The Silent Treatment

9 Jan 2012

“I don’t want to be sort of a poodle dog when I’m out there, and a friendly sort of presence in people’s lives,” explained New York Times reporter David Carr in an October 2011 interview with Fresh Air host Terry Gross, “and then come back and do something that’s really mean or aggressive.”

“And if it’s gonna be a hard story, one of things I always say is: This is gonna be a really serious story, and I’m asking very serious questions. And it behooves you to think it through and really work on answering, and defending yourself, because this is not a friendly story. And if they don’t engage, I just tell them: Well, you know what? You better put the nut-cup on, because this is not gonna be pleasant for anyone.”

Two months later, I heard the interview as part of a year-end compilation of the show’s most memorable conversations. Carr’s comments struck a chord; just three weeks earlier, following the publication of “Perceived Predation Risk Reduces the Number of Offspring Songbirds Produce per Year” in Science, I was unable to get co-authors Liana Zanette and Michael Clinchy to “engage.”

Which I found both frustrating and puzzling.

Clearly, these two are eager to talk about domestic cats (see, for example, Clinchy’s comments in ScienceNOW and Zanette’s in the Winnipeg Free Press), even when their work has nothing at all to do with them (or, given the absurd methods employed, real-world predation in general). And here I am—pretty much all cats, all the time—reaching out, only to be snubbed.

During his Fresh Air interview, Carr refers to his October 23 column (“basically a screed,” he says), in which he took on big media—in particular, The Tribune Company and Gannett.

“I spent four days [in June] trying to get comments on Gannett [executive] bonuses, and on Sunday night they said, ‘We’re not going to comment on these bonuses.’ And I just said: Really? You’re a newspaper company. You’re a publicly held company. These bonuses are a matter of public record, and you have nothing to say about them? And I just found that appalling, and I think some of that was reflected in the piece.”

“Clearly,” added Carr, explaining the crux of his frustration, “they were living a life beyond consequence.”

Again, I’m reminded of Zanette and Clinchy. These two led a study in which contrived methods rendered the work nearly worthless—and then went on to misrepresent the study’s implications to the media. And what consequences will they face? None, I suspect. After all, the research did receive funding, and the resulting paper was published in a prestigious journal.

All of which paves the way for more of the same.

Not that Zanette and Clinchy are exceptional in this regard. Since launching this blog in April 2010, I’ve had numerous e-mail inquiries go unanswered. Scientists, journalists, officials of various agencies and organizations, etc.—people eager to get their message out, clearly, but unwilling to respond when that message is challenged. I’d always thought such scrutiny not only came with the territory, but was also welcome—a necessary tool for shaping better science, reporting, and policy.

Others apparently disagree. Among those with whom I have a decidedly one-way correspondence:

Melissa Miller, Wildlife Pathologist, California Department of Fish and Game
Miller was one of 14 co-authors to link the Type X strain of T. gondii—responsible for nearly three-quarters of sea otter infections, according to one study [1]—to wild felids (e.g., mountain lions and bobcats) rather than domestic cats.

“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.” [2]

Now, one needs to be very careful about making conclusions based on such small sample sizes. Nevertheless, given (1) the unprecedented (as far as I can tell) nature of these findings, and (2) the nature of the current “cat debate”—in which free-roaming cats are being vilified in both the scientific literature and mainstream media—this would certainly seem to be newsworthy.

And yet, just two paragraphs later, the paper goes into detail about the estimated mass of “feline fecal deposition” created by domestic cats in the communities near Estero Bay. Suddenly, the focus is back on domestic cats.

I asked her about this in July of 2010, but received no response.

(Nine months later, in a special section of the Spring issue of The Wildlife Professional, Miller and David Jessup (another of the 14 co-authors on the 2008 paper, and a colleague of Miller’s at the California Department of Fish and Game) were at it again, arguing simply, “the science points to cats.” [3])

Christine Stracey, Assistant professor of biology at Westminster College
“I thought the cats probably really hammered them when they were fledglings,” said Stracey, a former University of Florida doctoral student in a UF press release about her study of Northern mockingbirds, “but when they were in the nests, I didn’t really expect the cats to be a huge problem. But I was really wrong about that.”

Once again, the underlying science fails to live up to the dramatic press release. Dig into the details of Stracey’s study, and it becomes clear that she’s probably overestimating the strength of cats as urban predators. Perhaps considerably. In fact, her nest camera placement almost certainly biased her data.

In short, it seems Stracey observed predation by cats largely because she placed the cameras where the cats were.

“We need to think hard about the feral cat problem,” warns Stracey in the press release. But if, as she suggests, cats are a “huge problem,” then how to explain the fact—as Stracey notes in the very same press release—Northern mockingbirds have proven “able to not only live with us, but do really well living with us” [and our cats]? These birds are, as she puts it, “urban winners.”

I asked Stracey about all of this by way of e-mail, but received no response. My follow-up e-mail also went unanswered, but I did notice some Website traffic from the Salt Lake City area (where Westminster College is located) that same day. Coincidence? Could be.

