology. 2009. 136(Special Issue 14): p. 1877-1885. http://dx.doi.org/10.1017/S0031182009990941

7. Sroka, J., Szymańska, J., and Wójcik-Fatla, A., “The occurrence of Toxoplasma gondii and Borrelia burgdorferi sensu lato in Ixodes ricinus ticks from eastern Poland with the use of PCR.” Annals of Agricultural and Environmental Medicine. 2009. 16(2): p. 313–319.

8. Prestrud, K.W., et al., “Serosurvey for Toxoplasma gondii in arctic foxes and possible sources of infection in the high Arctic of Svalbard.” Veterinary Parasitology. 2007. 150(1–2): p. 6–12. http://www.sciencedirect.com/science/article/B6TD7-4PYR4P2-2/2/fcc91fcf1d1426cd1b750bd3840bdb31

9. Oksanen, A., et al., “Prevalence of Antibodies Against Toxoplasma gondii in Polar Bears (Ursus maritimus) From Svalbard and East Greenland.” Journal of Parasitology. 2009. 95(1): p. 89–94. http://dx.doi.org/10.1645/GE-1590.1

10. Jessup, D.A. and Miller, M.A., “The Trickle-Down Effect.” The Wildlife Professional. 2011. 5(1): p. 62–64.

11. Conrad, P.A., et al., “Transmission of Toxoplasma: Clues from the study of sea otters as sentinels of Toxoplasma gondii flow into the marine environment.” International Journal for Parasitology. 2005. 35(11-12): p. 1155-1168. http://www.sciencedirect.com/science/article/B6T7F-4GWC8KV-2/2/2845abdbb0fd82c37b952f18ce9d0a5f

12. Miller, M.A., et al., “Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores from coastal California: New linkages between terrestrial mammals, runoff and toxoplasmosis of sea otters.” International Journal for Parasitology. 2008. 38(11): p. 1319-1328. http://www.sciencedirect.com/science/article/B6T7F-4RXJYTT-2/2/32d387fa3048882d7bd91083e7566117

13. Gibson, A.K., et al., “Polyparasitism Is Associated with Increased Disease Severity in Toxoplasma gondii-Infected Marine Sentinel Species.” PLoS Neglected Tropical Diseases. 2011. 5(5): p. e1142. http://dx.doi.org/10.1371%2Fjournal.pntd.0001142

14. Koch, C., “Protozoa Could Be Controlling Your Brain.” Scientific American. 2011. http://www.scientificamerican.com/article.cfm?id=fatal-attraction

More Cats, Less Brain Cancer

“Evidence continues to pile up,” writes Michael Hutchins, Executive Director and CEO of The Wildlife Society, in yesterday’s blog post, “that Toxoplasmosis, a disease caused by a parasite (Toxoplasma gondii) that lives in the guts of cats, may be responsible for serious human health problems.”

Hutchins was referring to a recent study in which researchers found “Infection with T. gondii was associated with a 1.8-fold increase in the risk of brain cancers across the range of T. gondii prevalence in our dataset (4–67 percent).” [1]

True to form, Hutchins used the opportunity to call for “doing away with managed cat colonies and TNR (trap-neuter-release) management practices for feral cats,” making a public plea to “public health officials, including the CDC.”

But what exactly does this latest study contribute to Hutchins’ “pile of evidence”?

The Study
According to a news release from the U.S. Geological Survey, “the study analyzed 37 countries for several population factors” and “showed that countries where Toxoplasma gondii is common also had higher incidences of adult brain cancers than in those countries where the organism is not common.”

“The study does not prove that Toxoplasma gondii directly causes cancer in humans, and the study does not imply that an infected person automatically has high cancer risk,” says [Kevin] Lafferty, who is based at the USGS Western Ecological Research Center. “However, we do know that Toxoplasma gondii behaves in ways that could stimulate cells towards cancerous states, so the discovery of this correlation offers a new hypothesis for an infectious link to cancer.”

According to the study’s abstract (I’ve been unable to access the paper), the authors took into account several factors:

“We corrected reports of incidence for national gross domestic product because wealth probably increases the ability to detect cancer. We also included gender, cell phone use and latitude as variables in our initial models. Prevalence of T. gondii explained 19 per cent of the residual variance in brain cancer incidence after controlling for the positive effects of gross domestic product and latitude among nations.” [1]

It will be interesting to compare—once I’m able to review the study in detail—these findings with those published earlier this year in the Journal of the National Cancer Institute (a collaborative effort involving several agencies, including, as it happens, the CDC):

“The relatively low variation in incidence and death rates for cancer of the brain and [other nervous system] nationally and internationally suggests that environmental risk factors do not play a major role in this disease. In fact, other than hereditary tumor syndromes and increased familial risk without a known syndrome, the only known modifiable causal risk factor for brain tumors is exposure to ionizing radiation.” [2, in-line citations removed for readability]

Correlation ≠ Causation
To illustrate the critical difference between correlation and causation, author Charles Seife uses the dramatic example of the mid-1990s NutraSweet scare—which, incredibly, was also linked brain cancer (falsely, as it turns out).

“Lots of people… don’t eat foods that contain the artificial sweetener NutraSweet for fear of developing brain cancer,” writes Seife, tracing the mythical connection to “a bunch of psychiatrists led by Washington University’s John Olney.”

“These scientists noticed that there was an alarming rise in brain tumor rates about three or four years after NutraSweet was introduced in the market.

Aha! The psychiatrists quickly came to the obvious conclusion: NutraSweet is causing brain cancer! They published their findings in a peer-reviewed journal, the Journal of Neuropathology and Experimental Neurology, and their paper immediately grabbed headlines around the world.

But a closer look at the data shows how unconvincing the link really is. Sure, NutraSweet consumption was going up at the same time brain tumor rates were, but a lot of other things were on the rise, too, such as cable TV, Sony Walkmen, Tom Cruise’s career. When Ronald Reagan took office in 1981, government spending increased just as dramatically as brain tumor rates… The correlation between government overspending and brain cancer is just as solid as the link between NutraSweet and brain cancer.” [3]

Sounds eerily familiar, doesn’t it?

Given the numerous factors and interrelationships involved in developing brain cancer—some of which, of course, we don’t even know—Hutchins’ eager indictment of cats is, at the very least, premature. In fact, Hutchins is going to have a difficult time connecting the dots in light of recent research.

More Cats, Less Brain Cancer
If brain cancer is more common where T. gondii is more common, then one might expect rates of brain cancer to increase over time as the prevalence of T. gondii increases. Which would seem to be the case here in the U.S., if cats are indeed the culprit.

According to data compiled last year in Conservation Biology, the population of pet cats tripled over the past 40 years, from approximately 31 million in 1971 to more than 90 million today. [4]

So what about brain cancer?

In 2006, researchers using data from the Surveillance, Epidemiology, and End Results Program for 1973–2001 were surprised to find incident rates decreasing. Following an increase of 1.68 percent between 1973 and 1987, the incident rate began to drop off by 0.44 percent annually (as indicated in the chart below; EAPC = estimated annual percentage of change).

“The cause for this decline,” suggest the study’s authors, “is unclear because of the paucity of definitive knowledge on the risk factors of brain cancer, but solace can be taken from the fact that brain cancers are not rising in this era of increasing environmental toxic exposures.” [5]

More recently, a report published by the Central Brain Tumor Registry of the United States (PDF) found “no statistically significant trend in incidence rates of all primary brain tumors from 2004 through 2007.” [6]

•     •     •

Lafferty and his colleagues concede that their work is “correlational,” a jumping-off point for further investigation. Again, I haven’t been able to read the paper yet, but I’m skeptical that their line of inquiry is headed anywhere productive. Cast a net as wide as they did—surveying the prevalence of T. gondii and incidence of brain cancer across 37 countries—and you’re bound to catch something.

Of course, something is all Michael Hutchins needs for his witch-hunt.

Hutchins refers to piles of evidence without taking the trouble to examine any of it, simply ignoring what doesn’t fit neatly into his narrative—declining brain cancer rates in the U.S., for example. Or, some rather interesting comments from Lafferty himself (which, strangely, were omitted from USGS’s news release, but were mentioned by several other news outlets, including LiveScience and Fox News):

“…one shouldn’t be panicking about owning cats… The risk factors for getting Toxoplasma are really hygiene and eating undercooked meat. One should be more concerned about those than pets.”

That sounds familiar, too. It’s the same advice the CDC provides on its Website.

Literature Cited
1. Thomas, F., et al., “Incidence of adult brain cancers is higher in countries where the protozoan parasite Toxoplasma gondii is common.” Biology Letters. 2011.

2. Kohler, B.A., et al., “Annual Report to the Nation on the Status of Cancer, 1975, Featuring Tumors of the Brain and Other Nervous System.” Journal of the National Cancer Institute. 2011. http://jnci.oxfordjournals.org/content/early/2011/03/31/jnci.djr077.abstract

3. Seife, C., Proofiness: The Dark Arts of Mathematical Deception. 2010: Viking Adult.

4. Lepczyk, C.A., et al., “What Conservation Biologists Can Do to Counter Trap-Neuter-Return: Response to Longcore et al.” Conservation Biology. 2010. 24(2): p. 627–629. www.abcbirds.org/abcprograms/policy/cats/pdf/Lepczyk-2010-Conservation%2520Biology.pdf

5. Deorah, S., et al., “Trends in brain cancer incidence and survival in the United States: Surveillance, Epidemiology, and End Results Program, 1973 to 2001.” Neurological Focus. 2006. 20(April): p. E1. thejns.org/doi/pdf/10.3171/foc.2006.20.4.E1

6. n.a., CBTRUS Statistical Report: Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2004-2007. 2011, Central Brain Tumor Registry of the United States: Hinsdale, IL. www.cbtrus.org/2011-NPCR-SEER/WEB-0407-Report-3-3-2011.pdf

Loose Threads

OpossumNorth American Opossum with winter coat. Photo courtesy of Wikimedia Commons and Cody Pope.

A study published last month in the online open-access journal PLoS Neglected Tropical Diseases suggests a new twist in the relationship between free-roaming cats, Toxoplasma gondii, and toxoplasmosis infections in marine mammals.

“The most remarkable finding of our study,” notes co-author Dr. Michael E. Grigg in a press release from the National Institutes of Health “was the exacerbating role that [Sarcocystis] neurona appears to play in causing more severe disease symptoms in those animals that are also infected with T. gondii.” What I found most remarkable, though, was the straightforward relationship between infections in land mammals and infected marine mammals implied in Grigg’s comments:

“Identifying the threads that connect these parasites from wild and domestic land animals to marine mammals helps us to see ways that those threads might be cut… by, for example, managing feral cat and opossum populations, reducing run-off from urban areas near the coast, monitoring water quality and controlling erosion to prevent parasites from entering the marine food chain.”

The Wildlife Society’s Michael Hutchins used the opportunity to once again call for the “control” of feral cats, which, he argues are “a menace to our native wildlife.” According to Hutchins, the study by Grigg (who serves as Chief of the National Institute of Allergy and Infectious Diseases’ Molecular Parasitology Unit) and his colleagues “is yet another demonstration that Trap-Neuter-Release (TNR) management of feral house cats must be stopped if we value our native wildlife.”

But, of course, the threads that make up the ecological “fabric” are interwoven with many others. Cut even one of them, as Grigg suggests, and the whole thing can begin to unravel.

Which is what surprised me about Grigg’s narrow focus on cats (considered the definitive host for T. gondii) and opossums (considered the definitive host of S. neurona), neither of which was mentioned in the paper itself.

Toxoplasma gondii
Cats pass the mature, infective form of T. gondii in their feces—a process called “shedding oocysts.” T. gondii infection, or toxoplasmosis, in humans can be traced to “ingestion of oocyst-contaminated soil and water, from tissue cysts in undercooked meat, by transplantation, blood transfusion, laboratory accidents, or congenitally.” [1]

Numerous studies have suggested a link between toxoplasmosis in marine life and freshwater run-off. In contrast to the “stress placed on the importance of the cat in the scientific literature,” [2] however, several studies have challenged the importance of environmental contamination in the transmission of T. gondii.

In the Absence of Cats
Researchers at the University of Salford’s Centre for Parasitology and Disease Research, for instance, observed high levels (e.g., 75 percent) of congenital transmission of T. gondii in a “wild population of mice,” leading them to conclude “that this phenomenon might be more widespread than previously thought.” [2] Another team of researchers from the same lab, citing studies of T. gondii infections in sheep, also make a compelling argument that congenital transmission “may be more important than previously considered.” [3]

And then there are the studies in the Arctic.

