Vol. 21, No. 2, 1995


Schizophrenia Be a Viral Zoonosis Transmitted From House Cats?

By E. Fuller Torrey and Robert H. Yolken


Studies have

suggested that some cases of schizophrenia may be caused by

viruses. We hypothesize that such cases may be cases of viral

zoonosis transmitted primarily from house cats. Epidemiological

aspects of schizophrenia and a case-control questionnaire support

this hypothesis.


Bulletin, 21(2): 167-171, 1995.

Several lines of

research have suggested that some cases of schizophrenia may be

caused by viruses. Known cerebral viral infections occasionally

present with symptoms of schizophrenia (Torrey 1996), and

immunological and virological abnormalities have been reported in

some individuals with this disease (Stevens and Hallick 1992;

Kirch 1993). There is also evidence that prenatal and perinatal

events may affect the later development of schizophrenia

(Weinberger 1987; McNeil 1988; Murray et al. 1992), including

studies suggesting that prenatal exposure to influenza is a risk

factor (Mednick et al. 1988; Barr et al. 1990; O’Callaghan

et al. 1991; Sham et al. 1992).

A viral theory

may also account for epidemiological aspects of schizophrenia.

Past studies using admissions to public psychiatric hospitals

– these studies have methodological limitations, but they

are the only ones available – suggest that the incidence of

admissions began increasing sharply in the 1870s (Stroup and

Manderscheid 1988) (Figure 1); schizophrenia was the single

largest diagnostic group accounting for this increase. The

disease occurs more commonly in northern areas of Europe and

America and is comparatively rare in most tropical countries

(Torrey 1980). A high incidence has been reported, for example,

in western Ireland (Torrey et al. 1984), in northern Sweden (Book

et al. 1978), among Afro-Caribbeans in England (Harrison et al.

1988; Wessely et al. 1991), and among the offspring of Dutch

women who were pregnant during the 1944-45 famine in Holland when

Nazi troops cut off all food supplies (Susser and Lin 1992).

Conversely, a very low incidence has been reported among groups

such as the Hutterites who live in rural areas of the United

States and Canada (Eaton and Weil 1955). There are also

suggestions that urban living and crowding are risk factors

(Torrey and Bowler 1990), and an excess winter and spring birth

seasonality has been demonstrated in more than 40 studies

(Bradbury and Miller 1985; Boyd et al. 1986).

The authors

hypothesize that an infectious agent transmitted primarily from

house cats could account for these observations of schizophrenia.

Transmission of toxoplasmosis from cats to pregnant women has

been well documented and can result in the transplacental

infection of the fetus; presumably, a virus could be similarly

transmitted either during pregnancy or after birth. Exposure to

influenza, other concurrent infections, or perinatal trauma

resulting in disruption of placental barriers might increase the

risk of transmission.

Cats were rarely

kept as pets in Europe or America until the 19th

century; before then they were generally associated with the

devil, often burned on religious holidays, and kept primarily in

barns and granaries to control rodents (Mery 1967). During the

second half of the 19th century, cats increased

rapidly in popularity as pets; the first English cat show took

place in London’s Crystal Palace in 1871, and the first show

in America was in Bangor, Maine in 1884 (Simpson 1903). The

American increase was referred to as a “cat craze” or

“cat cult” (Repplier 1892); in advertising it was said

that “the 1850s would prove to be the beginning of the boom,

for cats would be seen everywhere until the last 1920s”

(Lynnlee 1990, p. 25).

House cats, like

schizophrenia, are common in northern areas in Europe and America

and much less common in tropical countries. Northern European

countries are said to be “famous for their love of

cats” (Mery 1967, p. 288), and house cats are abundant in

western Ireland and northern Sweden. It is possible that exposure

to English house cats accounts for the high incidence of

schizophrenia among Afro-Caribbean immigrants, especially since

the increased incidence is more marked in the second-generation

immigrants who are born in England (Harrison et al. 1988; Wessely

et al. 1991). Regarding the reported increased incidence of

schizophrenia among the offspring of the 1944-45 Dutch famine, it

is known that the Dutch people, presumably including pregnant

women, ate cats as the famine progressed (Dr. Ezra Susser,

personal communications, March 1994).

In the United

States studies since 1880 have consistently shown the New England

and Pacific Coast States to have comparatively high prevalences

of schizophrenia (Torrey and Bowler 1990). Maine, well known for

its coon cats, was a leader in popularizing house cats in

America, as were the New England States in general (Winslow 1900;

Tibbetts 1903). Large numbers of cats also accompanied miners to

the Pacific Coast States during the Gold Rush years (Bretnar

1978). Even today, the New England and Pacific Coast States have

a high incidence of cat ownership in comparison with other States

(American Veterinary Medical Association 1992). By comparison,

the rural Hutterites, among whom the prevalence of schizophrenia

is very low (Eaton and Weil 1955), are reported to restrict cats

to the barn and almost never keep them as house pets (Dr. John A.

Hostetler, personal communication, October 1993).