The same goes for the traffic from Columbus, OH, following my e-mail to Amanda Rodewald, professor of wildlife ecology at Ohio State University.

“There are a lot of loud voices that deny cats are important predators of birds in our cities,” argued Rodewald (whose relationship to Stracey’s work remains a mystery) in the UF press release. “But this study shows clearly that cats were the dominant predator in this Florida system—and that wasn’t presumed, it was recorded on video, so it was fact.”

When I wrote to Rodewald, I identified myself as one of those “loud voices,” explaining that I wasn’t asking her to speak for Stracey, nor to defend the research. But, given her own research interest—and her obvious concern with Stracey’s work—perhaps she might be able to answer one question for me: What impact might we expect on the area’s Northern mockingbird populations if the cats were removed from the environment?

It was, apparently, one question too many.

Michael E. Grigg, National Institutes of Health
Like Zanette and Clinchy, Grigg, who serves as Chief of the Molecular Parasitology Unit at the National Institute of Allergy and Infectious Diseases (part of NIH), used a PR opportunity to misrepresent his work. “The most remarkable finding of our study,” notes Grigg in an NIH press release, “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.”

So, the story is more complicated than is typically acknowledged—T. gondii may not be the culprit it’s so often made out to be.

But Grigg is still hanging his hat—in spite of his own findings—on simple environmental contamination:

“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.”

In fact, Grigg and his colleagues found that “T. gondii infections peaked in 2007 then declined relative to S. neurona.” [4] Could it be that free-roaming domestic cats—generally presumed to be the primary source of T. gondii contamination—are also on the decline? TNR opponents don’t seem to think so.

And the researchers observed that infection rates associated with inland waters were no greater than in mammals found along the outer coast. Again, this raises serious questions about the role of domestic cats (which, one would presume, are more numerous inland). As do the numerous studies pointing to sources other than environmental contamination [5–7]—vertical transmission, [5] for example, and possibly ticks [8]—none of which Grigg and his colleagues acknowledge.

Then, of course, there are Grigg’s proposed solutions—first and foremost: “managing feral cat and opossum populations.” Even setting aside for the moment the numerous hurdles (e.g., ethical, economic, etc.) involved with the mass removal/reduction/eradication of these animals, what impact could we realistically expect in terms of T. gondii and/or S. neurona infections in marine mammals? (And what other consequences would we then face?)

I assume Grigg has given the subject considerable thought, but—so far, anyhow—he’s been unwilling to share those thoughts with me.

Steve Klett, Crocodile Lake National Wildlife Refuge Manager
I first ran across Klett’s name in the Florida Keys National Wildlife Refuges Complex Integrated Predator Management Plan/Draft Environmental Assessment, where he was cited as the source for the claim that “cats accounted for 77 percent of the mortality during a recent re-introduction of the Key Largo woodrat.” [9] If, as USFWS has suggested, there are only about 500 woodrats in the wild, [10] why not disclose precisely how many were involved in this “recent re-introduction”? Seventy-seven percent out of how many?

Thirteen, as far as I’ve been able to determine. That’s how many were apparently released in November 2010—following the release of 14 others in February. And, according to attorney and Endangered Species Act blogger Keith Rizzardi, 13 more were released in April 2011.

I e-mailed Klett in July, asking him to clarify that 77 percent figure (which, let’s face it: does a far better job of fanning the flames of the witch-hunt for feral cats than, say, “10 out of 13” does), but never heard back.

Klett retired in December, but Chad Anderson, USFWS biologist at the refuge, assures me that I can “look forward to that [77 percent figure] going from a personal comm. quote to a referenced white paper in the final IPM plan.”

I’m not holding my breath.

Timothy O’Hara, Reporter for the Key West Citizen
In an August 30, 2011 story for the Key West Citizen, Timothy O’Hara writes: “Research indicates that cat predation accounts for 50 percent to 77 percent of the deaths of Lower Keys marsh rabbits and Key Largo woodrats.”

One-half to three-quarters? Really?

Actually, no.

That 77 percent, of course, comes from Klett’s “personal communication”—and seems to reflect the 10 mortalities described above. (Another question I asked Klett was how they could be sure that cats were the culprits. It’s been suggested by a volunteer involved with the re-introductions that the evidence comes from camera traps on the refuge, but I know of no such information coming from refuge officials.)

The 50 percent figure, I’m quite sure, can be traced to Elizabeth Forys’ PhD work, done in the early 1990s on Navy-owned land on Boca Chica and Saddlebush Key. Forys found that 13 of 24 marsh rabbits monitored over the course of her two-and-a-half year study were killed by cats. [11] (USFWS misrepresents this, too, in its Predator Management Plan, once again omitting the number of mortalities: “Free-roaming domestic cat predation accounted for 50 percent of adult Lower Keys marsh rabbit mortality during radio telemetry studies…” [9])

Turns out, O’Hara wasn’t interested in being fact-checked; he never replied to my e-mail.