Among the “arctic foxes (n=594), Svalbard reindeer (n=390), sibling voles (n=361), walruses (n=17), kittiwakes (n=58), barnacle geese (n=149), and glaucous gulls (n=27),” tested, Prestrud et al. found T. gondii only in the arctic foxes (257, or 43 percent), geese (11, or 7 percent), and walruses (1, or 6 percent). [4] The fact that these researchers found no T. gondii-infected reindeer or sibling voles “indicates that infection by oocysts is not an important mode of transmission on Svalbard.” [4] In the end, Prestrud et al. suggest:

“…T. gondii most likely is brought to Svalbard by migratory birds that become infected in temperate agricultural areas in the winter. However, marine sources of infection may exist. The high seroprevalence of T. gondii in the arctic fox population on Svalbard may be due to: (1) infection from migratory bird species through predation; (2) vertical transmission; and (3) tissue cyst transmission within the Svalbard ecosystem through scavenging and cannibalism. Together, these transmission routes cause a surprisingly high seroprevalence of T. gondii in a top predator living in an ecosystem with very few cats.” [4]

A study of polar bears provides further evidence: “It would… be inconceivable to assume that the few cats would play a major role in the epidemiology of T. gondii in the vast high Arctic. This is apparently the case in East Greenland as well.” [5]

Ticks and Tick-bites
In a paper published in 2009, Polish researchers proposed yet another possibility. The “high incidence of T. gondii found, among others, in free-living ruminants,” write Sroka et al., “suggests a possibility of other, so far unknown, paths of transmission of this protozoan.”

“Due to the fact that they are widespread, and tick-bites occur frequently both in humans and in animals, ticks might play an important role in toxoplasmosis transmission.” [6]

Sarcocystis neurona and Opossums
The links between opossums and S. neurona infections, too, are not quite as straightforward as Grigg’s comment suggests. Researchers were surprised to find S. neurona in central Wyoming, for example—“outside the known range of the opossum.” [7]

“Finding antibodies to S. neurona… in at least 18 horses native to Wyoming is unexpected and unexplained. Opossums are not known to occur in central Wyoming, and there has not been any confirmed case of [equine protozoal myeloencephalitis] from horses native to Wyoming.” [7]

Their findings, write Dubey et al., “suggest that another definitive host may be involved or that the parasite shares antigens with another protozoan.” [7]

Conspicuously Absent
Grigg and his colleagues make no reference to these studies, nor do they acknowledge the alternative transmission routes suggested therein. To be clear, though, the paper focuses mostly on infection rates; it’s the press release that refers to cats and opossums as the ultimate source of infection.

(If all of this sounds familiar, it may be because I referred to many of the same studies in my response last month to a press release about a study of T. gondii-infected mammals in a “natural area in central Illinois” by Shannon Fredebaugh and Nohra Mateus-Pinilla.)

Stray Threads
Grigg and his colleagues found infection rates among mammals living in the inland waters of Washington, Oregon, and southern British Columbia were no greater than in those found along the outer coast, as illustrated in the figure below (blue dots indicating inland infection, red dots indicating infection among outer coast individuals).

But if environmental contamination plays such a critical role, shouldn’t that be reflected in higher infection rates inland (nearer, presumably, to greater concentrations of contaminated soil)?

Perhaps the most puzzling of their findings, though, is this: “T. gondii infections peaked in 2007 then declined relative to S. neurona” (as illustrated in the bar chart below).

Again, if environmental contamination is the culprit, does this mean that the population of free-roaming cats in the area also peaked around 2007? Could this, in fact, be empirical evidence of the positive impact of TNR? (At last, something for Hutchins to blog about!)

Obviously, there’s not enough evidence here to make that leap. Still, the data challenge assertions by the American Bird Conservancy that the feral cat population continues to rise—as well as the conventional wisdom about the presumed cause of T. Gondii-infected marine mammals, articulated most recently by David Jessup and Melissa Miller: “the science points to cats.” [8]

And finally, let’s say we were able to remove all of the cats and opossums from the environment. Setting aside for the moment the numerous hurdles (e.g., ethical, economic, etc.) involved, what impact could we expect in terms of T. gondii and/or S. neurona infections in marine mammals? Or in rodents, whose populations would surely skyrocket?

I’m skeptical that the benefits would be all that great. Skeptical, too, that we could predict with much accuracy the actual outcomes (to say nothing of the unintended consequences).

As for what Grigg thinks, he’s yet to respond to my e-mail inquiries on the subject.

Literature Cited
1. Elmore, S.A., et al., “Toxoplasma gondii: epidemiology, feline clinical aspects, and prevention.” Trends in Parasitology. 2010. 26(4): p. 190–196. http://www.sciencedirect.com/science/article/B6W7G-4YHFWNM-1/2/2a468a936eb06649fde0463deae4e92f

2. Marshall, P.A., et al., “Detection of high levels of congenital transmission of Toxoplasma gondii in natural urban populations of Mus domesticus.” Parasitology. 2004. 128(01): p. 39–42. http://dx.doi.org/10.1017/S0031182003004189

3. Hide, G., et al., “Evidence for high levels of vertical transmission in Toxoplasma gondii.” Parasitology. 2009. 136(Special Issue 14): p. 1877-1885. http://dx.doi.org/10.1017/S0031182009990941

4. Prestrud, K.W., et al., “Serosurvey for Toxoplasma gondii in arctic foxes and possible sources of infection in the high Arctic of Svalbard.” Veterinary Parasitology. 2007. 150(1-2): p. 6–12. http://www.sciencedirect.com/science/article/B6TD7-4PYR4P2-2/2/fcc91fcf1d1426cd1b750bd3840bdb31

5. Oksanen, A., et al., “Prevalence of Antibodies Against Toxoplasma gondii in Polar Bears (Ursus maritimus) From Svalbard and East Greenland.” Journal of Parasitology. 2009. 95(1): p. 89–94. http://dx.doi.org/10.1645/GE-1590.1

6. Sroka, J., Szymańska, J., and Wójcik-Fatla, A., “The occurrence of Toxoplasma gondii and Borrelia burgdorferi sensu lato in Ixodes ricinus ticks from eastern Poland with the use of PCR.” Annals of Agricultural and Environmental Medicine. 2009. 16(2): p. 313–319.

7. Dubey, J.P., et al., “Prevalence of Antibodies to Neospora caninum, Sarcocystis neurona, and Toxoplasma gondii in Wild Horses from Central Wyoming.” Journal of Parasitology. 2003. 89(4): p. 716–720. http://dx.doi.org/10.1645/GE-66R

8. Jessup, D.A. and Miller, M.A., “The Trickle-Down Effect.” The Wildlife Professional. 2011. 5(1): p. 62–64.

Close Enough?

Among the findings of a recent study:

Five of 18 cats trapped “between the spring and fall of 2008 and 2009” in central Illinois’ 1,500-acre Robert Allerton Park tested positive for Toxoplasma gondii antibodies. Five of the seropositive cats were trapped at the same site; there, one white-footed mouse (of 21 trapped) also tested positive, and a gray squirrel tested negative. The site where the sixth seropositive cat was trapped revealed similar results among the “small home range” (SHR) mammals found there: one of 34 white-footed mice was seropositive; a fox squirrel was negative.

All of which means… what, exactly?

Although there were five times as many “infected” cats at the first site, infection rates among SHR mammals were only about one-and-a-half times as high as those at the second site. Put another way: given the infection rate among SHR mammals at the second site, one would have expected three seropositive SHR mammals at the first site.

In fact, a press release put out last week put a very different spin on Shannon Fredebaugh’s thesis work (downloadable PDF):

One third of the cats sampled were infected with T gondii, as were significant numbers of the wild animals found at every site. Animals that inhabit or range over territories of 247 acres (100 hectares) or more, such as raccoons and opossums, were more likely to be infected than those with smaller ranges.

But these animals “could have acquired T. gondii infection somewhere outside of the park,” said Nohra Mateus-Pinilla, a wildlife veterinary epidemiologist at the University of Illinois Prairie Research Institute and leader of the study. Animals with smaller home ranges likely picked up the infection close to where they were trapped, she said. This makes these animals good sentinels of disease in a natural area. “The small animals are screening the environment for us,” she said. “So when we sample one of those animals, we are really sampling their lifestyle.”

The absence of bobcats in the park combined with the occurrence of domestic cats and T. gondii infection in wildlife that inhabit small territories strongly suggest that feral, free-ranging or abandoned house cats are the source of the infection, Mateus-Pinilla said. Cats are vital for the survival of the parasite, and so they are—either directly or indirectly—spreading T. gondii to the wildlife in the park. “There’s no other option,” she said.

Well, “one third of the cats” certainly sounds more impressive than “six of 18.” And “significant numbers of the wild animals found at every site” had an undeniable allure to it—though, in fact, the statement applies only to the park’s “large home range” (LHR) mammals (mostly raccoons and opossums).

Far more troubling, though, is the alleged connection between cats, T. gondii, and infected SHR mammals.

Environmental Contamination
“If one infected cat defecates there, any area can become infected,” Fredebaugh said in the press release. “It just takes one cat to bring disease to an area.”

But, as Fredebaugh points out, “environmental detection of oocysts is difficult and was not evaluated in this study.” [1] She simply assumes a causal link between “infected” cats and environmental contamination: more seropositive cats means more contaminated soil.

In fact, Fredebaugh goes further, assuming that the mere presence of cats—seropositive or not—is the key factor in SHR infection rates. In addition to trapping data, she uses data from scent stations and motion detection cameras (which proved largely ineffective, capturing photos of just four cats over the course of the research) to designate each of the eight sites as either high or low “cat occurrence,” as indicated in the following table (please forgive the tiny type):

Table: Shannon Fredebaugh's Thesis

Fredebaugh acknowledges that “scent stations should only be used to identify trends in animal populations and as a supplemental tool in conjunction with other population estimates,” [1] thereby raising serious questions about their use in her study. (She’s not interested in trends, her scent station and trapping data correlate quite poorly, and her use of scent station data is hardly “supplemental.”)

But back to the environmental contamination.

Cats (both domestic and wild) are T. gondii’s definitive host—the animal in which the parasite reproduces sexually. Cats pass the mature, infective form of T. gondii in their feces—a process called “shedding oocysts.”

Although oocysts can survive in soil for up to 18 months, and are resistant to disinfectants, cats typically “shed oocysts only once in their life.” [see discussion in 2] Indeed, according to Dubey and Jones, “Most cats seroconvert after they have shed oocysts. Thus, it is a reasonable assumption that most seropositive cats have already shed oocysts.” [2]

So, who’s to say that the “infected” cats Fredebaugh trapped shed oocysts in the area where they were found? Indeed, we don’t even know that these cats shed oocysts in the park. It’s been suggested (based on a small sample of cats monitored closely from 1974 to 1977) that home ranges of unsterilized feral females can exceed 500 acres, while those of unsterilized feral males may approach 2,500 acres. (Even house-based males, which were also unsterilized, had large home ranges: 865–939 acres.) [3]

What’s more, Fredebaugh points out that, given their “relatively good physical condition,” some of these cats might have been “recently abandoned at RAP.” [1] In which case, they wouldn’t have been “contributing” any oocysts to the park’s soil—assuming they were seropositive to begin with.

Odds Ratios
Fredebaugh expresses her results using odds ratios, a measure easy enough to calculate but rather difficult to grasp intuitively (especially for those of us, myself included, unfamiliar with the measure). A page on the Children’s Mercy Hospital (Kansas City, MO) Website explains odd ratios this way:

“An odds ratio of 1 implies that the event is equally likely in both groups. An odds ratio greater than one implies that the event is more likely in the first group. An odds ratio less than one implies that the event is less likely in the first group.”

(Some examples are discussed in detail here.)

It seems to me that, in this case at least, odds ratios obscure more than they reveal. When Fredebaugh reports “a significant difference in the seroprevalence of T. gondii for SHR mammals at sites with a high frequency of cat occurrence,” we know nothing of sample size or the overall fit of the data (which, ranges from pretty good—for LHR mammals—to pretty lousy—for SHR mammals).

A simple x-y graph illustrates this point:

Chart: Shannon Fredebaugh's Thesis

By (mis?)representing the data in odds ratios, Fredebaugh suggests a connection that’s not actually supported by her research findings.

