Transmission of T. gondii

Although Toxoplasma gondii, the protozoan parasite that causes toxoplasmosis, was identified in 1908, it took more than half a century to identify felines as its primary host. By 1959 it was alleged that “dogs and cats have been most frequently suspected”(1) but it was the work of William Hutchinson in the 1960s that convincingly demonstrated the importance of oocysts shed in cat feces in the transmission of T. gondii (2-3) This was followed in 1969 by Gordon Wallace’s report showing an absence of T. gondii on remote Pacific islands where there were no cats (4). Therefore, in 1971, the United States Public Health Service recommended that pregnant women should avoid contact with cat feces to avoid becoming infected.

T. gondii can be acquired by humans in several different ways. It may be transmitted as a tissue cyst, usually by eating undercooked meat from an infected animal, or as an oocyst.

Ingestion of Tissue cysts

The infection of mammals with T. gondii  is widespread. Such infections occur when farm animals ingest feed containing cat feces; when grazing animals inhale or ingest dried cat feces deposited on the ground; and when an animal eats a smaller animal, such as a mouse or rat that is infected. T. gondii  then invades many parts of the body, especially muscles, where it becomes tissue cysts and remains for life. When the muscle is eaten as meat, especially if it has not been thoroughly cooked, the person becomes infected.

Lamb and pork are thought to be the most common source of T. gondii  tissue cysts for humans, although cysts also occur in beef, chicken, and wild animal meat (e.g., deer, moose, bear). There have even been epidemics of adult toxoplasmosis among individuals who ate undercooked meat, such as hamburger, from a common source (5).

Ingestion or Inhalation of Oocysts

As previously noted, approximately 1.5 million cats (1 percent of 150 million) in the United States are excreting oocysts on any given day; they may excrete up to 20 million oocysts per day, and the oocysts may live for a year or longer. Thus, wherever cats defecate is likely to be a source of contamination. Children’s play areas and sandboxes are common places for cats to defecate because they can use the area’s loose soil or sand to bury their feces. Children may become infected by putting dirty hands, including oocysts, in their mouths. One study of young children reported that children who are under three years of age put their hands or other objects in their mouths every 2 to 3 minutes (6) Another study, which included 64 children between one and four years old, carried out in a Massachusetts day care center reported that the children ingested a median of 40 mg of soil per day; furthermore, one child consumed 5 to 8 g of soil per day on average (7) A family epidemic was described as having occurred this way (8).

As the cat feces dry, the oocysts may become aerosolized. They can thus be inhaled by a person changing cat litter or just walking in an area where cats have defecated. An outbreak of toxoplasmosis among patrons of a riding stable was thought to have occurred in this manner (9).

Sandboxes (also called sandpits) are of special interest. Studies of sandboxes in public parks have been carried out in Japan. In one study, 12 of the 13 sandboxes were contaminated with animal feces; the “mean number of feces found in 1 square meter of the sandpits was 35” (10) In another study of three public sandboxes observed over 140 days, an average of 2.3 cat defecations occurred each day in each sandbox (11).

Assuming that 1 percent of the cats were infected, that each infected cat excreted 10 million oocysts each time it defecated, and that the oocysts remained viable for one year, each sandbox would contain approximately 85 million viable oocysts at any given time. For children playing in such a sandbox, the chances of inhaling or ingesting (e.g., by putting fingers in mouth) T. gondii  oocysts would appear to be high. This mode of transmission should not surprise us; as early as 1981 Frenkel and Ruiz, based on their studies in Costa Rica, speculated that “children start to become infected when they play in soil and sand, at an age when they are particularly prone to place their (soiled) fingers in their mouths” (12) .

Gardens are also commonly used by cats for defecation and are also thought to be a common source of infection by inhalation for gardeners. Unwashed vegetables from gardens can also carry oocysts. Studies have also shown that cockroaches and flies can carry oocysts from cat feces to fruits and vegetables (13-14). Another possible mode of transmission is by dogs that roll in cat feces. One study reported that 23 percent of dogs did this, suggesting “the contamination of fur, after rolling in cat feces containing oocysts, might make these accessible to children who pet dogs” (15).

Water infected with T. gondii  oocysts is increasingly suspected of being a major source of transmission (16). The water is thought to become contaminated by runoff from areas where cats defecate. Several epidemics of toxoplasmosis have been reported due to contaminated water, most notably a 1995 epidemic in Victoria, British Columbia, due to the contamination of the city water supply by cat feces (17).

