Toxoplasma

 

Originally published as a National Pork Board/American Meat Science Association Fact Sheet

 

Reviewed July 2020

 

Introduction

Toxoplasma gondii is a protozoan (single-celled) parasite found in muscle and other tissues of many warm-blooded animals including pigs and people. Cats and other felids are the only hosts in which the parasite can complete its entire life cycle, and the only animals that excrete the environmentally resistant and infectious stage called the oocyst (eggs) in feces. Infection occurs when pigs and other animals, accidentally ingest oocysts in soil or water or eat tissues of rodents, wildlife or meat containing cysts. Ingested oocysts or tissue cysts enter the intestine and release sporozoites or bradyzoites, respectively. These stages penetrate intestinal cells and transform into rapidly dividing tachyzoites. Tachyzoites are dispersed throughout the body by the circulatory and lymphatic systems, eventually entering and encysting as bradyzoites (tissue cysts) in skeletal muscle and other organs of the body (brain, heart, liver). These cysts remain alive in the body for the lifetime of the animal, and are infective when eaten by other hosts, such as humans. Once tissue cysts have formed, most animals are resistant to a second infection. In the cat, a series of asexual stages in the intestine is followed by sexual reproduction of the parasite and finally the production of oocysts that are passed in the feces. Cats can shed more than 10 million oocysts per day for 3-10 days after infection. Oocysts must mature (sporulate) in the environment for 1-5 days to become infective for a new host. Transplacental transmission of infection can occur in some hosts, including humans, who become infected during pregnancy.

 

Objectives

• Describe the general life cycle of Toxoplasma gondii
• Understand the zoonotic potential of T. gondii
• Describe the prevalence, transmission, control and prevention measures of T. gondii
• Understand the inactivation of T. gondii during pork processing

 

Toxoplasmosis in Humans

Human infection with T. gondii is quite high relative to most other diseases. Serological surveys report population infection rates of nearly 100% in some countries. Prevalence rates in France, for example, are reported to range from 42-84% of the population. In the United States, the rate of infection with T. gondii appears to be declining. In the most recent serological survey (National Health and Nutrition Examination Survey) involving over 17,000 people, 23% were positive for T. gondii antibodies, indicating infection with the parasite. Of the women of child bearing age that were tested, 14% were positive for T. gondii. Prevalence of infection was lower in a younger population (military recruits), declining from 14.4% in a 1962 study, to 9.5% in a similar 1989 study.

 

Exposure of healthy adults to T. gondii generally results in either an asymptomatic infection or a mild flu-like illness. A major health problem associated with T. gondii is transmission of the parasite from a pregnant woman to her unborn baby. At risk are women who acquire a primary infection either during, or shortly before, pregnancy. Women who have previously been exposed to T. gondii and who have a healthy immune system, have minimal risk of transmitting the parasite to the fetus. Transplacental infection can result in miscarriage, stillbirth, or live birth with congenital infection. Infant mortality may be as high as 12%, and 30% may have severe birth defects, including mental retardation. Congenital toxoplasmosis may be expressed as either a neonatal disease (in approximately 15% of cases), or appear later during infancy, childhood, adolescence or adulthood (approximately 85% of cases). Typical consequences of neonatal disease can affect the brain and eye resulting in hydrocephalus (water on the brain), intracranial (brain) calcification, and chorioretinitis (eye inflammation).

 

Most postnatal cases of toxoplasmosis are mild with only a flu-like illness for several days before immunity occurs. The disease can be reactivated in immunosuppressed people, and can result in severe illness and death. Toxoplasmic encephalitis, a disease caused by parasites multiplying in the brain, results from either acute infection or reactivation of a latent infection. It is the second most common opportunistic infection of the central nervous system in Acquired Immunodeficiency Syndrome (AIDS) patients. In healthy adults, most infections with T. gondii are subclinical; however, acute disease occurs occasionally and includes lymphadenopathy (enlarged lymph nodes), chorioretinitis, or central nervous system infection. Human toxoplasmosis in the United States is estimated to cost $5.26 billion annually in medical costs, losses in personal productivity, and costs of special education and residential care. An additional $100 million is attributed to medical costs of toxoplasmic encephalitis in AIDS cases.

 

Table 1. Prevalence of Toxoplasma gondii in pigs in the United States.

