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

Arkansas Game and Fish Commission Targets Feral Cats

“The Barnett Access on the Little Red River is being overrun with feral cats,” reported last Tuesday’s edition of The Sun-Times, the local paper in Heber Springs, Arkansas. “Due to the interaction between the public and feral cats, and the risk to human health, the Arkansas Game and Fish Commission is going to begin a trapping effort in July to remove the cats.” [1]

Interaction between the public and feral cats?

Huh. The feral cats I’m familiar with don’t really interact with the public. They’re… you know, feral.

What’s going on here?

“Tom Bly, fisheries biologist with the AGFC said that feral cats are considered an invasive species by conservation agencies and organizations nationwide. ‘Cats are the most significant invasive species affecting native bird populations and are also estimated to kill twice as many mammals as birds. There are also numerous human health concerns associated with feral cat colonies. Through feces, fleas, bites, or scratches cats can pass a variety of parasitic, bacterial and viral illnesses including rabies, toxoplasmosis, hook worms, and typhus,’ Bly said.” [1]

Sounds like Bly’s been drinking TNR opponents’ Kool-Aid. Read more

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

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.

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

Parasite Lost

Until now, my posts have focused almost exclusively on wildlife impacts (real and otherwise) related to predation by cats, a topic I’ll be returning to soon enough. Over the past week or so, however, I’ve been researching the Toxoplasma gondii parasite (another subject that will keep me busy well into the future). As it turns out, there’s big news on the T. gondii front—though in this case, the “news” is actually two years old.

Toxoplasma gondii
Toxoplasma gondii
is found in many mammals and birds, but its definitive host—the animal in which the parasite reproduces—is the cat, both domestic and wild species. Cats pass the mature, infective form of the parasite 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]

How often cats shed oocysts, and to what extent, is a complex issue—one I’ll save for later. For now, I will simply note that, in general, it is thought that most cats build up immunity to re-shedding oocysts (though exceptions have been documented in laboratory testing). [2] (For a concise overview of T. gondii’s prevalence in, and risks to, humans, download Toxoplasma gondii: Epidemiology, feline clinical aspects, and prevention.”)

T. Gondii, Cats, and Sea Otters
In recent years, T. gondii has been linked to the illness and death of marine life, primarily sea otters [2], thereby prompting investigation into the possible role of free-roaming (both owned and feral) cats. [3, 4] It’s generally thought that oocysts are transferred from soil contaminated with infected feces to coastal waterways by way of freshwater run-off. [4] And it’s also generally thought that domestic cats are the culprits—or at least it was.

As I was sifting through my growing pile of T. gondii studies, I was rather shocked to find this:

“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.” [4] (italics mine)

Let me explain. There are multiple strains of T. Gondii. Studies of southern sea otters from coastal California found that 36 of 50 otters were infected with the Type X strain. [5] In other words, 72% of the otters were infected with a strain of T. gondii that has yet to be traced to domestic cats.

Now, I’ll be the first to admit that these results are to be treated with caution—as Miller et al. note, “subsequent studies” are in order. For one thing, 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). In addition, this area of research is quite active—and, as this study illustrates, the results can be surprising. Future research intended to confirm or refute this work could just as easily take us off in another direction altogether.

That said, this is still big news. Nearly two years old now, however, it’s not exactly breaking news. So why is this the first I’ve heard about these important findings?

What’s the Story?
For some reason, Miller et al. downplay their findings. Worse, they confuse matters by going into detail about the estimated mass of “feline fecal deposition” created by domestic cats in the communities adjacent to their study site. Suddenly, the focus is back on domestic cats. Given the authors’ findings, I’m not sure how this is relevant, other than as background—previous assumptions being called into question by their results. Perhaps it’s merely the inevitable result of 14 co-authors (one of whom, it should be noted, is David Jessup, of whose work I have been critical in the past) collaborating on a single paper.

But I’m unwilling to give Longcore et al. the same benefit of the doubt. In their essay, Longcore et al. [6] dissemble to such an extent that readers are likely to come away missing the point entirely:

“The large quantity of waste from feral and free-roaming cats containing Toxoplasma oocysts [3, 7] and the correlation between freshwater runoff and toxoplasmosis in marine mammals [8] has led researchers to suspect domestic cats as the source of the infections, although further research is needed to determine the relative importance of native versus exotic felids as sources of this parasite [4].”

While technically correct, Longcore et al. gloss over the fact that, based on the very study they cite, “the relative importance of native versus exotic felids as sources of this parasite” might be something like three-to-one.

And it’s not as if these authors are unwilling to consider speculative findings—such as those by Baker et al. [9] and Hawkins [10]. Longcore et al. even take seriously the Wisconsin Study [11] and its findings that “aren’t actual data.” [12] And they leave out plenty, too—which in the case of the Miller et al. work, might have been a more honorable approach.

Something else they should have omitted:

“Felids, including feral and free-roaming cats, shed Toxoplasma oocysts that infect southern sea otters [8, 5], Pacific harbor seals, and California sea lions.” [6]

In fact, Conrad et al. examined just one harbor seal and one sea lion—and in both cases found the Type X strain of T. gondii. [5] Which, when combined with the results from Miller et al., suggests wild felids as the more likely source, rather than domestic cats.

These two studies not only contradict the specific claims made by Longcore et al., they also challenge the native-good/non-native-bad dichotomy that seems to be at the root of so many feral cat/TNR complaints.

*     *     *

I sent an e-mail to Melissa Miller, lead author of “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,” asking her to comment on my reading of the study. I have not yet received a response.

Literature Cited
1. Elmore, S.A., et al., “Toxoplasma gondii: epidemiology, feline clinical aspects, and prevention.” Trends in Parasitology. 26(4): p. 190-196.

2. Jones, J.L. and Dubey, J.P., “Waterborne toxoplasmosis—Recent developments.” Experimental Parasitology. 124(1): p. 10-25.

3. 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.

4. 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.

5. 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.

6. Longcore, T., Rich, C., and Sullivan, L.M., “Critical Assessment of Claims Regarding Management of Feral Cats by Trap–Neuter–Return.” Conservation Biology. 2009. 23(4): p. 887–894.

7. Dabritz, H.A., et al., “Detection of Toxoplasma gondii-like oocysts in cat feces and estimates of the environmental oocyst burden.” Journal of the American Veterinary Medical Association. 2007. 231(11): p. 1676-1684.

8. Miller, M.A., et al., “Coastal freshwater runoff is a risk factor for Toxoplasma gondii infection of southern sea otters (Enhydra lutris nereis).” International Journal for Parasitology. 2002. 32(8): p. 997-1006.

9. Baker, P.J., et al., “Impact of predation by domestic cats Felis catus in an urban area.” Mammal Review. 2005. 35(3/4): p. 302-312.

10. Hawkins, C.C., Impact of a subsidized exotic predator on native biota: Effect of house cats (Felis catus) on California birds and rodents. 1998, Texas A&M University

11. Coleman, J.S. and Temple, S.A., On the Prowl, in Wisconsin Natural Resources. 1996, Wisconsin Department of Natural Resources: Madison, WI. p. 4–8. http://dnr.wi.gov/wnrmag/html/stories/1996/dec96/cats.htm

12. Elliott, J., The Accused, in The Sonoma County Independent. 1994. p. 1, 10.