Finally, in a disturbing finding, researchers reported that you may even become infected with T. gondii oocysts by touching the keypad of an ATM.  Presumably the previous user had been gardening and had oocysts on their fingers (18).

The relative importance of different modes of T. gondii  transmission has been widely debated but minimally studied. In countries like France, which has a high rate of T. gondii -infected individuals, the most important source of transmission is thought to be cysts in undercooked meat. Studies of pregnant women in Europe have identified the eating of raw or undercooked meat as the most likely source of transmission (19-21).  In countries like the United States, in which meat is generally well cooked, direct transmission of oocysts from cats especially via water, and contaminated fruits and vegetables, is thought to be more important (22). Recent studies have reported that the majority of congenital infections (23) and postnatal acute infections (24) in the United States are from oocysts.

The question has been raised whether the clinical outcome is different if a human becomes infected by a tissue cyst or an oocyst. In mice, infection by oocysts appears to be more pathogenic. In humans, “circumstantial evidence suggests that oocyst-induced infections…are clinically more severe than tissue cyst-acquired infections” (25). There are also suggestions that reinfection can occur with different strains of T. gondii (26). 

 Vertical Transmission from Infected Mother to Offspring

In humans, it is well known that if a previously uninfected woman is infected with T. gondii  while pregnant, the T. gondii  may cross the placenta and cause brain damage (e.g., cysts, seizures, mental retardation) in the offspring. This is why women are cautioned to not change cat litter while they are pregnant.

In female mice, it is known that a mouse which has been infected with T. gondii, even before becoming pregnant, may pass along the T. gondii  to their offspring. This may occur in subsequent litters as well so that the infected mouse mother may infect many offspring (27).  More surprising is the vertical transmission of T. gondii  from an infected mouse to its offspring, then from this offspring to its offspring, and on for up to five generations (28). This would give the appearance of being a genetic disease with maternal inheritance, but in reality, would simply be the vertical transmission of an infectious agent.

A nice summary of the studies supporting the vertical transmission of T. gondii was published in 2016 (29).

Sexual Transmission of T. gondii

A study in dogs demonstrated that T. gondii  can be transmitted sexually in that species. Male dogs were infected by T. gondii ; it was then found in their semen. The infected semen was then used to artificially inseminate four uninfected female dogs. Seven days after insemination, all four dogs had antibodies to T. gondii. Two of the pregnant dogs had miscarriages; the other two delivered four puppies, none of whom lived longer than three weeks and all of which had cysts containing T. gondii  in their brains (30). Another study demonstrated that T. gondii  can be sexually transmitted in rats; 43 of 69 rat pup offspring, following sexual transmission, were found to be infected (31). Most recently, it was demonstrated that T. gondii  can be sexually transmitted in sheep; infected males were able to infect previously-uninfected females and the infection was then transmitted vertically to their lambs (32).

There is also evidence that T. gondii  can be sexually transmitted in humans. How often this actually happens and its clinical importance are unknown. A study in Germany examined semen collected from 125 men who were being examined for possible infertility. Among the 125, 3 men had evidence of T. gondii in their semen. Two of the men also had blood antibodies to T. gondii, but the third did not. One man had urethritis and another had gonorrhea (33).

An American study examined the testes of 10 men who had died from AIDS and T. gondii  opportunistic infection. In 6 of the 10 cases bradyzoite-filled cysts were identified in the testes. In 4 of these 6 cases, the only other organ in which T. gondii  was found was the brain (34). In another study 22% of the semen of male sheep was infected with T. gondii (35).

Timing of Infection by T. Gondii

Since many people are infected by T. gondii who show no apparent effects of the infection, the question is why. Genetic differences and strain differences are likely explanations. Another possible explanation is difference in the timing of the infection since the human brain is undergoing constant change during childhood and adolescence.

To test this hypothesis Kannan et. al. at Johns Hopkins infected juvenile mice (33 days) and adult mice with T. gondii and assessed differences in outcomes. Significant differences were seen on several measures including prepulse inhibition; immune response; and the distribution in brain areas of several neurotransmitters (GABA, glutamate, dopamine, serotonin, norepinephrine) (36).

Do people with close cat contact have a greater chance of being infected with T. gondii?

As noted previously, T. gondii  can be transmitted from cats to humans in many different ways. Being bitten by a cat, however, apparently does not cause the transmission of T. gondii  (37). Some of the means of transmission require no contact whatever between cats and humans, e.g., through tissue cysts in undercooked lamb, drinking water infected with oocysts, oocysts deposited by a neighborhood cat in your garden. For this reason, attempts to show a correlation between having antibodies to T. gondii  and past contact with cats have yielded very inconsistent results.