That said, she’s is hardly the first to imply causation where nothing more than correlation has been demonstrated (and, again, even that is dicey). In “The Impact of Free Ranging Cats,” a special section of the Spring Issue of The Wildlife Professional, for example, David Jessup and Melissa Miller argue that “the science points to cats,” but provide little more than “proximity” and “sheer numbers” to support their claim that “outdoor pet and feral domestic cats may be the most important source of T. gondii oocysts in near-shore marine waters.” [4]

(No?) Other Options
The fact that the researchers are so certain of their conclusions—that the only explanation for T. gondii in Robert Allerton Park is the presence of cats—is telling. I can’t help but think that they knew going in what they would find (a perception reinforced by what’s included in, and omitted from, Fredebaugh’s literature review, as described below).

In fact, Mateus-Pinilla’s comment—“There’s no other option.”—is challenged by several recent studies.

“Among white-footed mice,” writes Fredebaugh, “I found a 6 percent seroprevalence of T. gondii antibodies, which was high, compared to other studies… Mice have a short life span, thus the findings that mice, including some juveniles, were seropositive implies an active infection and recent T. gondii contamination in RAP.” [1]

Actually, researchers at the University of Salford’s Centre for Parasitology and Disease Research found an overall prevalence of 59 percent among the “200 mice… trapped from within houses in the Cheetham Hill area of Manchester.” [5] More important, they observed “high levels of congenital transmission… with 75 percent of female mice transmitting parasites to foetuses prior to birth” (emphasis added), leading them to conclude:

“These high levels of congenital transmission in this wild population of mice, taken together with other recent data on congenital transmission in sheep, suggests that this phenomenon might be more widespread than previously thought.” [5]

Fredebaugh, by contrast, mentions congenital transmission only in passing.

In another paper, researchers from the Centre for Parasitology and Disease Research challenge the conventional wisdom surrounding the transmission of T. gondii (note: I’ve removed several in-text citations for the sake of readability):

“The life cycle is well understood and three principal routes are recognised: ingestion of infective oocysts shed by the cat, consumption of undercooked meat containing Toxoplasma cysts and congenital transmission. Traditionally, the main route of infection is considered to be infection by oocysts deposited in faeces by the definitive host, the cat. This would imply that a high degree of contact with cats would be required to explain the very high prevalences found in many animal and human populations. Toxoplasma gondii has been reported in a very wide range of species. However, this also includes some species that would not normally come into contact with cats.” [6]

“Congenital transmission,” suggest Hide et al., “offers another possible mode of parasite transmission in the absence of cats.” [6]

“One way of determining the importance of transmission routes is to investigate transmission in a system where one of the routes of transmission is absent or minimal. For example, the carnivorous route could be excluded as a source of transmission in a herbivorous species such as sheep.” [6]

On the basis of multiple studies (see [7] and [8] for details of the study with sheep), Hide and his colleagues make a compelling argument that congenital transmission “may be more important than previously considered.” [6]

Researchers working in “the remote, virtually cat-free, high arctic islands of Svalbard” (the northern-most part of Norway) [9] came to similar conclusions. Among the “arctic foxes (n  = 594), Svalbard reindeer (n  = 390), sibling voles (n  = 361), walruses (n  = 17), kittiwakes (n  = 58), barnacle geese (n  = 149), and glaucous gulls (n  = 27),” tested, Prestrud et al. found T. gondii only in the arctic foxes (257, or 43 percent), geese (11, or 7 percent), and walruses (1, or 6 percent). [10]

“The finding of no seropositive reindeer or sibling voles,” they argue, “indicates that infection by oocysts is not an important mode of transmission on Svalbard.” [10] (Also of interest is their suggestion that the seropositive walrus demonstrates “that T. gondii is present in the marine food chain.” [10])

So where does the T. gondii come from?

“…we suggest that T. gondii most likely is brought to Svalbard by migratory birds that become infected in temperate agricultural areas in the winter. However, marine sources of infection may exist. The high seroprevalence of T. gondii in the arctic fox population on Svalbard may be due to: (1) infection from migratory bird species through predation; (2) vertical transmission; and (3) tissue cyst transmission within the Svalbard ecosystem through scavenging and cannibalism. Together, these transmission routes cause a surprisingly high seroprevalence of T. gondii in a top predator living in an ecosystem with very few cats.” [10]

A study of polar bears is further evidence that “other options” do indeed exist:

“In Svalbard cats are banned by the Norwegian authorities; however, a few cats may exist in Russian mining communities. Thus, the possibility of cats as a source of infection for polar bears cannot totally be excluded. Nonetheless, the existing cat population is very limited and local, and the proportion of seropositive polar bears is rather high, indicating that polar bears are commonly infected with T. gondii. It would, therefore, be inconceivable to assume that the few cats would play a major role in the epidemiology of T. gondii in the vast high Arctic. This is apparently the case in East Greenland as well.” [11]

As with the single seropositive walrus discussed above, the results of the polar bear study indicates “that there might be marine sources of T. gondii in the region.” [9]

And finally, in a paper published in 2009, Polish researchers proposed yet another possibility. The “high incidence of T. gondii found, among others, in free-living ruminants,” write Sroka et al., “suggests a possibility of other, so far unknown, paths of transmission of this protozoan.”

“Due to the fact that they are widespread, and tick-bites occur frequently both in humans and in animals, ticks might play an important role in toxoplasmosis transmission.” [12] (Note: the authors acknowledge both support for, and differing opinions about, the possibility of such a pathway.)

Fredebaugh mentions none of this work in her thesis; none of the author’s names appear in her lengthy list of references (which, to most people, probably appears comprehensive). And still, both she and Mateus-Pinilla (who chaired Fredebaugh’s thesis advisory committee) are committed to the proposition that, as Jessup and Miller suggest, “the science points to cats.”

Greater (Mis)Understanding
Fredebaugh concludes her thesis by suggesting that her results:

“provide a greater understanding of how feral cats and wildlife utilize natural areas in a highly fragmented landscape and how feral cat land use may impact wildlife parasite prevalence both directly and indirectly. With this information, I more clearly understand the association between wildlife and feral cats and can suggest better control strategies for feral cat populations. Using wildlife with small spatial scale habitat use as sentinels of parasite presence in the environment, I can gain a better understanding of the epidemiologic impact of T. gondii in different urban and rural settings to prevent human and wildlife infection. Further collaborative research is needed to determine the most effective management strategy for feral cat populations in natural areas and to evaluate the direct relationship between feral cats and their impacts on wildlife.” [1]

At the risk of being overly critical, I’m suggesting that Fredebaugh’s work has not only failed to clarify our understanding of feral cats, wildlife, and the transmission of T. gondii, but has—due to its problematic methodology and incomplete literature review—actually made matters worse (especially with regard to possible “control strategies”).

•     •     •

Not surprisingly, The Wildlife Society’s CEO/Executive Director Michael Hutchins immediately endorsed the study (his summary conveniently omits the small sample size involved, the inverse relationship between “infected” cats and “infected” SHR mammals, and several other important aspects of the research) and its misguided conclusions, pleading:

“How many more peer reviewed studies do we need to convince leaders to change the way that we are currently dealing with the feral cat population explosion in this country?”

I don’t want to suggest that Hutchins and I are on the same page here, but omit the word explosion, and that’s pretty much the same question I’ve been asking for a while now.

Literature Cited
1. Fredebaugh, S.L., Habitat Overlap and Seroprevalence of Toxoplasma Gondii in Wildlife and Feral Cats in a Natural Area. 2010, University of Illinois at Urbana-Champaign: Urbana-Champaign, IL. p. 88. http://www.ideals.illinois.edu/bitstream/handle/2142/16185/1_Fredebaugh_Shannon.pdf?sequence=6

2. Dubey, J.P. and Jones, J.L., “Toxoplasma gondii infection in humans and animals in the United States.” International Journal for Parasitology. 2008. 38(11): p. 1257–1278. http://www.sciencedirect.com/science/article/B6T7F-4S85DPK-1/2/2a1f9e590e7c7ec35d1072e06b2fa99d

3. Liberg, O., “Home range and territoriality in free-ranging house cats.” Acta Zoologica Fennica. 1984. 171: p. 283–285.

4. Jessup, D.A. and Miller, M.A., “The Trickle-Down Effect.” The Wildlife Professional. 2011. 5(1): p. 62–64.

5. Marshall, P.A., et al., “Detection of high levels of congenital transmission of Toxoplasma gondii in natural urban populations of Mus domesticus.” Parasitology. 2004. 128(01): p. 39–42. http://dx.doi.org/10.1017/S0031182003004189

6. Hide, G., et al., “Evidence for high levels of vertical transmission in Toxoplasma gondii.” Parasitology. 2009. 136(Special Issue 14): p. 1877-1885. http://dx.doi.org/10.1017/S0031182009990941

7. Morley, E.K., et al., “Significant familial differences in the frequency of abortion and Toxoplasma gondii infection within a flock of Charollais sheep.” Parasitology. 2005. 131(02): p. 181–185. http://dx.doi.org/10.1017/S0031182005007614

8. Morley, E.K., et al., “Evidence that primary infection of Charollais sheep with Toxoplasma gondii may not prevent foetal infection and abortion in subsequent lambings.” Parasitology. 2008. 135(02): p. 169–173. http://dx.doi.org/10.1017/S0031182007003721

9. Prestrud, K.W., et al., “Direct high-resolution genotyping of Toxoplasma gondii in arctic foxes (Vulpes lagopus) in the remote arctic Svalbard archipelago reveals widespread clonal Type II lineage.” Veterinary Parasitology. 2008. 158(1-2): p. 121–128. http://www.sciencedirect.com/science/article/B6TD7-4TDK6Y8-2/2/1e5b02861f7a0c81f2277f65f42e6be9

10. Prestrud, K.W., et al., “Serosurvey for Toxoplasma gondii in arctic foxes and possible sources of infection in the high Arctic of Svalbard.” Veterinary Parasitology. 2007. 150(1-2): p. 6–12. http://www.sciencedirect.com/science/article/B6TD7-4PYR4P2-2/2/fcc91fcf1d1426cd1b750bd3840bdb31

11. Oksanen, A., et al., “Prevalence of Antibodies Against Toxoplasma gondii in Polar Bears (Ursus maritimus) From Svalbard and East Greenland.” Journal of Parasitology. 2009. 95(1): p. 89–94. http://dx.doi.org/10.1645/GE-1590.1

12. Sroka, J., Szymańska, J., and Wójcik-Fatla, A., “The occurrence of Toxoplasma gondii and Borrelia burgdorferi sensu lato in Ixodes ricinus ticks from eastern Poland with the use of PCR.” Annals of Agricultural and Environmental Medicine. 2009. 16(2): p. 313–319.

It’s Not the Media, It’s the Message

To hear The Wildlife Society’s staunch opponents of TNR tell it, the media’s just not interested in stories about “the impacts of free-ranging and feral cats on wildlife.”

“This January when thousands of blackbirds fell from the sky in Arkansas, articles about mass extinctions and bird conservation were a dime-a-dozen. When the Deepwater Horizon oil spill killed 6,000 birds between April to October 2010, news organizations ran ‘Breaking News’ about the negative impacts on the environment. Meanwhile it is estimated that one million birds are killed everyday by cats, and the only news organizations covering it are small, local branches. The bigger problem is being shuffled to the backburner for more sensational news.”

According to The Wildlife Society (TWS), however, “the bigger problem” is “greater than almost any other single-issue.”

In their effort to get the issue on the front burner, TWS has “gathered the facts about these cats, and published them in the Spring Issue of The Wildlife Professional in a special section called ‘The Impact of Free Ranging Cats.’” (available free via issuu.com)

Thus armed, readers are expected to, as it says on the cover, “Pick One: Outdoor Cats or Conservation”

Back Burner or Hot Topic?
Before we get to the “facts,” it’s worth looking back over the past 15 months to see just how neglectful the media have been re: “the bigger problem.”

  • January 9, 2010: Travis Longcore, science director for the Urban Wildlands Group, tells Southern California Public Radio: “Feral cats are documented predators of native wildlife. We do not support release of this non-native predator into our open spaces and neighborhoods, where they kill birds and other wildlife.”
  • January 17, 2010 Longcore, whose Urban Wildlands Group was lead plaintiff in a lawsuit aimed to put an end to publicly supported TNR in Los Angeles, tells the L.A. Times: “It’s ugly; it’s gotten very vicious. It’s not like we’ve got a vendetta here. This is a real environmental issue, a real public health issue.” In the same story, American Bird Conservancy’s Senior Policy Advisor, Steve Holmer, tells the Times: “The latest estimates are that there are about . . . 160 million feral cats [nationwide]… It’s conservatively estimated that they kill about 500 million birds a year.”