(If O’Hara is interested in real journalism, he might consider an investigative piece about how USFWS routinely plays misleads the public to whom they are ostensibly accountable.)

Darin Schroeder, ABC’s Vice President for Conservation Advocacy
In October, Schroeder sent a letter (PDF) to the mayors of the 50 largest cities in the country, urging them “to oppose Trap-Neuter-Re-abandon (TNR) programs and the outdoor feeding of cats as a feral cat management option.” In it, he trots out the usual laundry list of misleading complaints: predation, rabies, vague threats regarding the possible implications of the Endangered Species Act and the Migratory Bird Treaty Act, etc.

When I wrote to Schroeder, I made it clear that we need not get into all of this. I just wanted him to explain how feeding bans and policy directives opposing TNR would, as ABC suggests in its November 9 media release, “stop the spread of feral cats.” After all, common sense—and science—tells us that such policies (assuming they could be enforced, of course) would only drive population numbers upward. If, as Schroeder claims, there are “well-documented impacts of cat predation on wildlife,” how could an increase in the population of cats possibly be a benefit?

That was nearly two months ago now; I’m still waiting for Schroeder to connect the dots for me.

• • •

At the risk of stating the obvious, I’m not David Carr. And this is not the New York Times. I suppose my inquiries are easily ignored—coming, as they do, from an “outsider” whose blog has just 330-some subscribers. On the other hand—and not to put too fine a point on it—I’m asking the kinds of questions these people should be asked, by their colleagues, the press, and, in the case of the non-profits like the American Bird Conservancy, their donors.

That seems to be changing though—which means these folks had better get to work on better responses (or, as Carr suggests, put the nut-cup on). In the meantime, the fact that they refuse to engage speaks volumes.

Literature Cited
1. 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

2. 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

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

4. 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

5. 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

6. 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

7. 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

8. 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.

9. n.a., Draft Environmental Assessment: Florida Keys National Wildlife Refuges Complex Integrated Predator Management Plan. 2011, U.S. Fish & Wildlife Service: Big Pine Key, FL. http://www.fws.gov/nationalkeydeer/predatormgmt.html

10. n.a., “Around the Refuge System: Florida and Arizona.” Refuge Update. 2010. 2. p. 17.

11. Forys, E.A. and Humphrey, S.R., “Use of Population Viability Analysis to Evaluate Management Options for the Endangered Lower Keys Marsh Rabbit.” The Journal of Wildlife Management. 1999. 63(1): p. 251–260. http://www.jstor.org/stable/3802507

Loose Threads

17 Jun 2011

North 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)?

Polyparasitism (Gibson et al. 2011) Fig. 1b_590px

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!)

Polyparasitism (Gibson et al. 2011) Fig. 3_590px

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?

17 May 2011

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):

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:

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

19 Mar 2011

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.”

May 8, 2010: Austin American-Statesman writer Mike Leggett devoted his column to the defense of his cat-killing neighbor. According to Leggett, the man’s killed more than 20 feral cats—he “just cannot tolerate what cats do to wild birds.” And, offers Leggett, “none of us should.”

June 17, 2010: An Associated Press story about a proposed feeding ban in Barre, VT, (subsequently picked up by MSNBC) includes multiple quotes from ABC’s Cats Indoors! campaign.

September 10, 2010: Jonathan Franzen, winner of the 2001 National Book Award and a Pulitzer Prize finalist the following year—also an ABC board member—tells Studio 360 host Kurt Andersen that housecats kill a million songbirds a day, just as Franzen depicts in his latest novel Freedom. “Minimum, minimum,” insists Franzen. “Cats should be indoors.”

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.

October 2010: The Smithsonian Migratory Bird Center posts “Baby Catbird Survival” on its Website (the page is currently “under renovation”), claiming that cats were responsible for “alarmingly high rates of nest predation and fledging [sic] mortality.”The evidence? It seems “several guilty-looking cats were found in close proximity to dead birds. Our guess is that closer examination would have revealed feathers in their whiskers.”

December 20, 2010: Feral cats are included among “The World’s Worst Invasive Mammals,” as determined by the Smithsonian (which, by the way, has yet to approve my comment). The article’s misinformation is as sensational as its headline: “In addition to carrying rabies, 62 to 82 percent of cats in a recent study tested positive for toxoplasmosis.”

December 2010: “Feral Cats and Their Management” is picked up by numerous media outlets, many of which mistake it for actual research.

January 17, 2011: Toronto Star reporters do the dirty work for TNR opponent David Bird (“The more cats, the fewer birds”) and Maureen Palmer, director of the recently released documentary Cat Crazed:

“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.”

March 7, 2011: Once again, the Smithsonian is promoting Peter Marra’s gray catbird research. Among the first to pick it up is Discovery News. Two days later, the story is featured on Science at the Smithsonian, “a new Website from the Smithsonian Office of Public Affairs.”

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

Parasite Lost

30 Jul 2010

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.