A review of 30 such studies reported that half of them found a correlation, but half did not (38). Those studies that were negative were more likely to have been studies of adults, e.g., pregnant women who were asked if they presently owned a cat. Those studies that were positive were more likely to have included children and teenagers, such as studies done in Costa Rica and Panama (39-40). The results varied depending on how the question was asked, with cat ownership in childhood more likely to yield a positive correlation with T. gondii  antibodies than cat ownership in adulthood. The complexity of studying human–cat contact was also illustrated by a Norwegian study that asked about cat contact in great detail. Becoming infected with T. gondii  was not statistically related to “living in a neighborhood with a cat” (p=0.71) or “living in a household with a cat” (p=0.13) but was statistically significantly related to “living in a household with a kitten less than 1 year old” (p=0.04) (41). An American study reported that living in a household with one or two kittens was not a significant risk factor for becoming infected with T. gondii, but living in a household with three or more kittens was a highly significant risk factor (OR 35.4) (42).

Assessing the transmission from cats to humans is made even more complex by the fact that some breeds of cats are more likely to carry T. gondii than other breeds are; a study of 8 cat breeds reported that T. gondii seropositivity varied widely from a low of 16-18% among Korats and Burmese to 60% among Persians (43).

Do children with close cat contact have a greater chance of developing schizophrenia?

In view of the above, it is of interest that all four studies that have assessed cat contact during childhood reported that it was significantly more common in individuals with schizophrenia than in controls. In the first study of 165 parents of individuals with schizophrenia and bipolar disorder, 51 percent reported that they owned a cat during pregnancy or during the first 10 years of life of the affected individuals, compared to 38 percent among matched controls (p=0.02, chi square; however, this was not corrected for the number of questions asked, which would require a p<0.01 using a Bonferroni correction). The question was asked for four different periods, and the results were as follows:

Owned cat
During pregnancy Birth to 1 yr 1–5 yrs 6–10 yrs
Subjects 18% 16% 29% 43%
Controls 13% 15% 28% 34%

Thus, the largest difference in the ages for cat ownership was for ages 6–10. Dog or other pet ownership was not included in this questionnaire (44).

The second study included 264 mothers of individuals with schizophrenia or bipolar disorder and 528 matched controls and included questions on both cat and dog ownership as follows:

Owned cat Owned dog
During pregnancy Birth to age 13 During pregnancy Birth to age 13
Subjects 17% 52% 31% 73%
Controls 16% 42% 39% 78%

Families in which the individual later developed schizophrenia or bipolar disorder were significantly more likely to have owned a cat, but not a dog, between birth and age 13 (p=0.0072) but not during the pregnancy (45).

A third study, based on a 1982 questionnaire to 2,125 members of NAMI, used 4,847 controls that were not ideally matched to the cases, yet produced results that were very similar to the first two studies; 51% of the cases had owned a cat between birth and age 13 compared to 43% of the controls (46).

Finally, a fourth study, carried out in Turkey, reported a striking difference in cat ownership in childhood among 300 individuals with schizophrenia (59%) and 150 blood donor controls (9%) (47).

These four studies are summarized on the following table:

Cases Controls
1992 questionnaire Cat in house, birth to age 10 84/165 (51%) 65/165 (39%) p=.03; OR= 1.60 (1.00-2.53)
1997 survey Cat ownership, birth to age 13 136/262 (52%) 220/522 (42%) p=.01; OR=1.48 (1.09-2.02)
1982 questionnaire Cat ownership, birth to age 13 1075/2125 (51%) 2065/4847 (43%) p≤.0001; OR=1.38 (1.25-1.53)
2010 Turkish study Cat ownership, birth to age 13 176/300 (59%) 14/150 (9%) p< .001


Dog ownership in childhood shows no association with schizophrenia.  Cat ownership in childhood is thus a clearly established risk factor for later being diagnosed with this disease.

A few of the T. gondii  antibody studies (see section V) have also collected information on cat exposure. For example, a Turkish study of 73 patients with first-episode schizophrenia and 40 controls reported that 15/73 (28%) of the patients had a cat in their house compared to 1/40 (3%) of the controls (p=0.006) (48).



