Public Health Agency of Canada
Symbol of the Government of Canada

Share this page

Toxoplasma gondii - Pathogen Safety Data Sheet

SECTION I - INFECTIOUS AGENT

NAME: Toxoplasma gondii

SYNONYM OR CROSS REFERENCE: Toxoplasmosis, congenital toxoplasmosis, toxoplasma infection Footnote 1Footnote 2.

CHARACTERISTICS: Toxoplasma gondii belong to the phylum Apicomplexa and family Sarcocystidae. They are obligate intracellular parasitic protozoa Footnote 3. Toxoplasma gondii is a parasite of birds and mammals. Felines are the only definitive host and the only animals that pass infective oocysts in their feces. Warm-blooded animals, including humans, are intermediate hosts that harbour tissue cysts in their bodies. Three major infectious stages and major morphological forms occur: oocyst-containing two sporocysts and four sporozoites each, quickly-multiplying tachyzoites, and slow-growing bradyzoites contained in persistent tissue cysts Footnote 3. Infection is most often initiated through the ingestion of oocysts containing sporozoites or cysts containing bradyzoites in contaminated food or water. Following ingestion, the sporozoites or bradyzoites invade the intestinal epithelium and differentiate to tachyzoites, which disseminate and replicate within the new host. In feline infections, T.gondii sexual reproduction is enteroepithelial and asexual reproduction is extraintestinal. Intermediate hosts only experience extraintestinal infection Footnote 4. Generally, oocysts are spherical and measure 10x12 µm, sporozoites measure 2x6 µm, tachyzoites are crescent-shaped and 2x6 µm, tissue cysts are spheroid and have a diameter of 5 µm - 70 µm, bradyzoites measure 7x1.5 µm Footnote 4Footnote 5.

SECTION II - HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Toxoplasma gondii infection is usually non-pathogenic in immunocompetent adults. The major pathogenic factor is proliferation of tachyzoites, destroying host cells faster than they can regenerate. In acute infection, mild symptoms can arise, including fever, rash, headache, lymphadenopathy, organomegaly (liver and/or spleen), weight loss, weakness, pneumonia, and myalgia Footnote 6. More severe symptoms are rare and mostly affect immunocompromised patients, although they can also develop in immunocompetent individuals. These include retinochoroiditis, and severe encephalitis Footnote 6. Congenital infection can result in abortion or stillbirth, and live births may demonstrate the congenital toxoplasmosis syndrome - mental retardation, malformation, retinochoroiditis, strabismus, nystagmus, microphthalmia, and cataracts Footnote 6Footnote 7. Severity of transplacental infection is inversely proportional to gestational age, but the rate of vertical transmission is more frequent as the pregnancy progresses Footnote 7. Persisting tissue cysts in a victim’s brain may cause psychosis Footnote 8. Ocular toxoplasmosis is responsible for 30% – 60% of retinochoroiditis cases Footnote 6.

EPIDEMIOLOGY: Worldwide distribution. An estimated 15% - 85% of adults have a chronic infection, depending on where they live Footnote 3. In France, seropositivity is near 90% Footnote 6. There is a higher prevalence of oocysts in the environment in moist and hot regions than in dry or cold regions Footnote 2. A documented outbreak of acute toxoplasmosis due to contaminated drinking water affected 110 individuals in Vancouver in 1995 Footnote 2.

HOST RANGE: Cats and other felines, humans, and warm-blooded vertebrates, including most mammals and birds Footnote 3. Flies and cockroaches that have fed on infected cat feces can transmit oocysts to food in their own feces Footnote 2Footnote 9.

INFECTIOUS DOSE: As few as 10 sporulated oocysts in intermediate hosts Footnote 2.