 

Humans become infected with T. gondii in three ways: 1) accidental ingestion of the oocysts excreted by cats in their feces, 2) ingestion of tissue cysts by consumption or improper handling of undercooked or raw meat from infected animals, and 3) congenitally, in the case of previously unexposed women who become infected around and during pregnancy. The oocysts excreted by cats are very resistant to environmental fluctuations and survive for years in soil, even in adverse conditions. Humans can be exposed to oocysts deposited in cat feces through gardening activities, eating unwashed fruits and vegetables, drinking water contaminated with cat feces, cleaning a cat litter box, contact with cat feces in sandboxes, etc. Once infection has occurred, it is not possible, based on tools currently available, to determine whether a person was infected by ingestion of oocysts or by consumption of contaminated and undercooked meat. The Centers for Disease Control (CDC) estimates that 50% of all human exposures in the U.S. are foodborne and that T. gondii is responsible for approximately 20% of all deaths attributed to foodborne pathogens. Of the major meat animal species investigated thus far, pigs are the only species shown to frequently harbor the parasite. Uncooked pork was identified as the source of two outbreaks in healthy adults in Korea resulting in chorioretinitis (3 patients) and lymphadenopathy (5 patients). In a cross-sectional study of adults, a group known to avoid eating meat (Seventh Day Adventists) had a significantly lower rate of infection (18%) as compared with the non-Seventh Day Adventists in the study (40%); however, cat ownership and association with oocyst-contaminated environments were not investigated.

 

Toxoplasma and Pork

Most species of livestock, including sheep, goats, and pigs, are susceptible to infection with T. gondii; however, animals exposed to T. gondii rarely show signs of infection. Animals are infected in a similar manner to humans: ingestion of oocysts from the environment; consumption of infected animals such as mice, birds, and other wildlife; consumption of undercooked meat scraps; and in some species, through in utero transmission.

 

Prevalence of T. gondii in pigs varies, but generally exceeds 10-20% in most countries. Infection rates are higher in breeding populations than in market pigs, reflecting that length of exposure is a factor in acquiring T. gondii infection. A number of serologic surveys for T. gondii have been conducted in the U.S. (Table 1). Infection was estimated at 23.9% of pigs in 1983-1984 with higher rates in breeders (42%) than in market pigs (23%). When pigs from these same areas were tested in 1992, the percentage had dropped to 20.8% of breeders and 3.1% of finisher pigs. Prevalence of T. gondii was 20% in sows tested in the 1990 National Animal Health Monitoring System (NAHMS) swine survey. Using sera from the NAHMS swine survey conducted in 1995, sow prevalence had fallen to 15% and finisher pigs had a seroprevalence of 3.2%. These results suggest that the frequency of T. gondii infection in pigs is declining, and that there is a clear difference in prevalence rates between breeding animals (sows) and market hogs.

 

Disease Spread

Transmission of T. gondii to pigs on the farm occurs by various means. Risk factors for transmission include exposure to live or dead rodents and other wildlife, as well as deliberate or inadvertent feeding of raw or undercooked meat scraps containing infective stages of the parasite. More importantly, pigs can acquire T. gondii from ingesting the environmentally resistant oocyst stage shed by cats. In several studies of management factors, outside housing of swine, access of cats to swine, infection in cats and mice, and small herd size were positively correlated with T. gondii infection. Once established, T. gondii can rapidly spread through an entire herd via cannibalism.

 

In a study of 47 farms in Illinois with typical rates of Toxoplasma gondii infection (15.1% in sows and 2.3% in finishers), a variety of reservoir hosts were found, including cats (68.3% infected), raccoons (67% infected), skunks (38.9% infected), opossums (22.7% infected), rats (6.3% infected) and mice (2.2% infected). In this same study, oocysts were found in samples of feed, soil, and cat feces. Oocysts can be found virtually anywhere, including pig feed and pig barns where cats reside. An infected cat can shed millions of oocysts each day for up to one week, and these stages can survive in most climates for several years. Avoiding environmental contamination is a major hurdle in reducing pig exposure to T. gondii.

 

Control: Slaughter Testing

There are no programs for the slaughter inspection of pigs for toxoplasmosis. It is not possible to detect the microscopic tissue cysts by visual inspection. Methods for testing pigs include serology and bioassay. Serological (blood) tests include various forms of agglutination (clumping) tests and Enzyme-Linked Immunosorbent Assay (ELISA). The most sensitive and specific test method is the modified agglutination test using preserved whole tachyzoites. This test, however, is not suitable for use in the slaughterhouse or in the field due to the length of time required to obtain a result. The availability of an ELISA that is both sensitive and specific would allow wider use of serologic testing. The most definitive method for the detection of T. gondii infection is by bioassay, in which portions of tissue are inoculated into mice or cats. This procedure requires several weeks to determine the presence of parasites and is therefore not suitable for testing slaughtered animals. Another option to try attempt to identify T. gondii is to submit infected tissue (muscle, brain, placenta) for microscopic evaluation and advanced staining.