  1. Beattie CP. Discussion on Toxoplasmosis, Epidemiology of Toxoplasmosis, Proc Roy Soc Med 1959;53: 108-110.
  2. Hutchinson WM. Experimental transmission of Toxoplasma gondii. Nature. 1965;206: 961-2
  3. Hutchinson WM. The nematode transmission of Toxoplasma gondiiTrans Roy Soc Trop Med Hyg. 1967; 61: 80-89.
  4. Wallace GD. Serologic and epidemiologic observations on toxoplasmosis on three pacific atolls. Am J Epidemiol. 1969; 90: 103-111.
  5. Kean BH, Kimball AC, Christenson WN. An epidemic of acute toxoplasmosis. JAMA. 1969;208:1002–1004.
  6. Black RE, Merson MH, Huq I, Alim AR, Yunus M. Incidence and severity of rotavirus and Escherichia colidiarrhoea in rural Bangladesh. Implications for vaccine development. Lancet. 1981;1:141-3.
  7. Calabrese EJ, Barnes R, Stanek EJ 3rd, et al. How much soil do young children ingest: an epidemiologic study. Regul Toxicol Pharmacol. 1989;10:123-37.
  8. Stagno S, Dykes AC, Amos CS, et al. An outbreak of toxoplasmosis linked to cats Pediatrics. 1980;65:758–762, copyright 1980, the American Academy of Pediatrics; linked to PDF file with permission.
  9. Teutsch SM, Juranek DD, Sulzer A, et al. Epidemic toxoplasmosis associated with infected cats. N Engl J Med. 1979;300:695–699.
  10. Uga S. Prevalence of Toxocara eggs and number of faecal deposits from dogs and cats in sandpits of public parks in Japan. J Helminthol. 1993;67:78–82
  11. Uga S. Minami T, Nagata K. Defecation habits of cats and dogs and contamination by Toxocara eggs in public park sandpits. Am J Trop Med Hyg. 1996;54:122–126.
  12. Frenkel JK, Ruiz A. Endemicity of toxoplasmosis in Costa Rica. Am J Epidemiol. 1981; 113: 254-258.
  13. Wallace GD. Experimental transmission of Toxoplasma gondii by cockroaches. J Infect Dis. 1972;126:545–547.
  14. Wallace GD. Experimental transmission of Toxoplasma gondii by filth-flies. Am J Trop Med Hyg. 1971;20:411–413.
  15. Frenkel JK, Parker BB. An apparent role of dogs in the transmission of Toxoplasma gondii : the probable importance of xenosmophilia. Ann NY Acad Sci. 1996;791:402–407.
  16. Dubey JP. Toxoplasmosis—a waterborne zoonosis. Vet Parisit. 2004;126:57–72.
  17. Bowie WR, King AS, Werker DH, et al. Outbreak of toxoplasmosis associated with municipal drinking water. Lancet. 1997;350:173–177, copyright 1997; linked to PDF file with permission from Elsevier.
  18. Bik, H.M., Maritz, J.M., Luong, A. et al. Microbial Community Patterns Associated with Automated Teller Machine keypads in New York City. mSphere 2016; 1 (6). Doi: 10.1128/mSphere00226-16.
  19. Kapperud G, Jenum PA, Stray-Pedersen B, et al. Risk factors forToxoplasma gondii infection in pregnancy: results of a prospective case-control study in Norway. Am J Epidemiology. 1996;144:405–412.
  20. Baril L, Ancelle T, Goulet V, et al. Risk factors for Toxoplasmainfection in pregnancy: a case-control study in France. Scand J Infect Dis. 1999;31:305–309.
  21. Cook AJC, Gilbert RE, Buffolano W, et al. Sources of Toxoplasma infection in pregnant women: European multicentre case-control study. Br Med J. 2000;321:142–147.
  22. Boyer K, Hill D, Mui, E, et al. Unrecognized ingestion of Toxoplasma gondii oocysts leads to congenital toxoplasmosis and causes epidemics in North America. Clin Infect Dis. 2011;53:1081-9.
  23. Boyer K, Hill D, Mui E, et al. Unrecognized ingestion of Toxoplasma gondii oocysts leads to congenital toxoplasmosis and causes epidemics in North America. Clin Infect Dis. 2011;53:1081-9.
  24. Hill D, Coss C, Dubey JP, et al. Identification of a sporozoite-specific antigen from Toxoplasma gondii. J Parasitol. 2011;97:328-37.
  25. Dubey JP. Toxoplasmosis—a waterborne zoonosis. Vet Parisit. 2004;126:57–72.