Urban living

might be a risk factor for schizophrenia, because cats are kept

as house pets more commonly in cities than in rural areas, where

they often remain outdoors or in the barn. Crowding might

increase the exposure of pregnant women and young children to

house cats by increasing cat-human contacts. The observed excess

winter-spring seasonality of schizophrenia births might be due to

cats and people spending more time indoors during the cooler and

rainier months.

If schizophrenia

is a feline zoonosis, it could be caused by a known feline

infectious agent, a yet-to-be-characterized infectious agent, or

an environmental factor associated with exposure to cats.

Infectious diseases known to be capable of being spread from cats

to humans include diseases caused by the following: viruses

(rabies, cowpox); bacteria (anthrax, campylobacter infection, cat

scratch disease, diphtheria, leptospirosis, listeriosis, Lyme

disease, plague, salmonellosis, shigellosis, streptococcal

infection, tularemia, and yersinia infection); rickettsia (Q

fever); fungi (blastomycocis, dermatophytoses, sporotrichosis);

helminths (cutaneous and visceral larval migrans); cestodes

(diphylidiasis, echinococcus); protozoa (amebiasis,

cryptosporidiosis, giardiasis, toxoplasmosis, trichomoniasis);

and ectoparasites (scabies) (Lappin 1993). Transmission of these

agents from cats to humans may occur through direct contact

(e.g., a bite in rabies or a scratch in cat scratch disease),

exposure to urine or feces (e.g., flea bites in plague), or

contaminated foods (e.g., milk in Q fever), or through a

combination of these contacts. Feline zoonosis usually involves

more than one animal reservoir, especially in rural areas where

farm animals are common.

In addition to

these known causes of feline zoonoses, numerous feline

retroviruses have been identified that cause systemic and

neurological feline diseases. Human infection with the type C

exogenous retrovirus feline leukemia virus has been suspected

because of the fact that the virus can infect human cells in

vitro, but human transmission has not been proven (Loar 1987).

Another feline retrovirus, the feline immunodeficiency virus, has

been intensively studied regarding its possible transmission to

humans (Sparger 1993). One strain (Hardy Zuckerman-5) of a

related feline retrovirus, the feline sarcoma virus, has

nucleotide sequence homology to human receptors for the cytokine

colony-stimulating factor (CSF-1). This virus contains within its

genome coding region a 30-nucleotide CAG triplet repeat similar

to the nucleotide triplet repeats associated with

Huntington’s disease, fragile X syndrome, myotonic

dystrophy, and other human genetic diseases with behavioral

manifestations (Ross et al. 1993).

The hypothesis

that schizophrenia is a feline viral zoonosis is also compatible

with the genetics of schizophrenia, since virtually all viral

infections are known to have genetically determined

susceptibilities. A possible interaction of viruses and genes

might occur if a feline retrovirus became incorporated into the

human genome. Alternatively, some familial clustering of

schizophrenia that appears to be genetic may in fact be caused by

a chronically infected family cats, a type of “typhoid

tabby,” as has been documented to account for some clusters

of human toxoplasmosis (Teutsch et al. 1979).

To test the

hypothesis that schizophrenia is a feline zoonosis, a

questionnaire was administered to 165 parents who were members of

the National Alliance for the Mentally Ill and whose child had

been diagnosed as being seriously mentally ill, mostly with

schizophrenia. Under a case-control method the parents were asked

to have a friend whose child had not become mentally ill complete

an identical questionnaire. A question regarding exposure to cats

during pregnancy or childhood (up to age 10) was included in a

two-page questionnaire covering such subjects as breastfeeding,

developmental milestones, coordination, childhood social

interaction, family history of serious mental illnesses,

rheumatoid arthritis, and multiple sclerosis. The only two

questions on which there were differences between the groups were

on breastfeeding (mentally ill individuals were more likely to

have been breastfed, (p=0.002, c 2) and on

exposure to cats. Among the individuals with serious mental

illnesses, 84 of the 165 (51%) had had a house cat in childhood

versus 65 (38%) of the 165 case controls (p=0.02, c 2; however,

with the Bonferroni correction for number of questions asked,

statistical significance would require p<0.01).

In summary, it

is suggested that house cats may be an important environmental

factor in the development of schizophrenia. It should be

emphasized that this suggestion is preliminary and that there is

no reason at this time for anyone to change behavior toward cats

or cat ownership. Future studies should be directed at confirming

this epidemiological association. If it is confirmed, additional

efforts should be directed at characterizing the agents involved

in disease transmission and in developing methods for reducing or

eliminating the environmental risk.

Note: The

authors wish to emphasize that nobody needs to change behavior

toward cats on the basis of the following preliminary hypothesis.

One of the authors continues to own two cats; the other author

continues to allow the neighbor’s cat, who believes she owns

all houses in the neighborhood, to visit regularly.


requests should be sent to Dr. E. F. Torrey, NIMH Neuroscience

Center, St. Elizabeths Hospital, Washington, DC 20032.



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