 

Processing

Currently, no regulations require that pork be inspected for T. gondii and no further processing is mandated to inactivate the parasite. However, many of the methods that are in place for processing pork for inactivation of Trichinella spiralis (trichinae) are also effective for the inactivation of T. gondii. The following discussion summarizes the inactivation of T. gondii by processing methods.

 

Cooking

Thermal death curves for the interaction of temperature and time required to kill T. gondii in meat have been generated. From these data, we know that T. gondii is killed in 336 seconds at 49°C, in 44 seconds at 55°C, and in 6 seconds at 61°C. These times and temperatures apply only when the product reaches and maintains temperatures evenly distributed throughout the meat. The temperatures reported to kill Toxoplasma gondii are lower than those required for Trichinella spiralis. Thus methods prescribed for the destruction of trichinae in the USDA’s Code of Federal Regulations are effective for the destruction of T. gondii also. The use of microwaves is not effective in killing T. gondii, probably because of uneven heating throughout the meat.

 

Freezing

Thermal death curves establishing the effect of cold on the viability of T. gondii in pork have been generated. Although tissue cysts remained viable at temperatures slightly below freezing (11.2 days at -6.7°C and 22.4 days at -3.9 and -1.0°C) parasites were inactivated almost instantaneously at temperatures of -9.4°C and lower. Based on the data, the predicted times required to kill T. gondii are shorter than those required to kill trichinae; thus, processing times for pork prescribed by the USDA’s Code of Federal Regulations to kill trichinae will also be effective for T. gondii. There is no evidence that there are strains of T. gondii with different freezing susceptibilities.

 

Curing

Our knowledge of the effect of various curing processes on T. gondii is limited and additional studies are needed to determine the effectiveness of curing for the destruction of T. gondii in pork and pork products.

 

Irradiation

1. gondii tissue cysts were rendered non-infectious by treatment with 40-50 krad of cesium-137, indicating that irradiation is a suitable method for eliminating the risk of this parasite in pork products.

 

Prevention of Infection

Despite the widespread distribution of T. gondii in wildlife and the opportunity for cats to contaminate the environment with the resistant oocyst stage, it is possible to raise pigs free from T. gondii infection, as evidenced by many negative swine production sites found in recent seroprevalence studies. Prevention of infection in swine is accomplished through on-farm adherence to good production practices (GPPs), which include: 1) adopting an effective rodent control program to minimize mouse populations, 2) creating a level of biosecurity which reduces or eliminates exposure of swine to wildlife, 3) eliminating feral cats or securing feed and swine areas from access by cats, 4) prompt removal of dead pigs, and, 5) changing or thoroughly washing boots before entering barns to avoid tracking in oocysts.

 

The contribution of cats to the spread of T. gondii infection in pigs cannot be overemphasized. Since it takes only one oocyst to infect a pig, protection of pigs from environmental contamination, contamination of feed, and transport of oocysts on boots is vital to control. In prevalence studies, from 41.9-70.7% of farm cats were seropositive for T. gondii infection. Cats only shed oocysts for 1–3 weeks; however, in one study, 1.8% of farm cats tested were actively shedding oocysts. Even more important was the finding of viable oocysts in soil and feed samples from these farms, suggesting that oocysts shed by cats become widely dispersed in the environment. Risk analysis of management factors associated with positive pigs showed that infection correlated with the presence of infected young cats (sources of oocysts) and T. gondii infected mice. Thus, a high level of biosecurity and GPPs which take into account the possible sources of environmental and feed contamination are necessary to assure the raising of pigs free from T. gondii infection.

 

Summary

Toxoplasma gondii can be found in muscle and tissue of infected animals and people. The protozoan completes its life cycle in felids and is spread to other species by oocysts passed in feces. T. gondii is zoonotic, causing major health problems in immunosuppressed individuals and pregnant women due to transplacental infection of their fetus. The protozoa commonly impacts the developing brain and eyes of infected neonates. Healthy adults can also be infected, but experience more of a flu-like illness for several days. For humans, infection occurs via accidental ingestion of oocysts from cat feces, ingestion of tissue cysts (raw or improperly handled meat) and transplacentally. Most livestock species are susceptible to T. gondii, but rarely show clinical signs of infection. Transmission between pigs is typically due to felids, rodents, wildlife and cannibalism. Since T. gondii cannot be seen during visual inspection, there is no program in place for slaughter inspection or testing. It is important to note that the processing steps to inactivate Trichinella spiralis are also effective at inactivating Toxoplasma gondii. To prevent entry into a farm, swine facilities should maintain control programs for felids, rodents and wildlife. Other steps to consider include protocols to prevent oocyst spread and prompt removal of dead pigs to prevent cannibalism.