MODE OF TRANSMISSION: Transmitted by consuming poorly-cooked infected meats (pork, mutton, beef) Footnote 10; ingestion of water, food, or milk contaminated with oocysts Footnote 8; inhalation of aerosols containing oocysts Footnote 11; and contact with sand or soil contaminated by cat feces Footnote 10. Transplacental transmission is possible if the mother has an acute infection during pregnancy Footnote 7. Transmission is also possible through blood transfusions and organ transplants Footnote 12. Food can be infected either by flies and cockroaches or by the use of tainted water in the agricultural industry Footnote 2Footnote 9. Consumption of unwashed raw vegetables or fruits also increases risk of infection Footnote 2. Children can be infected via contaminated sandboxes or playgroundsFootnote 13.

INCUBATION PERIOD: If inoculated with a mixture of tachyzoites and bradyzoites, tissue cysts can form as early as 2-3 days post-infection, although a clinical presentation of toxoplasmosis may not arise Footnote 5; 4-20 days (in cats) Footnote 4.

COMMUNICABILITY: Toxoplasma gondii are not horizontally transmitted from person-to-person but can be transmitted vertically, or during organ transplants Footnote 7Footnote 12. Oocysts shed by cats become infective (sporulate) 1-5 days later, depending on aeration and temperature Footnote 14.

SECTION III - DISSEMINTATION

RESERVOIR: The definitive hosts are cats. The intermediate hosts are warm-blooded animals, including most mammals and birds Footnote 3.

ZOONOSIS: Yes, direct or indirect contact of mucous membranes with oocysts from feces of infected animals Footnote 3. Flies and cockroaches that have fed on oocyst infected cat feces can transmit them to food Footnote 2Footnote 9.

VECTORS: None, however cockroaches and flies can transmit oocysts in their feces, contaminating human food Footnote 9.

SECTION IV - STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Although tissue cysts cannot be specifically targeted, many drugs are used against the other morphological forms. This includes pyrimethamine trimethoprim-sulfamethoxazole (160 mg/800 mg), pyrimethamine-sulfadoxin (75 mg/1500 mg), sulfadiazine-pyrimethamine, with or without folinic acid rescue Footnote 12Footnote 15.

SUSCEPTIBILITY TO DISINFECTANTS: Tachyzoites and tissue cysts are susceptible to detergents, including 1% sodium hypochlorite, and 70% ethanol Footnote 2Footnote 16. Oocysts are resistant to most disinfectants, but 10% formalin decreases viability significantly Footnote 17. Treatment of oocysts with 1.3% sodium hypochlorite removes the outer layer Footnote 5. Bradyzoites are resistant to acid-pepsin digestion Footnote 5.

PHYSICAL INACTIVATION: Tissue cysts die in 6% NaCl solutions Footnote 2. Cysts can be killed with gamma irradiation at a dose of 1.0 kGy Footnote 2. High pressure processing at 300 MPa or higher inactivates tissue cysts Footnote 2. Heating tissue cysts to 67°C will kill them instantly Footnote 2. Cysts in meat can be killed by heating the meat to >60 °C or freezing it at -20 °C Footnote 18. Oocysts are killed if kept at a temperature of 55-60°C for 1-2 minutes Footnote 2. Tachyzoites are inactivated at a pH lower than 4.0 Footnote 19Footnote 20.

SURVIVAL OUTSIDE HOST: Oocysts can survive in moist soil or water for up to 18 months Footnote 2Footnote 21. They can survive in uncovered feces for 46 days and for 334 days when covered Footnote 1.

SECTION V - FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms and confirm by positive serology for IgM and IgG antibodies (i.e. by ELFA or ELISA) Footnote 6Footnote 22. Identification can also be confirmed through isolation of the parasite, PCR, and ultrasound imaging Footnote 7. Women who are intending on becoming pregnant and are at risk of exposure should be tested for Toxoplasma gondii infection Footnote 9. Fetal diagnosis can involve molecular evaluation of amniotic fluid or direct identification of the parasite by inoculation of amniotic liquid and/or fetal blood in mice Footnote 7.

