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.

, 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.


Veterinary Medical Association. The Veterinary Service Market
for Companion Animals 1992
. Schaumberg, IL: Center for
Information Management, American Veterinary Medical Association,

Barr, C.E.;
Mednick, S.A.; and Munk-Jørgensen, P. Exposure to influenza
epidemics during gestation and adult schizophrenia. Archives
of General Psychiatry
, 47:869-874, 1990.

Book, J.A.;
Wetterberg, L.; and Modrzewska, K. Schizophrenia in a North
Swedish geographical isolate 1900-1977: Epidemiology, genetics
and biochemistry. Clinical Genetics, 14:373-394, 1978.

Boyd, J.H.;
Pulver, A.E.; and Stewart, W. Season of birth: Schizophrenia and
Bipolar Disorder. Schizophrenia Bulletin, 12(2):173-186,

Bradbury, T.N.,
and Miller, G.A. Season of birth in schizophrenia: A review of
evidence, methodology and etiology. Psychological Bulletin,
98:569-594, 1985.

Bretnar, R.
Bring cats! The American West, 15:32-60, 1978.

Eaton, J.W., and
Weil, R.J. Culture and Mental Disorders: A Comparative Study
of the Hutterites and Other Populations
. Glencoe, IL: Free
Press, 1955.

Harrison, G.;
Owens, D.; Holton, A.; Neilson, D.; and Boot, D. A prospective
study of severe mental disorder in Afro-Caribbean patients.
Psychological Medicine
, 18:643-657, 1988.

Kirch, D.G.
Infection and autoimmunity as etiologic factors in schizophrenia:
A review and reappraisal. Schizophrenia Bulletin,
19(2):355-370, 1993.

Lappin, M.R.
Feline zoonotic diseases. Veterinary Clinics of North America
Small Animal Practice
, 23:57-78, 1993.

Loar, A.S. The
zoonotic potential of feline leukemia virus. Veterinary
Clinics of North America Small Animal Practice
, 17:105-115,

Lynnlee, J.L.
Purrfection: The Cat. West Chester, PA: Schiffer
Publishing Company, 1990.

McNeil, T.F.
Obstetric factors and perinatal injuries. In: Tsuang, M.T., and
Simpson, J.C., eds. Handbook of Schizophrenia: Nosology,
Epidemiology and Genetics
. Vol. 3. Amsterdam, The
Netherlands: Elsevier, 1988. pp. 319-344.

Mednick, S.A.;
Machon, R.A.; Huttunen, M.O.; and Bonnett, D. Adult schizophrenia
following prenatal exposure to an influenza epidemic. Archives
of General Psychiatry
, 45:189-192, 1988.

Mery, F. The
Life, History and Magic of the Cat
. London, England: Paul
Hamlyn, 1967.

Murray, R.M.;
O’Callaghan, E.; Castle, D.J.; and Lewis, S.W. A
neurodevelopmental approach to the classification of
schizophrenia. Schizophrenia Bulletin, 18(2):319-332,

E.; Sham, P.; Takei, N.; Glover, G.; and Murray, R.M.
Schizophrenia after prenatal exposure to 1957 A2 influenza
epidemic. Lancet, 337:1248-1250, 1991.

Repplier, A.
Agrippina. Atlantic Monthly, 69:753-763, 1892.

Ross, C.A.;
McInnis, M.G.; Margolis, R.L.; and Li, S.H. Genes with triplet
repeats: Candidate mediators of neuropsychiatric disorders. Trends
in Neuroscience
, 16:254-260, 1993.

Sham, P.C.;
O’Callaghan, E.; Takei, N.; Murray, G.K.; Hare, E.H.; and
Murray, R.M. Schizophrenia following pre-natal exposure to
influenza epidemics between 1939 and 1960. British Journal of
, 160:461-466, 1992.

Simpson, F. The
Book of the Cat
. New York, NY: Cassell and Company, 1903. pp.

Sparger, E.E.
Current thoughts of feline-immunodeficiency virus infection. Veterinary
Clinics of North America Small Animal Practice
, 23:173-191,

Stevens, J.R.,
and Hallick, L.M. Viruses and schizophrenia. In: Specter, S.;
Bendinell, M.; and Friedman, H., eds. Neuropathogenic Viruses
and Immunity
. New York, NY: Plenum Press, 1992. pp. 303-316.

Stroup, A.L.,
and Manderscheid, R.W. The development of the State mental
hospital system in the United States: 1840-1980. Journal of
the Washington Academy of Sciences
, 78:59-68, 1988.

Susser, E.S.,
and Lin, S.lP. Schizophrenia after prenatal exposure to the Dutch
hunger winter of 1944-1945. Archives of General Psychiatry,
49:983-988, 1992.

Teutsch, S.M.;
Juranek, D.D.; Sulzer, A.; Dubey, J.P.; and Sikes, R.K. Epidemic
toxoplasmosis associated with infected cats. New England
Journal of Medicine
, 300:696-699, 1979.

Tibbetts, E.L.
The long-haired cat in Maine. Fortnightly Cattarian,
3:119-120, 1903.

Torrey, E.F. Schizophrenia
and Civilization
. New York, NY: Jason Aronson, 1980.

Torrey, E.F.
Functional psychoses and viral encephalitis. Integrative
, 4:224-236, 1986.

Torrey, E.F.,
and Bowler, A. Geographical distribution of insanity in America:
Evidence for an urban factor. Schizophrenia Bulletin,
16(4):591-604, 1990.

Torrey, E.F.;
McGuire, M.; O’Hare, A.; Walsh, D.; and Speilman, M.P.
Endemic psychosis in western Ireland. American Journal of
, 141:966-969, 1984.

Weinberger, D.R.
Implications of normal brain development for the pathogenesis of
schizophrenia. Archives of General Psychiatry, 44:660-669,

Wessely, S.;
Castly, D.J.; Der, G.; and Murray, R.M. Schizophrenia and
Afro-Caribbeans. British Journal of Psychiatry,
159:795-801, 1991.

Winslow, H.M.
Concerning Cats. Boston, MA: Lothrop, 1900. pp. 133-138.