  • September 30, 2010: “Scientists are quietly raging about the effects that cats, both owned and stray, are having on bird populations,” claims Washington Post columnist Adrian Higgins. “It’s not an issue that has received much attention, but with an estimated 90 million pet cats in the United States, two-thirds of them allowed outdoors, the cumulative effect on birds is significant, according to experts.” Higgins’ story is riddled with misinformation, courtesy of the American Bird Conservancy (ABC), The Wildlife Society, and Dauphine and Cooper’s 2009 Partners in Flight paper.

“Palmer said one of the most ‘heartbreaking’ scenes during filming was at a volunteer spay-neuter clinic in Los Angeles that sterilized 80 ferals a day. She said most of the cats had infections that never healed, as well as broken bones, large abscesses around their teeth and mange.” (A claim easily discredited, if only the reporters had bothered to check.)

  • January 2011: Utah Representative Curtis Oda sponsors HB 210, which would permit “the humane shooting of an animal in an unincorporated area of a county, where hunting is not prohibited, if the person doing the shooting has a reasonable belief that the animal is a feral animal.”

Yet, the folks at TWS would have us believe that “the only news organizations covering [the cat-bird issue] are small, local branches.” As is often the case, their story doesn’t hold up well alongside the facts.

Indeed, other than when Higgins got Executive Director/CEO Michael Hutchins’ name wrong, it’s hard to see what TWS has to complain about.

The Art of Selling Science
“After years of arguments,” laments Nico Dauphine and Robert Cooper, recalling last year’s decision by Athens, GA, to adopt TNR, “the vote was cast: 9–1 in favor of the ordinance, with an additional 7–3 vote establishing a $10,000 annual budget to support the TNR program.”

“How could this happen in a progressive community like Athens, Georgia, home to one of the nation’s finest university programs in wildlife science? The answer is a complex mix of money, politics, intense emotions, and deeply divergent perspectives on animal welfare… If we’re going to win the battle to save wildlife from cats, then we’ll need to be smarter about how we communicate the science.” [1]

Something tells me this “smarter” communication doesn’t allow for much in the way of honesty and transparency—attributes already in short supply.

Old Habits
“The Impact of Free Ranging Cats” has given its contributors the opportunity to revive and reinforce a range of dubious claims, including the ever-popular exaggerations about the number of free-roaming cats in the environment.

According to Dauphine and Cooper, “The number of outdoor pet cats, strays, and feral cats in the U.S. alone now totals approximately 117 to 157 million,” [1] an estimate rooted in their earlier creative accounting. Colin Gillin, president of the American Association of Wildlife Veterinarians, who penned this issue’s “Leadership Letter” (more on that later), follows suit, claiming  “60 million or more pet cats are allowed outdoors to roam free.” [2]

The American Pet Products Association 2008 National Pet Owners Survey, though, indicates that 64 percent of pet cats are indoor-only during the daytime, and 69 percent are kept in at night [3]. Of those that are allowed outdoors, approximately half are outside for less than three hours each day. [4, 5]

This information is widely available—and has been for years—yet many TNR opponents continue to inflate by a factor of two the number of free-roaming pet cats.

And it only gets worse from here.

Dense and Denser
Not content to inflate absolute cat numbers, Dauphine and Cooper go on to misrepresent research into population demographics as well. “Local densities can be extremely high,” they write, “reaching up to 1,580 cats per square kilometer in urban areas.” [1] In fact, the very paper they cite paints a rather different picture. For one thing, there’s quite a range involved: 132–1,579 cats per square kilometer (a point recognized by Yolanda van Heezik, another contributor to the special issue [6].)

Also, this is a highly skewed distribution—there are lots of instances of low/medium density, while high densities are far less common. As a result, the median (417) is used “as a measure of central tendency” [7] rather than the mean (856). So, although densities “reaching up to 1,580 cats per square kilometer in urban areas” were observed, more than half fell between 132 and 417 cats per square kilometer (or 51–161 cats per square mile).

Even more interesting, however, are what Sims et al. learned when they compared bird density and cat density: in many cases, there were more birds in the very areas where there were more cats—even species considered especially vulnerable to predation by cats. It may be, suggest Sims et al., that, because high cat density corresponds closely to high housing density, this measure is also an indication of those areas “where humans provide more supplementary food for birds.” [7]

Another explanation: “consistently high cat densities in our study areas… and thus uniformly high impacts of cat populations on urban avian assemblages.” [7] (Interestingly, the authors never consider that they might be observing uniformly low impacts.)

The bottom line? It’s difficult enough to show a direct link between observed predation and population impacts; suggesting a causal connection between high cat densities and declining bird populations is misleading and irresponsible. (Not that Dauphine and Cooper are the only ones to attempt it; recall that no predation data from Coleman and Temple’s “Wisconsin Study” were ever published, despite numerous news stories in which Temple referred to their existence in some detail [8–10].)

Predation Pressure
Dauphine and Cooper make a similar leap when, to buttress their claim that “TNR does not reduce predation pressure on native wildlife,” [1] they cite a study not about predation, but about the home ranges of 27 feral cats on Catalina Island.

While it’s true that the researchers found “no significant differences… in home-range areas or overlap between sterilized and intact cats,” [11] this has as much due to their tiny sample size as anything else. And the difference in range size between the four intact males and the four sterilized males was—while not statistically significant—revealing.

The range of intact males was 33–116 percent larger during the non-breeding season, and 68–80 percent larger during the breeding season. In his study of “house-bound” cats, Liberg, too, found differences: “breeding males had ranges of 350–380 hectares; ranges of subordinate, non-breeding males were around 80 hectares, or not much larger than those of females.” [12]

All of which suggests smaller ranges for males that are part of TNR programs. What any of this has to do with “predation pressure on native wildlife,” however, remains an open question.

On the other hand, Castillo and Clarke (whose paper Dauphine and Cooper cite) actually documented remarkably little predation among the TNR colonies they studied. In fact, over the course of approximately 300 hours of observation (this, in addition to “several months identifying, describing, and photographing each of the cats living in the colonies” [13] prior to beginning their research), Castillo and Clarke “saw cats kill a juvenile common yellowthroat and a blue jay. Cats also caught and ate green anoles, bark anoles, and brown anoles. In addition, we found the carcasses of a gray catbird and a juvenile opossum in the feeding area” [13].

Another of Dauphine and Cooper’s “facts”—that “TNR does not typically reduce feral cat populations”—is contradicted by another one of the studies they cite. Contrary to what the authors suggest, Felicia Nutter’s PhD thesis work showed that “colonies managed by trap-neuter-return were stable in composition and declining in size throughout the seven year follow-up period.” [14]

Indeed, Nutter observed a mean decrease of 36 percent (range: 30–89 percent) in the six TNR colonies they studied over two years. By contrast, the three control colonies increased in size an average of 47 percent. [15]

Additional TNR success stories Dauphine and Cooper fail to acknowledge:

  • Natoli et al. reported a 16–32 percent decrease in population size over a 10-year period across 103 colonies in Rome—despite a 21 percent rate of “cat immigration.” [16]
  • As of 2004, ORCAT, run by the Ocean Reef Community Associa­tion (in the Florida Keys), had reduced its “overall population from approximately 2,000 cats to 500 cats.” [17] Accord­ing to the ORCAT Website, the population today is approximately 350, of which only about 250 are free-roaming.

Toxoplasma gondii
In recent years, Toxoplasma gondii has been linked to the illness and death of marine life, primarily sea otters [18], prompting investigation into the possible role of free-roaming (both owned and feral) cats. [19, 20] But if, as the authors claim, “the science points to cats,” then it does so rather obliquely, an acknowledgement Jessup and Miller make begrudgingly:

“Based on proximity and sheer numbers, outdoor pet and feral domestic cats may be the most important source of T. gondii oocysts in near-shore marine waters. Mountain lions and bobcats rarely dwell near the ocean or in areas of high human population density, where sea otter infections are more common.” [21, emphasis mine]

Correlation, however, is not the same as causation. And not all T. gondii is the same.

In a study of southern sea otters from coastal California, conducted between 1998 and 2004, a team of researches—including Jessup and Miller—found that 36 of 50 otters were infected with the Type X strain of T. gondii, one of at least four known strains. [22] Jessup and Miller were also among 14 co-authors of a 2008 paper (referenced in their contribution to “The Impact of Free Ranging Cats”) in which the Type X strain was linked not to domestic cats, but to wild felids:

“Three of the Type X-infected carnivores were wild felids (two mountain lions and a bobcat), but no domestic cats were Type X-positive. Examination of larger samples of wild and domestic felids will help clarify these initial findings. If Type X strains are detected more commonly from wild felids in subsequent studies, this could suggest that these animals are more important land-based sources of T. gondii for marine wildlife than are domestic cats.” [20, emphasis mine]

Combining the results of the two studies, then, nearly three-quarters of the sea otters examined as part of the 1998–2004 study were infected with a strain of T. gondii that hasn’t been traced to domestic cats. (I found this to be such surprising news that, months ago, I tried to contact Miller about it. Was I missing something? What studies were being conducted that might confirm or refute these finings? Etc. I never received a reply.)

As Miller et al. note, “subsequent studies” are in order. And it’s important to keep in mind their sample size was quite small: three bobcats, 26 mountain lions, and seven domestic cats (although the authors suggest at one point that only five domestic cats were included).

Still, a recently published study from Germany seems to support the hypothesis that the Type X strain isn’t found in domestic cats. Herrmann et al. analyzed 68 T. gondii-positive fecal samples (all from pet cats) and found no Type X strain. [23] (It’s interesting to note, too, that only 0.25 percent of the 18,259 samples tested positive for T. gondii.)

This is not to say that there’s no connection between domestic cats and Toxoplasmosis in sea otters, but that any “trickle-down effect,” as Jessup and Miller describe it, is not nearly as well understood as they imply. There’s too much we simply don’t know.

Money and Politics
I agree with Dauphine and Cooper that science is only part of the TNR debate—that it also involves “a complex mix of money, politics, intense emotions, and deeply divergent perspectives on animal welfare.” And I agree with their assessment of the progress being made by TNR supporters:

“Advocates of TNR have gained tremendous political strength in the U.S. in recent years. With millions of dollars in donor funding, they are influencing legislation and the policies of major animal-oriented nonprofit organizations.” [1]

What I find puzzling is Dauphine’s rather David-and-Goliath portrayal of the “cat lobby” (my term, not hers) they’re up against—in particular, her complaint, “promotion of TNR is big business, with such large amounts of money in play that conservation scientists opposing TNR can’t begin to compete.” [24]

The Cat Lobby
In “Follow the Money: The Economics of TNR Advocacy,” she notes that Best Friends Animal Society, “one of the largest organizations promoting TNR, took in over $40 million in revenue in 2009.” [24] Fair enough, but this needs to be weighed against expenses of $35.6 million—of which $15.5 million was spent on “animal care activities.”

But Dauphine’s got it wrong when she claims that Best Friends “spent more than $11 million on cat advocacy campaigns that year.” [24] Their financials—spelled out in the same document Dauphine cites—are unambiguous: $11.7 million in expenditures went to all “campaigns and other national outreach.” Indeed, there is no breakdown for “cat advocacy campaigns.”

Dauphine does a better job describing Alley Cat Allies’ 2010 financials: of the $5.2 million they took in, $3.3 million was spent in public outreach. But she’s overreaching in suggesting that their “Every Kitty, Every City” campaign is nationwide. For now, at least, it’s up and running in just “five major U.S. cities.”

Echoing Dauphine’s concerns, Florida attorney Pamela Jo Hatley decries ORCAT’s resources: “At a meeting hosted by the Ocean Reef Resort in June 2004,” recalls Hatley, “I learned that the ORCAT colony then had about 500 free-ranging cats, several paid employees, and an annual operating budget of some $100,000.” [25]

What Hatley fails to mention is how those resources have been used to make ORCAT a model for the rest of the country—using private donations. Hatley doesn’t seem to object to the U.S. Fish and Wildlife Service shelling out $50,000—of tax dollars—in 2007 to round up fewer than 20 cats (some of which were clearly not feral) along with 81 raccoons (53 of which were released alive) in the Florida Keys. [26, 27]

Following the Money
According to their 2008 Form 990, ORCAT took in about $278,000 in revenue, compared to $310,000 in expenses. How does that compare to some of the organizations opposing TNR? A quick visit to Guidestar.com helps put things in perspective.