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Spiramycin can be taken by women in their first trimester to prevent transplacental transmission (3.0 g/day) Footnote 7. For pregnant women in their third trimester, sulfadiazine (75 mg/Kg/day to a maximum of 4.0 g/day), and folinic acid (15 mg/3 days) are indicated Footnote 7. Pyrimethamine is teratogenic and should not be used during the first trimester Footnote 23. Prednisone is also used as an adjunct when the patient has retinochoroiditis Footnote 6.

IMMUNIZATION: None Footnote 7.

PROPHYLAXIS: Effective prophylaxis for seronegative organ transplant recipients includes pyrimethamine (25 mg/day), cotrimoxazole (trimethoprim-sulfamethoxazole), pyrimethamine-sulfadoxin (75 mg/1500 mg) Footnote 12. A treatment of sulfadiazine-pyrimethamine, and folinic acid is suitable for most patients Footnote 12Footnote 15.

SECTION VI - LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: 47 cases of laboratory infections have been reported as of 1999, as well as one death Footnote 11.

SOURCE/SPECIMENS: Infective stages may be present in blood, saliva, sputum, urine, tears, semen, milk, feces, and tissue Footnote 2Footnote 10Footnote 12.

PRIMARY HAZARDS: Parenteral inoculation, exposure to mucous membrane or skin lesions (wound), ingestion, aerosols Footnote 11.

SPECIAL HAZARDS: Feces from infected animals, for example, changing litter Footnote 1.

SECTION VII - EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes Footnote 24.

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities Footnote 24.

SECTION VIII - HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled.

SECTION IX - REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: November 2011

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Copyright © Public Health Agency of Canada, 2011 Canada