  26. (Elbez-Rubinstein A, Ajzenberg D, Dardé M-L, et al. Congenital toxoplasmosis and reinfection during pregnancy: case report, strain characterization, experimental model of reinfection, and review. J Infect Dis. 2009;199:280–285.
  27. Owen MR, Trees AJ. Vertical transmission ofToxoplasma gondii from chronically infected house (Mus musculus) and field (Apodemus sylvaticus) mice determined by polymerase chain reaction. Parasitology. 1998;116:299-304.
  28. Beverly JKA. Congenital transmission of Toxoplasmosis through successive generations of mice. Nature. 1959;183:1348-1349.
  29. Hide G, Role of vertical transmission of Toxoplasma gondii in prevalence of infection. 2016. Expert Review of Anti-Infective Therapy 14: 335-344.
  30. Arantes TP, Lopes WD, Ferreira RM, et al. Toxoplasma gondii : evidence for the transmission by semen in dogs. Exp Parasitol. 2009;123:190–194.
  31. Dass SAH, Vasudevan A, Dutta D, et al. Protozoan parasite Toxoplasma gondii manipulate mate choice in rats by enhancing attractiveness of males. PLoS One. 2011;11:e27229. doi:10.1371/journal.pone.0027229.
  32. Lopes WDZ, Rodriguez JD, Souza FA, et al. Sexual transmission of Toxoplasma gondii in sheep. Vet Parasitol. 2013;195:47-56).
  33. Disko R. Braveny I, Vogel P. Untersuchungen zum Vorkommen vonToxoplasma gondii im menschlichen Ejakulat. [Studies on the occurrence of Toxoplasma gondii  in the human ejaculate]. Z. Tropenmed. Parasitol. 1971;22:391-6.
  34. De Paepe M, Guerrieri C, Waxman M. Opportunistic infections of the testis in the Acquired Immunodeficiency Syndrome. Mt Sinai J Med. 1990;57:25-29.
  35. Bezerra MJG, et al. Detection of Toxoplasma gondii DNA in Fresh and Frozen Semen from Rams in Brazil. Reprod Dom Anim.2014; 49: 753-755.
  36. Kannan et al. Anit-NMDA receptor autoantibodies and associated neurobehavioral pathology in mice are dependent on age of first exposure to Toxoplasma gondii. Neurobiology of Disease 2016. 91: 307-314.
  37. Westling K, Jorup-Ronstrom C, Evengard B. Toxoplasmosis not transmitted by cat bite, but high prevalence of antibodies to Toxoplasma gondii in patients bitten by their own cat. Scand J Infect Dis. 2010; 42:687–690.
  38. Hall S, Ryan M, Buxton D. The epidemiology of Toxoplasma infection. In Joynson DHM, Wreghitt TG, eds, Toxoplasmosis: A Comprehensive Clinical Guide, Cambridge: Cambridge University Press; 2001:85–91.
  39. Sousa OE, Saenz RD, Frenkel JK. Toxoplasmosis in Panama: a 10-year study. Am J Trop Med Hyg. 1988;38:315–322.
  40. Frenkel JK, Ruiz A. Human toxoplasmosis and cat contact in Costa Rica. Am J Trop Med Hyg. 1980;29:1167–1180.
  41. Kapperud G, Jenum PA, Stray-Pedersen, et al. Risk factors for Toxoplasma gondii infection in pregnancy: results of a prospective case-control study in Norway. Am J Epidemiol. 1996;144:405–412.
  42. Jones JL, Dargelas V, Roberts J, et al. Risk factors for Toxoplasma gondii infection in the United States. Clin Infect Dis. 2009;49:878–884.
  43. Hytonen M, Lohi H, Jokelainene P. Toxoplasma gondii seroprevalence in eight cat breeds. International Conference on Toxoplasmosis poster, Gettysburg, PA. June 2015.
  44. Torrey EF, Yolken RH. Could schizophrenia be a viral zoonosis transmitted from house cats? Schizophr Bull. 1995;21:167–171.
  45. Torrey EF, Rawlings R, Yolken RH. The antecedents of psychoses: a case-control study of selected risk factors. Schiz Res. 2000;46:17–23.
  46. Torrey EF, Simmons W, Yolken RH, Is childhood cat ownership a risk factor for schizophrenia later in life? Schiz Res 2015; 165: 1-2.
  47. Yuksel P, et al. The role of latent toxoplasmosis in the aetiopathogenesis of schizophrenia–the risk factor or an indication of a contact with cat? Folia Parasit. 2010; 57 (2): 121-128.
  48. Tanyuksel M, Uzun O, Araz E, et al. Possible role of toxoplasmosis in patients with first-episode schizophrenia. Turk J Med Sci. 2010;40:399–404.