  • In 2009, ABC took in just under $6 million, slightly more than their expenses.
  • TWS had $2.3 million in revenue in 2009, which was more than offset by expenses of $2.5 million.
  • Friends of the National Zoo, which oversees the Smithsonian Migratory Bird Center, showed $15 million in revenue, just exceeding their 2009 expenses of $14.7 million. (The Smithsonian Institute topped $1 billion in both the revenue and expense categories.)
  • And the National Audubon Society took in $61.6 million in 2008 (the most recent year for which information is available). And, despite expenses in excess of $86 million, finished the year with more than $255 million in net assets.

These numbers clearly don’t reflect the funding each organization dedicates to opposing TNR—but neither do they offer any evidence that, as Dauphine argues, “conservation scientists opposing TNR can’t begin to compete.”

Intense Emotions
Nobody familiar with the TNR debate would suggest that it’s not highly emotional. How can it be otherwise? Indeed, the very idea of decoupling our emotions from such important discourse is rather absurd.

Having an emotional investment in the debate does not, however, make one irrational or stupid.

“On the surface,” suggest Dauphine and Cooper, their tone unmistakably condescending, “TNR may sound reasonable, even logical.” [1] Gillin, for his part, bemoans the way the TNR debate “quickly shifts from statistics to politics to emotional arguments.” [2]

What’s particularly fascinating about all of this—the way TNR supporters are made out to be irrational (if not mentally ill—as in a letter to Conservation Biology last year, when several TNR opponents, including four contributors to “The Impact of Free Ranging Cats,” compared TNR to hoarding [28])—is just how emotionally charged the appeal of TNR opponents is.

Witness the “gruesome gallery of images,” for example, in which “one cat lies dead with a broken leg, one lies dying in a coat of maggots, and another suffers as ticks and ear mites plague its face.” [1] The idea, of course, is that these cats would have been better off if they’d been rounded up and killed “humanely.” A preemptive strike against the inevitability of “short, brutal lives.” (This phrase, which I first saw used by Jessup, [28] has become remarkably popular among TNR opponents.)

But is it that simple? Applying the same logic (if that’s what it is) to pelicans covered in oil, for instance, would we suggest that these birds should either be in captivity or “humanely euthanized”? Obviously not.

Divergent Perspectives on Animal Welfare
While I disagree that “the debate is predominately about whether cats should be allowed to run wild across the landscape and, if not, how to effectively and humanely manage them,” [29] I tend to agree with Lepczyk et al. when they write:

“It’s much more about human views and perceptions than science—a classic case where understanding the human dimensions of an issue is the key to mitigating the problem.” [29]

But, like Dauphine and Cooper, Lepczyk et al. seem more interested in broadcasting their message—loudly, ad nauseam—than in listening. “We need to understand whether people are even aware,” they write, “of the cumulative impact that their actions—choosing to let cats outdoors—can have on wildlife populations.” [29]

Although it’s packaged somewhat “softly,” we’re back to the same old speculative connections between predation and population impacts (familiar terrain for Lepczyk, who tried to connect these same dots in his PhD research). But how much of a connection is there, really? In their review of 61 predation studies, Mike Fitzgerald and Dennis Turner are unambiguous:

“We consider that we do not have enough information yet to attempt to estimate on average how many birds a cat kills each year. And there are few, if any studies apart from island ones that actually demonstrate that cats have reduced bird populations.” [30]

While the tone used by Lepczyk et al. is very much “we’re all in this together,” their prescription for “moving forward” suggests little common ground. (They actually cite that 2010 letter to Conservation Biology [28]—not much of an olive branch.)

“One approach is exemplified in Hawaii,” explain the authors, “where we’ve become part of a large coalition of stakeholders working together with the shared goal of reducing and eventually removing feral cats from the landscape.” [29] So, who’s involved?

“Our diverse group includes individuals from the Humane Society of the United States, the Hawaiian Humane Society, the U.S. Fish and Wildlife Service, the National Park Service, Hawaii’s Department of Land and Natural Resources, and the University of Hawaii. Our team also regularly interacts with other groups around the nation such as regional Audubon Societies and the American Bird Conservancy. Several stakeholders in the group have differing views, such as on whether or not euthanasia or culling is appropriate, or whether people should feed feral cats.” [29]

Other than the Humane Society organizations (whose position on TNR I don’t take for granted, considering they were early supporters of ABC’s Cats Indoors! campaign [31]), I don’t see a real diversity of views in this coalition.

I suppose it’s easy to make room at the table when you’re offering so few seats.

For Dauphine, though, any such collaboration approaches treason. Or selling out, at least.

“In some cases,” she explains, “conservation groups accept funding to join in efforts promoting TNR. The New Jersey Audubon Society, for example, had previously rejected TNR but began supporting it in 2005, acknowledging funding from the Frankenberg and Dodge Foundations for collaboration with TNR groups.” [24]

Dauphine doesn’t go into detail about the amount of funding, and it’s not clear what, if any, role it played in the decision by NJAS (which took in $6.8 million in 2008) to participate in the New Jersey Feral Cat-Wildlife Coalition—the kind of collaborative effort that should be encouraged, not derided:

“From 2002 to 2005, NJAS had actively opposed the practice of TNR in New Jersey. Despite this opposition, municipalities continued to adopt TNR ordinances. In 2005, NJAS, American Bird Conservancy, Neighborhood Cats and Burlington Feral Cat Initiative began exploratory dialogue about implementing standards to protect rare wildlife vulnerable to cat predation in towns which have already adopted TNR programs.” [32]

Message Received, Loud and Clear
Rather than wringing their hands over how to “better communicate the science” [1] or how to better facilitate “legal or policy changes, incentives, and increased education,” [29] TNR opponents might want to reconsider the message itself.

What they are proposing is the killing—on an unprecedented scale—of this country’s most popular pet.

I don’t imagine this tests well with focus groups and donors, of course, but there it is.

These people seem perplexed by a community’s willingness to adopt TNR (“In the end,” lament Lepczyk et al., referring to the decision in Athens, GA, “the professional opinion of wildlife biologists counted no more than that of any other citizen, a major reason for the defeat.” [29]) but fail to recognize how profoundly unpalatable their alternative is.

And, unworkable, too.

Which may explain why it’s virtually impossible to get them to discuss their “plan” in any detail. (I was unsuccessful, for example, in pinning down Travis Longcore during our back-and-forth on the Audubon magazine’s blog and couldn’t get Jessup or Hutchins to bite when I asked the same question during an online discussion of public health risks.)

In light of what’s involved with “successful” eradication programs, I’m not surprised by their eagerness to change the subject.

  • On Marion Island, it took 19 years to eradicate something like 2,200 cats—using disease (feline distemper), poisoning, intensive hunting and trapping, and dogs. This on an island that’s only 115 square miles in total area, barren, and uninhabited. [33, 34] The cost, I’m sure, was astronomical.
  • On the sparsely populated (fewer than 1,000, according to Wikipedia) Ascension Island (less than 34 total square miles), a 2003 eradication effort cost nearly $950,000 (adjusted to 2009 dollars). [35]
  • A 2000 effort on Tuhua (essentially uninhabited, and just 4.9 square miles) ran $78,591 (again, adjusted to 2009 dollars). [35]
  • Efforts on Macquarie Island (also small—47.3 square miles—and essentially uninhabited) proved particularly costly: $2.7 million in U.S. (2009) dollars. And still counting. The resulting rebound in rabbit and rodent numbers prompted “Federal and State governments in Australia [to commit] AU$24 million for an integrated rabbit, rat and mouse eradication programme.” [36] (To put this into context, Macquarie Island is about one-third the size of the Florida Keys.)

These examples represent, in many ways, low-hanging fruit. By contrast, “the presence of non-target species and the need to safely mitigate for possible harmful effects, along with substantial environmental compliance requirements raised the cost of the eradication.” [37] Eradicating rodents from Anacapa Island, “a small [1.2-square-mile] island just 80 miles from Los Angeles International Airport, cost about $2 million.” [38]

Now—setting aside the horrors involved—how exactly do TNR opponents propose to rid the U.S. of it’s millions of feral cats? [cue the sound track of crickets chirping]

I think the general public is starting to catch on. Even if they fall for the outlandish claims about predation, wildlife impacts, and all the rest—they don’t see anything in the way of a real solution. As Mark Kumpf, former president of the National Animal Control Association, put it in an interview with Animal Sheltering magazine, “the traditional methods that many communities use… are not necessarily the ones that communities are looking for today.” [39]

“Traditional” approaches to feral cat management (i.e., trap-and-kill) are, says Kumpf, akin to “bailing the ocean with a thimble.” [39]

For all their apparent interest—22 pages in the current issue of The Wildlife Professional alone—TWS might as well be handing out thimbles to its members. Although Gillin’s “Leadership Letter” invites “dialogue among all stakeholders,” it offers nothing substantive to advance the discussion:

“If removal and euthanasia of unadoptable feral cats is not acceptable to TNR proponents, then they need to offer the conservation community a logical, science-based proposal that will solve the problem of this invasive species and its effect on wildlife and the environment.” [2]

So much for leadership.

Literature Cited
1. Dauphine, N. and Cooper, R.J., “Pick One: Outdoor Cats or Conservation.” The Wildlife Professional. 2011. 5(1): p. 50–56.

2. Gillin, C., “The Cat Conundrum.” The Wildlife Professional. 2011. 5(1): p. 10, 12.

3. APPA, 2009–2010 APPA National Pet Owners Survey. 2009, American Pet Products Association: Greenwich, CT. http://www.americanpetproducts.org/pubs_survey.asp

4. Lord, L.K., “Attitudes toward and perceptions of free-roaming cats among individuals living in Ohio.” Journal of the American Veterinary Medical Association. 2008. 232(8): p. 1159-1167. http://www.avma.org/avmacollections/feral_cats/javma_232_8_1159.pdf

5. Clancy, E.A., Moore, A.S., and Bertone, E.R., “Evaluation of cat and owner characteristics and their relationships to outdoor access of owned cats.” Journal of the American Veterinary Medical Association. 2003. 222(11): p. 1541-1545. http://avmajournals.avma.org/doi/abs/10.2460/javma.2003.222.1541

6. van Heezik, Y., “A New Zealand Perspective.” The Wildlife Professional. 2011. 5(1): p. 70.

7. Sims, V., et al., “Avian assemblage structure and domestic cat densities in urban environments.” Diversity and Distributions. 2008. 14(2): p. 387–399. http://dx.doi.org/10.1111/j.1472-4642.2007.00444.x

8. Wilson, M. (1997). Cats Roaming Free Take a Toll on Songbirds. Boston Globe, p. 11.

9. Seppa, N. (1993, July 22). Millions of Songbirds, Rabbits Disappearing. Wisconsin State Journal, p. 1A.

10.  Wozniak, M.D. (1993, August 3). Feline felons: Barn cats are just murder on songbirds. The Milwaukee Journal, p. A1.

11. Guttilla, D.A. and Stapp, P., “Effects of sterilization on movements of feral cats at a wildland-urban interface.”Journal of Mammalogy. 2010. 91(2): p. 482–489. http://dx.doi.org/10.1644/09-MAMM-A-111.1

12. Liberg, O. and Sandell, M., Spatial organisation and reproductive tactics in the domestic cat and other felids, in The Domestic cat: The biology of its behaviour, D.C. Turner and P.P.G. Bateson, Editors. 1988, Cambridge University Press: Cambridge; New York. p. 83–98.

13. Castillo, D. and Clarke, A.L., “Trap/Neuter/Release Methods Ineffective in Controlling Domestic Cat “Colonies” on Public Lands.” Natural Areas Journal. 2003. 23: p. 247–253.

14. Nutter, F.B., Evaluation of a Trap-Neuter-Return Management Program for Feral Cat Colonies: Population Dynamics, Home Ranges, and Potentially Zoonotic Diseases, in Comparative Biomedical Department. 2005, North Carolina State University: Raleigh, NC. p. 224.