REFERENCES

Footnote 1
Dubey, J. P., & Jones, J. L. (2008). Toxoplasma gondii infection in humans and animals in the United States. International Journal for Parasitology, 38(11), 1257-1278. doi:10.1016/j.ijpara.2008.03.007
Footnote 2
Petersen, E., Vesco, G., Villari, S., & Buffolano, W. (2010). What do we know about risk factors for infection in humans with Toxoplasma gondii and how can we prevent infections? Zoonoses and Public Health, 57(1), 8-17. doi:10.1111/j.1863-2378.2009.01278.x
Footnote 3
Howe, D. K., & Sibley, L. D. (1995). Toxoplasma gondii comprises three clonal lineages: correlation of parasite genotype with human disease. The Journal of Infectious Diseases, 172(6), 1561-1566.
Footnote 4
Frenkel, J. K. (1974). Advances in the biology of sporozoa. Zeitschrift Fur Parasitenkunde (Berlin, Germany), 45(2), 125-162.
Footnote 5
Dubey, J. P., Lindsay, D. S., & Speer, C. A. (1998). Structures of Toxoplasma gondii tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts. Clinical Microbiology Reviews, 11(2), 267-299.
Footnote 6
Silva, C. S., Neves Ede, S., Benchimol, E. I., & Moraes, D. R. (2008). Postnatal acquired toxoplasmosis patients in an infectious diseases reference center. The Brazilian Journal of Infectious Diseases : An Official Publication of the Brazilian Society of Infectious Diseases, 12(5), 438-441.
Footnote 7
Lopes, F. M., Goncalves, D. D., Mitsuka-Bregano, R., Freire, R. L., & Navarro, I. T. (2007). Toxoplasma gondii infection in pregnancy. The Brazilian Journal of Infectious Diseases : An Official Publication of the Brazilian Society of Infectious Diseases, 11(5), 496-506.
Footnote 8
Zhu, S. (2009). Psychosis may be associated with toxoplasmosis. Medical Hypotheses, 73(5), 799-801. doi:10.1016/j.mehy.2009.04.013
Footnote 9
Frenkel, J. K., Hassanein, K. M., Hassanein, R. S., Brown, E., Thulliez, P., & Quintero-Nunez, R. (1995). Transmission of Toxoplasma gondii in Panama City, Panama: a five-year prospective cohort study of children, cats, rodents, birds, and soil. The American Journal of Tropical Medicine and Hygiene, 53(5), 458-468.
Footnote 10
Hofhuis, A., VAN Pelt, W., VAN Duynhoven, Y. T., Nijhuis, C. D., Mollema, L., VAN DER Klis, F. R., Havelaar, A. H., & Kortbeek, L. M. (2010). Decreased prevalence and age-specific risk factors for Toxoplasma gondii IgG antibodies in The Netherlands between 1995/1996 and 2006/2007. Epidemiology and Infection, , 1-9. doi:10.1017/S0950268810001044
Footnote 11
Herwaldt, B. L. (2001). Laboratory-acquired parasitic infections from accidental exposures. Clinical Microbiology Reviews, 14(4), 659-88, table of contents. doi:10.1128/CMR.14.3.659-688.2001
Footnote 12
Patrat-Delon, S., Gangneux, J. P., Lavoue, S., Lelong, B., Guiguen, C., le Tulzo, Y., & Robert-Gangneux, F. (2010). Correlation of parasite load by quantitative PCR and clinical outcome in a heart transplant patient with disseminated toxoplasmosis. Journal of Clinical Microbiology, doi:10.1128/JCM.00252-10
Footnote 13
dos Santos, T. R., Nunes, C. M., Luvizotto, M. C., de Moura, A. B., Lopes, W. D., da Costa, A. J., & Bresciani, K. D. (2010). Detection of Toxoplasma gondii oocysts in environmental samples from public schools. Veterinary Parasitology, 171(1-2), 53-57. doi:10.1016/j.vetpar.2010.02.045
Footnote 14
Frenkel, J. K., & Dubey, J. P. (1972). Toxoplasmosis and its prevention in cats and man. The Journal of Infectious Diseases, 126(6), 664-673.
Footnote 15
Andrade, G. M., Vasconcelos-Santos, D. V., Carellos, E. V., Romanelli, R. M., Vitor, R. W., Carneiro, A. C., & Januario, J. N. (2010). Congenital toxoplasmosis from a chronically infected woman with reactivation of retinochoroiditis during pregnancy. Jornal De Pediatria, 86(1), 85-88. doi:doi:10.2223/JPED.1948
Footnote 16
World Health Organization. (1993). Laboratory Biosafety Manual (2nd ed.)
Footnote 17
Villegas, E. N., Augustine, S. A., Villegas, L. F., Ware, M. W., See, M. J., Lindquist, H. D., Schaefer, F. W.,3rd, & Dubey, J. P. (2010). Using quantitative reverse transcriptase PCR and cell culture plaque assays to determine resistance of Toxoplasma gondii oocysts to chemical sanitizers. Journal of Microbiological Methods, 81(3), 219-225. doi:10.1016/j.mimet.2010.03.023
Footnote 18
Fauci, A. S., Fauci, A., STAT!Ref, & Teton Data Systems. (2008). Harrison's principles of internal medicine (17th ed.). New York: McGraw-Hill Medical Pub. Division. Retrieved from http://online.statref.com/document.aspx?FxId=55&DocID=1&grpalias=
Footnote 19
Sonar, S. S., & Brahmbhatt, M. N. (2010). Toxoplasmosis: An Important Protozoan Zoonosis. Veterinary World, 3(9), 436-439.
Footnote 20
Institute for International Cooperation in Animal Biologics. (2005). Toxoplasmosis. Toxoplasma Infection.. Ames, Iowa: Iowa State University. College of Veterinary Medecine. The Centre for Foor Security and Public Health.
Footnote 21
Ferguson, D. J. (2009). Toxoplasma gondii: 1908-2008, homage to Nicolle, Manceaux and Splendore. Memorias do Instituto Oswaldo Cruz, 104(2), 133-148.
Footnote 22
Ndao, M. (2009). Diagnosis of parasitic diseases: old and new approaches. Interdisciplinary Perspectives on Infectious Diseases, 2009, 278246. doi:10.1155/2009/278246
Footnote 23
Wong, S. Y., & Remington, J. S. (1994). Toxoplasmosis in pregnancy. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 18(6), 853-61; quiz 862.
Footnote 24
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.