15. Stoskopf, M.K. and Nutter, F.B., “Analyzing approaches to feral cat management—one size does not fit all.”Journal of the American Veterinary Medical Association. 2004. 225(9): p. 1361–1364. http://www.ncbi.nlm.nih.gov/pubmed/15552309

www.avma.org/avmacollections/feral_cats/javma_225_9_1361.pdf

16.  Natoli, E., et al., “Management of feral domestic cats in the urban environment of Rome (Italy).” Preventive Veterinary Medicine. 2006. 77(3-4): p. 180-185. http://www.sciencedirect.com/science/article/B6TBK-4M33VSW-1/2/0abfc80f245ab50e602f93060f88e6f9

www.kiccc.org.au/pics/FeralCatsRome2006.pdf

17. Levy, J.K. and Crawford, P.C., “Humane strategies for controlling feral cat populations.” Journal of the American Veterinary Medical Association. 2004. 225(9): p. 1354–1360. http://www.avma.org/avmacollections/feral_cats/default.asp

http://www.avma.org/avmacollections/feral_cats/javma_225_9_1354.pdf

18. Jones, J.L. and Dubey, J.P., “Waterborne toxoplasmosis – Recent developments.” Experimental Parasitology. 124(1): p. 10-25. http://www.sciencedirect.com/science/article/B6WFH-4VXB8YT-2/2/8f9562f64497fe1a30513ba3f000c8dc

19. Dabritz, H.A., et al., “Outdoor fecal deposition by free-roaming cats and attitudes of cat owners and nonowners toward stray pets, wildlife, and water pollution.” Journal of the American Veterinary Medical Association. 2006. 229(1): p. 74-81. http://www.avma.org/avmacollections/feral_cats/javma_229_1_74.pdf

20. Miller, M.A., et al., “Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores from coastal California: New linkages between terrestrial mammals, runoff and toxoplasmosis of sea otters.” International Journal for Parasitology. 2008. 38(11): p. 1319-1328. http://www.sciencedirect.com/science/article/B6T7F-4RXJYTT-2/2/32d387fa3048882d7bd91083e7566117

21. Jessup, D.A. and Miller, M.A., “The Trickle-Down Effect.” The Wildlife Professional. 2011. 5(1): p. 62–64.

22. Conrad, P.A., et al., “Transmission of Toxoplasma: Clues from the study of sea otters as sentinels of Toxoplasma gondii flow into the marine environment.” International Journal for Parasitology. 2005. 35(11-12): p. 1155-1168. http://www.sciencedirect.com/science/article/B6T7F-4GWC8KV-2/2/2845abdbb0fd82c37b952f18ce9d0a5f

23. Herrmann, D.C., et al., “Atypical Toxoplasma gondii genotypes identified in oocysts shed by cats in Germany.”International Journal for Parasitology. 2010. 40(3): p. 285–292. http://www.sciencedirect.com/science/article/B6T7F-4X1J771-2/2/dc32f5bba34a6cce28041d144acf1e7c

24. Dauphine, N., “Follow the Money: The Economics of TNR Advocacy.” The Wildlife Professional. 2011. 5(1): p. 54.

25. Hatley, P.J., “Incompatible Neighbors in the Florida Keys.” The Wildlife Professional. 2011. 5(1): p. 52–53.

26. O’Hara, T. (2007, April 3). Fish & Wildlife Service to begin removing cats from Keys refuges. The Key West Citizen, from http://keysnews.com/archives

27. n.a., Lower Florida Keys National Wildlife Refuges Comprehensive Conservation Plan. 2009, U.S. Department of the Interior, Fish and Wildlife Service: Atlanta, GA. http://www.fws.gov/nationalkeydeer/

http://www.fws.gov/southeast/planning/PDFdocuments/Florida%20Keys%20FINAL/TheKeysFinalCCPFormatted.pdf

28. Jessup, D.A., “The welfare of feral cats and wildlife.” Journal of the American Veterinary Medical Association. 2004. 225(9): p. 1377-1383. http://www.ncbi.nlm.nih.gov/pubmed/15552312

http://www.avma.org/avmacollections/feral_cats/javma_225_9_1377.pdf

29. Lepczyk, C.A., van Heezik, Y., and Cooper, R.J., “An Issue with All-Too-Human Dimensions.” The Wildlife Professional. 2011. 5(1): p. 68–70.

30. Fitzgerald, B.M. and Turner, D.C., Hunting Behaviour of domestic cats and their impact on prey populations, in The Domestic Cat: The biology of its behaviour, D.C. Turner and P.P.G. Bateson, Editors. 2000, Cambridge University Press: Cambridge, U.K.; New York. p. 151–175.

31. Berkeley, E.P., TNR Past present and future: A history of the trap-neuter-return movement. 2004, Bethesda, MD: Alley Cat Allies.

32. Stiles, E., NJAS Works with Coalition to Reduce Bird Mortality from Outdoor Cats. 2008, New Jersey Audubon Society. http://www.njaudubon.org/Portals/10/Conservation/PDF/ConsReportSpring08.pdf

33. Bester, M.N., et al., “A review of the successful eradication of feral cats from sub-Antarctic Marion Island, Southern Indian Ocean.” South African Journal of Wildlife Research. 2002. 32(1): p. 65–73.

http://www.ceru.up.ac.za/downloads/A_review_successful_eradication_feralcats.pdf

34. Bloomer, J.P. and Bester, M.N., “Control of feral cats on sub-Antarctic Marion Island, Indian Ocean.” Biological Conservation. 1992. 60(3): p. 211-219. http://www.sciencedirect.com/science/article/B6V5X-48XKBM6-T0/2/06492dd3a022e4a4f9e437a943dd1d8b

35. Martins, T.L.F., et al., “Costing eradications of alien mammals from islands.” Animal Conservation. 2006. 9(4): p. 439–444. http://onlinelibrary.wiley.com/doi/10.1111/j.1469-1795.2006.00058.x/abstract

http://i3n.iabin.net/documents/pdf/Costingeradicationsofalienmammalsfromislands.pdf

36. Bergstrom, D.M., et al., “Indirect effects of invasive species removal devastate World Heritage Island.” Journal of Applied Ecology. 2009. 46(1): p. 73-81. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2664.2008.01601.x/abstract

http://eprints.utas.edu.au/8384/4/JAppEcol_Bergstrom_etal_journal.pdf

37. Donlan, C.J. and Heneman, B., Maximizing Return on Investments for Island Restoration with a Focus on Seabird Conservation. 2007, Advanced Conservation Strategies: Santa Cruz, CA. http://www.advancedconservation.org/roi/ACS_Seabird_ROI_Report.pdf

38. Donlan, C.J. and Wilcox, C., Complexities of costing eradications, in Animal Conservation. 2007, Wiley-Blackwell. p. 154–156. http://onlinelibrary.wiley.com/doi/10.1111/j.1469-1795.2007.00101.x/abstract

http://www.advancedconservation.org/library/donlan_&_wilcox_2007a.pdf

39. Hettinger, J., Taking a Broader View of Cats in the Community, in Animal Sheltering. 2008. p. 8–9. http://www.animalsheltering.org/resource_library/magazine_articles/sep_oct_2008/taking_a_broader_view_of_cats.html

http://www.animalsheltering.org/resource_library/magazine_articles/sep_oct_2008/broader_view_of_cats.pdf

Revisiting “Reassessment”

“Reassessment: A Closer Look at ‘Critical Assessment of Claims Regarding Management of Feral Cats by Trap-Neuter-Return’” has been revised and expanded!

Image of "Reassessment" Document

This paper, a brief review and critique of the essay “Critical Assessment of Claims Regarding Management of Feral Cats by Trap-Neuter-Return” by Travis Longcore, Catherine Rich, and Lauren M. Sullivan, now includes sections on Toxoplasma gondii, the mesopredator release phenomenon, and more. In addition, links and downloadable PDFs have been added to the list of references.

Over the past year, “Critical Assessment” has gotten a great deal of traction among TNR opponents, despite its glaring omissions, blatant misrepresenta­tions, and obvious bias. “Reassessment”—intended to be a resource for a broad audience, including, wildlife and animal control professionals, policymakers, and the general public—shines a bright spotlight on these shortcomings, thereby bringing the key issues back into focus.

Act Locally
Politics is, as they say, local. This is certainly true of the debate surrounding TNR. Policies endorsing TNR, the feeding of feral cats, etc. typically begin with “Town Hall” meetings, or even meetings of neighborhood associations. “Reassessment” provides interested parties with a rigorous, science-based counter-argument to those using “Critical Assessment” as a weapon against feral cats/TNR.

So, once you’ve had a look for yourself, please share generously! Together, we can—in keeping with the mission of Vox Felina—improve the lives of feral cats through a more informed, conscientious discussion of feral cat issues in general, and TNR in particular.

Download PDF

On Invasion and Persuasion

Smithsonian magazine is, according to its website, “created for modern, well-rounded individuals with diverse interests” and “chronicles the arts, history, sciences and popular culture of the times.” Jess Righthand’s recent article, “The World’s Worst Invasive Mammals,” seems—despite its inclusion in the online edition’s “Science & Nature” section—better suited for the pop culture category.

Indeed, the story has more to do with sensationalism than science.

Feral Cat Population
Righthand’s claim that “there are an estimated 60 million feral cats in the United States alone” is conservative compared to some other estimates. David Jessup, for example, suggested in 2004 that there were 60–100 million [1], while, more recently, The American Bird Conservancy Guide to Bird Conservation puts the figure at 60–120 million [2] (neither cites a source).

Still, Merritt Clifton of Animal People, an independent newspaper dedicated to animal protection issues, makes a compelling argument that the population of feral cats in the U.S. is much smaller than is often reported, and may very well be on the decline. [3]

Clifton’s estimates are derived not from surveys of homeowners feeding stray and feral cats, but from “information about the typical numbers of cats found in common habitat types, gleaned from a national survey of cat rescuers… cross-compared with animal shelter intake data.” [4] In 2003, Clifton suggested that “the winter feral cat population may now be as low as 13 million and the summer peak is probably no more than 24 million.” [4]

Predation on Birds
Righthand puts the figure for annual bird deaths attributed to feral cats at “around 480 million.” Nowhere near the “one billion birds” proposed by Nico Dauphine and Robert Cooper, [5] of course, but more than enough to get the attention of Smithsonian readers.

But, as I’ve pointed out repeatedly, even high rates of predation do not equate to population declines (though, clearly, it’s easy to suggest as much). Many researchers have disputed the kind of broad, overreaching claims to which Righthand alludes. Biologist C.J. Mead, for example, reviewing the deaths of “ringed” (banded) birds reported by the British public, suggests that cats may be responsible for 6.2–31.3 percent of bird deaths. “Overall,” writes Mead, “it is clear that cat predation is a significant cause of death for most of the species examined.” Nevertheless, Mead concludes:

“there is no clear evidence of cats threatening to harm the overall population level of any particular species… Indeed, cats have been kept as pets for many years and hundreds of generations of birds breeding in suburban and rural areas have had to contend with their predatory intentions.” [6]

Mike Fitzgerald and Dennis Turner come to essentially the same conclusion: “We consider that we do not have enough information yet to attempt to estimate on average how many birds a cat kills each year. And there are few, if any studies apart from island ones that actually demonstrate that cats have reduced bird populations.” [7]

Then, too, there’s the critical distinction between compensatory and additive predation—again, a point I’ve made numerous times. Two very interesting studies have generated compelling evidence that birds killed by cats are, on average, significantly less healthy than those killed through non-predatory events (e.g., collisions with buildings). [8, 9] In other words, these birds probably weren’t going to live long enough to contribute to the overall population numbers; predation was compensatory rather than additive.

Public Health Threats
“When house cats are allowed free range outdoors by their owners,” argues Righthand, “or simply don’t have owners, they not only wreak havoc as opportunistic hunters, they can also spread disease. In addition to carrying rabies, 62 to 82 percent of cats in a recent study tested positive for toxoplasmosis.” Here, Righthand seems to be cribbing off of Hildreth, Vantassel, and Hygnstrom, of “Feral Cats and Their Management” fame—hardly a reputable source.

Rabies
Regarding rabies—a topic I’ll save for future posts—I think it’s important to put this into perspective. I happen to have data from Florida handy, and according to that state’s Department of Health, approximately 22,000 Florida residents have died of the flu or pneumonia since 2006 (actually, that figure accounts for only 24 of Florida’s 67 counties, so the total is surely much higher).

By way of comparison: from 2005 through mid-May of this year, there were 11 reported cases of rabies in humans across the entire country (though, I believe there were a handful of reported cases this summer as well).

In terms of public health, then, I think we’re all better off focusing on frequent hand washing, sneezing into our sleeves, and the like—as opposed to, say, exterminating this country’s most popular companion animal by the millions.

Toxoplasma gondii (I)
While it’s true that cats are the definitive host of Toxoplasma gondii, it’s important to note that “wild game can be a source of T. gondii infection in humans, cats, and other carnivores. Serologic data show that a significant number of feral pigs, bears, and cervids are exposed to T. gondii. [10]

“Humans,” write Elmore et al., “usually become infected through ingestion of oocyst-contaminated soil and water, tissue cysts in undercooked meat, or congenitally. Because of their fastidious nature, the passing of non-infective oocysts, and the short duration of oocyst shedding, direct contact with cats is not thought to be a primary risk for human infection.” [11]

But to Righthand’s point: the rate of cats testing positive—or seroprevalence—is, in any event, not a useful measure of their ability to infect other animals or people.

According to Dubey and Jones, “most cats seroconvert after they have shed oocysts. Thus, it is a reasonable assumption that most seropositive cats have already shed oocysts.” [12] “Testing positive,” in this case, is nothing more than the detection of antibodies resulting from seroconversion (the same process, by the way, that takes place in humans after receiving a flu shot).

So, what exactly is Righthand’s point? Did she simply not do her homework here, or is the idea to portray these cats as a threat far, far beyond what the scientific evidence supports? Both, I suspect.

Toxoplasma gondii (II)
T. gondii
, Righthand continues, “has been shown to cause neurological damage to sea otters and other marine mammals that are exposed when heavy rainfall washes infected cat feces into the water.” Again, this is terrain I’ve covered previously. (Righthand, it seems, could do herself—and Smithsonian readers—a favor by subscribing to Vox Felina!)

Yes, T. gondii has been linked to the illness and death of marine life, primarily sea otters [13], prompting investigation into the possible role of free-roaming (both owned and feral) cats. [14, 15] It’s generally thought that oocysts (the mature, infective form of the parasite) are transferred from soil contaminated with infected feces to coastal waterways by way of freshwater run-off. [15]

However, one study found that 36 of 50 sea otters from coastal California were infected with the Type X strain of T. gondii [16], a type linked to wild felids (mountain lions and a bobcat, in this case), but not to domestic cats. [15] A recently published study from Germany seems to corroborate these findings. Herrmann et al. analyzed 18,259 fecal samples (all from pet cats) for T. gondii and found no Type X strain. (It’s interesting to note, too, that only 0.25% of the samples tested positive for T. gondii). [17]

Once again, we’re back to the question: What is Righthand trying to accomplish here?

Population Impacts
“Cats have,” writes Righthand, “also hurt populations of birds, reptiles and other creatures. The black stilt of New Zealand (a seabird), the Okinawa woodpecker and the Cayman Island ground iguana are just a few of the dozens of endangered species at risk due to the proliferation of feral cats.”

At the risk of pointing out the obvious, endangered species are—by definition—at risk due to the proliferation of all sorts of threats. That’s how they became endangered in the first place. To suggest, as Righthand does, that cats are the sole threat these animals face is both misleading and irresponsible.

Righthand (taking a cue, perhaps, from the authors of The ABC Guide?) also makes the common mistake of using island impacts (which are, themselves, more complex than often acknowledged) to imply impacts elsewhere (better yet: everywhere). Readers, it seems, are on their own in terms of doing any research on the topic.

Mission Failure
How much of the blame we can put on Righthand, I don’t know. According to Smithsonian’s website, she’s an intern with the magazine. Had the editors wanted a more thoroughly researched article, they could have demanded one. (This, some readers will recall, is not the first time I’ve been disappointed with the Smithsonian’s lack of rigor.)

According to its website, the mission of the Smithsonian is straightforward but ambitious: “the increase and diffusion of knowledge.” Righthand’s article—misleading at best—falls well short. It seems she’s still struggling with how to best express the organization’s proclaimed values—in this case, going overboard on the creativity at the expense of excellence and integrity.

Literature Cited
1. Jessup, D.A., “The welfare of feral cats and wildlife.” Journal of the American Veterinary Medical Association. 2004. 225(9): p. 1377-1383. http://avmajournals.avma.org/doi/abs/10.2460/javma.2004.225.1377

2. Lebbin, D.J., Parr, M.J., and Fenwick, G.H., The American Bird Conservancy Guide to Bird Conservation. 2010, London: University of Chicago Press.

3. Clifton, M. (2003) Roadkills of cats fall 90% in 10 years—are feral cats on their way out? http://www.animalpeoplenews.org/03/11/roadkills1103.html Accessed May 23, 2010.

4. Clifton, M. Where cats belong—and where they don’t. Animal People 2003 [cited 2009 December 24].  http://www.animalpeoplenews.org/03/6/wherecatsBelong6.03.html.

5. Dauphiné, N. and Cooper, R.J., Impacts of Free-ranging Domestic Cats (Felis catus) on birds in the United States: A review of recent research with conservation and management recommendations, in Fourth International Partners in Flight Conference: Tundra to Tropics. 2009. p. 205–219. www.pwrc.usgs.gov/pif/pubs/McAllenProc/articles/PIF09_Anthropogenic%20Impacts/Dauphine_1_PIF09.pdf

6. Mead, C.J., “Ringed birds killed by cats.” Mammal Review. 1982. 12(4): p. 183-186. http://dx.doi.org/10.1111/j.1365-2907.1982.tb00014.x

7. Fitzgerald, B.M. and Turner, D.C., Hunting Behaviour of domestic cats and their impact on prey populations, in The Domestic Cat: The biology of its behaviour, D.C. Turner and P.P.G. Bateson, Editors. 2000, Cambridge University Press: Cambridge, U.K.; New York. p. 151–175.

8. Baker, P.J., et al., “Cats about town: is predation by free-ranging pet cats Felis catus likely to affect urban bird populations? Ibis. 2008. 150: p. 86-99. http://dx.doi.org/10.1111/j.1474-919X.2008.00836.x

9. Møller, A.P. and Erritzøe, J., “Predation against birds with low immunocompetence.” Oecologia. 2000. 122(4): p. 500-504. http://www.springerlink.com/content/ghnny9mcv016ljd8/

10. Hill, D.E., Chirukandoth, S., and Dubey, J.P., “Biology and epidemiology of Toxoplasma gondii in man and animals.” Animal Health Research Reviews. 2005. 6(01): p. 41-61. http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=775956&fulltextType=RA&fileId=S1466252305000034

11. Elmore, S.A., et al., “Toxoplasma gondii: epidemiology, feline clinical aspects, and prevention.” Trends in Parasitology. 26(4): p. 190-196. http://www.sciencedirect.com/science/article/B6W7G-4YHFWNM-1/2/2a468a936eb06649fde0463deae4e92f

12. Dubey, J.P. and Jones, J.L., “Toxoplasma gondii infection in humans and animals in the United States.” International Journal for Parasitology. 2008. 38(11): p. 1257-1278. http://www.sciencedirect.com/science/article/B6T7F-4S85DPK-1/2/2a1f9e590e7c7ec35d1072e06b2fa99d

13. Jones, J.L. and Dubey, J.P., “Waterborne toxoplasmosis – Recent developments.” Experimental Parasitology. 124(1): p. 10-25. http://www.sciencedirect.com/science/article/B6WFH-4VXB8YT-2/2/8f9562f64497fe1a30513ba3f000c8dc

14. Dabritz, H.A., et al., “Outdoor fecal deposition by free-roaming cats and attitudes of cat owners and nonowners toward stray pets, wildlife, and water pollution.” Journal of the American Veterinary Medical Association. 2006. 229(1): p. 74-81. http://avmajournals.avma.org/doi/abs/10.2460/javma.229.1.74

15. Miller, M.A., et al., “Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores from coastal California: New linkages between terrestrial mammals, runoff and toxoplasmosis of sea otters.” International Journal for Parasitology. 2008. 38(11): p. 1319-1328. http://www.sciencedirect.com/science/article/B6T7F-4RXJYTT-2/2/32d387fa3048882d7bd91083e7566117

16. Conrad, P.A., et al., “Transmission of Toxoplasma: Clues from the study of sea otters as sentinels of Toxoplasma gondii flow into the marine environment.” International Journal for Parasitology. 2005. 35(11-12): p. 1155-1168. http://www.sciencedirect.com/science/article/B6T7F-4GWC8KV-2/2/2845abdbb0fd82c37b952f18ce9d0a5f

17. Herrmann, D.C., et al., “Atypical Toxoplasma gondii genotypes identified in oocysts shed by cats in Germany.” International Journal for Parasitology. 2010. 40(3): p. 285–292. http://www.sciencedirect.com/science/article/B6T7F-4X1J771-2/2/dc32f5bba34a6cce28041d144acf1e7c

Adult Supervision Required II

In my haste to get my previous post online, I neglected to address a critical point (later brought to my attention by a particularly helpful reader). So, a brief follow-up…

In “Feral Cats and Their Management,” the authors point out—correctly, in this case—that “most feral cats (62 percent to 80 percent) tested positive for toxoplasmosis.” [1] But the rate of cats testing positive—or seroprevalence—is not a useful measure of their ability to infect other animals or people.

According to Dubey and Jones, “Most cats seroconvert after they have shed oocysts. Thus, it is a reasonable assumption that most seropositive cats have already shed oocysts.” [2]

“Testing positive,” in this case, is nothing more than the detection of antibodies resulting from seroconversion (the same process, by the way, that takes place in humans after receiving a flu shot).

And so, any argument for killing feral cats based on their high T. Gondii seroprevalence is deeply flawed (and, it should be obvious, on very shaky ground ethically). According to this line of reasoning, we might well consider quarantining humans testing positive for flu antibodies.

TNR: The Solution, Not the Problem
If T. gondii in feral cats is really the concern, then the focus should be on removing young cats from “high-risk” environments. Sound familiar? That’s a significant part of what TNR programs do.

As Dubey and Jones point out, T. gondii prevalence tends to be higher in feral cats than pet or owned cats. [2] So, getting kittens adopted—a key feature of TNR—reduces the likelihood of their becoming T. gondii “contributors” in the future.

And adoption numbers seem to be significant. In 2003, Merritt Clifton of Animal People, an independent newspaper dedicated to animal protection issues, suggested that “up to a third of all pet cats now appear to be recruited from the feral population.”

One can actually make the argument that TNR—dismissed more or less out of hand by Hildreth, Vantassel, and Hygnstrom—may well be the best defense currently available against the spread of Toxoplasmosis (not only in terms of stabilizing/reducing population numbers overall, but also in that it reduces number of kittens potentially exposed to T. gondii).

Hunting for Scapegoats
Finally, one more interesting note from Dubey and Jones (whose paper is referenced in “Feral Cats and Their Management”):

“In addition to live prey, eviscerated tissues (gut piles) from hunted deer and black bears would be a source of infection for wild cats… Prevalence of T. gondii in wild game and venison in the USA is very high and hunters need to be aware of the risk of transmission of infection to humans and, more importantly, spread of infection in the environment. The viscera of hunted animals need to be buried to prevent scavenging by animals, especially cats.” [2]

But Hildreth et al. prefer to focus (or, take aim, as the case may be) solely on feral cats. Though their motives aren’t clear to me, there’s no doubt whatsoever that they have little understanding of the key issues surrounding TNR—never mind the relevant science.

Literature Cited
1. Hildreth, A.M., Vantassel, S.M., and Hygnstrom, S.E., Feral Cats and Their Managment. 2010, University of Nebraska-Lincoln Extension: Lincoln, NE. http://elkhorn.unl.edu/epublic/live/ec1781/build/ec1781.pdf

2. Dubey, J.P. and Jones, J.L., “Toxoplasma gondii infection in humans and animals in the United States.” International Journal for Parasitology. 2008. 38(11): p. 1257-1278. http://www.sciencedirect.com/science/article/B6T7F-4S85DPK-1/2/2a1f9e590e7c7ec35d1072e06b2fa99d

3. Clifton, M. Where cats belong—and where they don’t. Animal People 2003 [cited 2009 December 24].  http://www.animalpeoplenews.org/03/6/wherecatsBelong6.03.html.

Adult Supervision Required

“Have you seen this already? This is awful.”

That’s what somebody posted on the Vox Felina Facebook page late last night—along with a link to an MSNBC news story. The headline was an attention-getter, no doubt about it: “Report: Kill feral cats to control their colonies.”

But beyond that, MSNBC had practically no details. A little digging around, however, led me to New England Cable News (NECN), which has the complete story.

“The report began in an undergraduate wildlife management class, with students writing reports on feral cats based on existing research. The students’ professor and other [University of Nebraska] researchers then compiled the report from the students’ work.” [1]

“Feral Cats and Their Management” claims, straightforwardly enough, to provide “research-based information on the management of feral cats.” [2] Management, in this case, meaning—as is so often the case in such contexts—killing, extermination, eradication, and so forth. Detailed advice is provided (e.g., “Body-gripping traps and snares can be used to quickly kill feral cats”).

And research? In this case, nothing more than a cursory review of all of the usual suspects: Coleman and Temple, Pamela Jo Hatley, Cole Hawkins, The Wildlife Society, Linda Winter. In other words, lots of Kool-Aid drinking.

It’s Like Science, Only Different
Among the research misinterpreted and/or misrepresented (none of which is cited in the text):

“As instinctive hunters, feral cats pose a serious threat to native wildlife, particularly birds.”

It’s no surprise that the authors of the report offer no evidence to support such a sweeping claim. “There are few if any studies,” write Mike Fitzgerald and Dennis Turner in their contribution to The Domestic Cat: The biology of its behaviour, “apart from island ones that actually demonstrate that cats have reduced bird populations.” [3]

Biologist C.J. Mead, reviewing the deaths of “ringed” (banded) birds reported by the British public, suggests that cats may be responsible for 6.2–31.3% of bird deaths. “Overall,” writes Mead, “it is clear that cat predation is a significant cause of death for most of the species examined.” Nevertheless, Mead concludes, “there is no clear evidence of cats threatening to harm the overall population level of any particular species… Indeed, cats have been kept as pets for many years and hundreds of generations of birds breeding in suburban and rural areas have had to contend with their predatory intentions.” [4]

The German zoologist Paul Leyhausen (1916–1998), who spent the bulk of his career studying the behavior of cats, found that cats, frustrated by the difficulties of catching them, “may soon give up hunting birds.” [5]

“During years in the field,” wrote Leyhausen, “I have observed countless times how cats have caught a mouse or a rat and just as often how they have stalked a bird. But I never saw them catch a healthy songbird that was capable of flying. Certainly it does happen, but, as I have said, seldom. I should feel sorry for the average domestic cat that had to live solely on catching birds.” [5]

“Cats kill an estimated 480 million birds per year (assuming eight birds killed per feral cat per year).”

Fitzgerald and Turner (whose work is not referenced in the report) argue that “we do not have enough information yet to attempt to estimate on average how many birds a cat kills each year.” [3] Though, of course, many studies have tried to do exactly that—few, it should be said, involve feral cats.

Unfortunately—and as I have pointed out time and time again—such work typically suffers from a range of methodological and analytical problems (e.g., statistical errors, small sample sizes, and inappropriate/baseless assumptions).

And—as with the UNL report—obvious bias.

“Estimates from Wisconsin indicate that between 500,000 and 8 million birds are killed by rural cats each year in that state…”

How anybody could misquote the numbers from the Wisconsin Study—easily the most widely circulated work on the subject—is a mystery. (On the other hand, the figures were, as Stanley Temple has said, “not actual data” [6] in the first place, so I suppose that does allow for some rather liberal interpretation.)

“The diets of well-fed house-based cats in Sweden consisted of 15 percent to 90 percent native prey, depending on availability.”

How important is it that the prey of feral cats is native, versus non-native? That’s a point of some debate—but not in this case. See, what Liberg actually wrote was this: “Most cats (80-85%) were house-based and obtained from 15 to 90% of their food from natural prey, depending on abundance and availability of the latter.” [7, emphasis mine] He was merely drawing the distinction between food provided by humans and any prey that cats might eat as food.

Liberg goes on to point out that the predation he documented did not, justify a conclusive assessment of the effects of cats on their prey populations, but… indicate[s] that cats by themselves were not limiting any of their prey.” [7] Even high rates of predation do not equate to population declines.

“In California, 67 percent of rodents, 95 percent of birds, and 100 percent of lizards brought home by cats were native species, and native birds were twice as likely to be seen in areas without cats.”

What looks to be truly damning evidence loses much of its impact when it’s seen in context. The reference to Crooks and Soulé’s 1999 paper, for example, omitted the sample size involved: “Identification of 68 prey items returned by cats bordering the fragments indicated that 67% of 26 rodents, 95% of 21 birds and 100% of 11 lizards were native species.” [8] It’s important to note, too, that these researchers asked residents to recall what kind of prey their cats returned—no prey items were collected—thereby raising questions about the accuracy of species attribution.

Furthermore, the cats involved with Crooks and Soulé’s study were all pet cats. How their habits compare with those of feral cats is an open question. Merritt Clifton of Animal People, an independent newspaper dedicated to animal protection issues, suggests, “feral cats appear to hunt no more, and perhaps less, than free-roaming pet cats. This is because, like other wild predators, they hunt not for sport but for food, and hunting more prey than they can eat is a pointless waste of energy.”

The second portion of the quote refers to Cole Hawkins’ PhD dissertation. Hawkins’ research methods and analysis are so problematic that the suggestion of a causal relationship between the presence of cats and the absence of birds (native or otherwise) is highly inappropriate (indeed, Hawkins scarcely investigates predation at all).

Among the key issues: Hawkins had no idea what the “cat” area of his study site was like before the cats were there; he merely assumes it was identical to the “no cat” area in terms of its fauna (though the two landscapes are actually quite different). It’s also interesting to note Hawkins’ emphasis on “the preference of ground feeding birds for the no-cat treatment” while downplaying the fact that five of the nine ground-feeding species included in the study showed no preference for either area. (For a more comprehensive analysis, please see my previous post on the subject.)

“…cats are the most important species in the life cycle of the parasite responsible for toxoplasmosis, and in 3 separate studies, most feral cats (62 percent to 80 percent) tested positive for toxoplasmosis.”

While cats are the “definitive host,” it’s important to note that “wild game can be a source of T. gondii infection in humans, cats, and other carnivores. Serologic data show that a significant number of feral pigs, bears, and cervids are exposed to T. gondii.” [9]

“Humans,” write Elmore et al., “usually become infected through ingestion of oocyst-contaminated soil and water, tissue cysts in undercooked meat, or congenitally. Because of their fastidious nature, the passing of non-infective oocysts, and the short duration of oocyst shedding, direct contact with cats is not thought to be a primary risk for human infection.” [10]

Toxoplasma gondii has been linked to the illness and death of marine life, primarily sea otters [11], prompting investigation into the possible role of free-roaming (both owned and feral) cats. [12, 13] It’s generally thought that oocysts (the mature, infective form of the parasite) are transferred from soil contaminated with infected feces to coastal waterways by way of freshwater run-off. [13]

However, a 2005 study found that 36 of 50 sea otters from coastal California were infected with the Type X strain of T. gondii [14], a type linked to wild felids (mountain lions and a bobcat, in this case), but not to domestic cats. [13] A recently published study from Germany seems to corroborate these findings. Herrmann et al. analyzed 18,259 fecal samples (all from pet cats) for T. gondii and found no Type X strain.  (It’s interesting to note, too, that only 0.25% of the samples tested positive for T. gondii). [15]

[NOTE: Please see follow-up post for additional information about cats and T. gondii.]

“Predation by cats on birds has an economic impact of more than $17 billion dollars [sic] per year in the U.S. The estimated cost per bird is $30, based on literature citing that bird watchers spend $0.40 per bird observed, hunters spend $216 per bird shot, and bird rearers spend $800 per bird released.”

According to this bizarre form of accounting, hunters value an individual bird more than 500 times as much as a birdwatcher does—suggesting, it seems, that dead birds are far more valuable than live birds. This is the kind of estimate that can be developed only through university (or perhaps government) research efforts.

Public Indecency
Stephen Vantassel, a wildlife damage project coordinator who worked on the study, said researchers were aware that some people would be ‘very offended that we offered any type of lethal control method.’ But he said the report was written for public consumption and wasn’t submitted to any science journals for publication.” [1]

For the record, Dr. Vantassel, I’m more offended by the way you’ve allowed such sloppy, grossly irresponsible work to pass for “research.” And the idea that such an undertaking is somehow acceptable because it’s meant for a mass audience is simply absurd!

Naturally, the American Bird Conservancy (ABC) embraced the report immediately, “with one official calling it ‘a must read for any community or government official thinking about what to do about feral cats.’” [1]

“‘Not surprisingly, the report validates everything American Bird Conservancy has been saying about the feral cat issue for many years—namely, TNR doesn’t work in controlling feral cat populations,’ Darin Schroeder, vice president of the Conservation Advocacy for American Bird Conservancy, said Tuesday.”

But validation requires far more than this report provides—beginning with a real interest in scientific inquiry and some basic critical thinking skills. And while we’re at it, a refresher in ethics wouldn’t hurt, either.

*     *     *

In my previous post, I’d indicated that my next post—this post—was going to focus on The American Bird Conservancy Guide to Bird Conservation. Obviously, something came up. Anyhow, the book will keep for a few more days…

Literature Cited
1. n.a. (2010) Report: Kill feral cats to control their colonieshttp://www.necn.com/11/30/10/Report-Kill-feral-cats-to-control-their-/landing_scitech.html?&blockID=3&apID=95afccc4d9564caf8e264f9d087f5732 Accessed December 1, 2010.

2. Hildreth, A.M., Vantassel, S.M., and Hygnstrom, S.E., Feral Cats and Their Managment. 2010, University of Nebraska-Lincoln Extension: Lincoln, NE. http://elkhorn.unl.edu/epublic/live/ec1781/build/ec1781.pdf

3. Fitzgerald, B.M. and Turner, D.C., Hunting Behaviour of domestic cats and their impact on prey populations, in The Domestic Cat: The biology of its behaviour, D.C. Turner and P.P.G. Bateson, Editors. 2000, Cambridge University Press: Cambridge, U.K.; New York. p. 151–175.

4. Mead, C.J., “Ringed birds killed by cats.” Mammal Review. 1982. 12(4): p. 183-186. http://dx.doi.org/10.1111/j.1365-2907.1982.tb00014.x

5. Leyhausen, P., Cat behavior: The predatory and social behavior of domestic and wild cats. Garland series in ethology. 1979, New York: Garland STPM Press.

6. Elliott, J. (1994, March 3–16). The Accused. The Sonoma County Independent, pp. 1, 10

7. Liberg, O., “Food Habits and Prey Impact by Feral and House-Based Domestic Cats in a Rural Area in Southern Sweden.” Journal of Mammalogy. 1984. 65(3): p. 424-432. http://www.jstor.org/stable/1381089

8. Crooks, K.R. and Soule, M.E., “Mesopredator release and avifaunal extinctions in a fragmented system.” Nature. 1999. 400(6744): p. 563.

9. Hill, D.E., Chirukandoth, S., and Dubey, J.P., “Biology and epidemiology of Toxoplasma gondii in man and animals.” Animal Health Research Reviews. 2005. 6(01): p. 41-61. http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=775956&fulltextType=RA&fileId=S1466252305000034

10. Elmore, S.A., et al., “Toxoplasma gondii: epidemiology, feline clinical aspects, and prevention.” Trends in Parasitology. 26(4): p. 190-196. http://www.sciencedirect.com/science/article/B6W7G-4YHFWNM-1/2/2a468a936eb06649fde0463deae4e92f

11. Jones, J.L. and Dubey, J.P., “Waterborne toxoplasmosis – Recent developments.” Experimental Parasitology. 124(1): p. 10-25. http://www.sciencedirect.com/science/article/B6WFH-4VXB8YT-2/2/8f9562f64497fe1a30513ba3f000c8dc

12. Dabritz, H.A., et al., “Outdoor fecal deposition by free-roaming cats and attitudes of cat owners and nonowners toward stray pets, wildlife, and water pollution.” Journal of the American Veterinary Medical Association. 2006. 229(1): p. 74-81. http://avmajournals.avma.org/doi/abs/10.2460/javma.229.1.74

13. Miller, M.A., et al., “Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores from coastal California: New linkages between terrestrial mammals, runoff and toxoplasmosis of sea otters.” International Journal for Parasitology. 2008. 38(11): p. 1319-1328. http://www.sciencedirect.com/science/article/B6T7F-4RXJYTT-2/2/32d387fa3048882d7bd91083e7566117

14. Conrad, P.A., et al., “Transmission of Toxoplasma: Clues from the study of sea otters as sentinels of Toxoplasma gondii flow into the marine environment.” International Journal for Parasitology. 2005. 35(11-12): p. 1155-1168. http://www.sciencedirect.com/science/article/B6T7F-4GWC8KV-2/2/2845abdbb0fd82c37b952f18ce9d0a5f

15. Herrmann, D.C., et al., “Atypical Toxoplasma gondii genotypes identified in oocysts shed by cats in Germany.” International Journal for Parasitology. 2010. 40(3): p. 285–292. http://www.sciencedirect.com/science/article/B6T7F-4X1J771-2/2/dc32f5bba34a6cce28041d144acf1e7c