 

References and Additional Reading

Assadi-Rad, A.M., New, J.C. and Patton, S. 1995. Risk factors associated with transmission of Toxoplasma gondii to sows kept in difference management systems in Tennessee. Vet. Parasitol. 57: 289-297.

 

Dubey J.P. 1990. Status of toxoplasmosis in pigs in the United States. J. Am. Vet. Med. Assoc. 196: 270-274.

 

Dubey J.P., Leighty J.C., Beal V.C., Anderson W.R., Andrews C.D. and Thulliez, Ph. 1991.

National seroprevalence of Toxoplasma gondii in pigs. J. Parasitol. 77: 517-521.

 

Dubey J.P., Kotula A.W., Sharar A., Andrews C.D., and Lindsay D.S. 1990. Effect of high temperature on infectivity of Toxoplasma gondii tissue cysts in pork. J. Parasitol. 76: 201-204.

 

Dubey J.P., Weigel R.M., Siegel A.M., Thulliez P., Kitron U.D., Mitchell M.A., Mannelli A., Mateus-Pinilla N.E., Shen S.K., Kwok O.C.H. and Todd K.S. 1995. Sources and reservoirs of Toxoplasma gondii infection on 47 swine farms in Illinois. J. Parasitol. 81: 723-729.

 

Dubey, J.P., Murrell, K.D., Hanbury, R.D., Anderson, W.R., Doby, P.B. and Miller, H.O. 1986. Epidemiologic findings on a swine farm with enzootic toxoplasmosis. J. Am. Vet. Med. Assoc. 189: 55-56.

 

Gamble, H.R., Brady, R.C. and Dubey, J.P. 1999. Prevalence of Toxoplasma gondii infection in domestic pigs in the New England states. Vet. Parasitol. 82: 129-136.

 

Kotula A.W., Dubey J.P., Sharar A.K., Andrews C.D., Shen S.K. and Lindsay D.S. 1991. Effect of freezing on infectivity of Toxoplasma gondii tissue cysts in pork. J. Food Prot. 54: 687-690.

 

Lopez, A., Dietz, V.J., Wilson, M., and Jones, J.L. 2000. Preventing congenital toxoplasmosis. MMWR 49: 59 – 75.

 

Mead, P.S., Slutsker, L., Dietz, V., McCaig, L.F., Bresee, J.S., Shapiro, C., Griffin, P.M. and Tauxe, R.V. 1999. Food-related illness and death in the United States. Emerg. Infect. Dis., 5(5): 1999 Sept.-Oct., available from: URL:http://www.cdc.gov/ncidod/EID/eid.htm

 

Patton, S., Zimmerman, J., Roberts, T., Faulkner, C., Diderrich, V., Assadi-Rad, A., Davies, P. and Kliebenstein, J. 1996. Seroprevalence of Toxoplasma gondii in hogs in the National Animal Health Monitoring System (NAHMS). J. Eucaryotic Microbiol. 43: 1215.

 

Roberts T., Weiss, M., Southard, L. 1993. Issues in pork safety: cost control and incentives. Agricultural Outlook AO-201, USDA-ERS, October: 28-32.

 

Roghmann, M-C., Faulkner, C.T., Lefkowitz, A., Patton, S., Zimmerman, J. and Morris, J.G. 1999. Decreased seroprevalence for Toxoplasma gondii in Seventh Day Adventists in Maryland. Am. J. Trop. Med. Hyg. 60: 790-792.

 

Smith K.E., Zimmerman J.J., Patton S., Beran G.W. and Hill H.T. 1992. The epidemiology of toxoplasmosis of Iowa swine farms with an emphasis on the roles of free-living mammals. Vet. Parasitol. 42: 199-211.

 

Smith, J.L. 1997. Long-term consequences of foodborne toxoplasmosis: effects on the unborn, the immunocompromised, the elderly and the immunocompetent. J. Food Protect. 60: 1595-1611.

 

Smith K.E., Zimmerman J.J., Patton S., Beran G.W. and Hill H.T. 1992. The epidemiology of toxoplasmosis of Iowa swine farms with an emphasis on the roles of free-living mammals. Vet. Parasitol. 42: 199-211.

 

Smith K.L., Wilson M., Hightower A.W., Kelley P.W., Struewing J.P, Juranek D.D. and McAuley J.B. 1996. Prevalence of Toxoplasma gondii antibodies in U.S. military recruits in 1989: comparison with data published in 1965. Clin. Infect. Dis. 23: 1182-1183.

 

Weigel R.M., Dubey J.P., Siegel A.M., Kitron U.D., Mannelli A., Mitchell M.A., Mateus-Pinilla N.E., Thulliez P., Shen S.K., Kwok O.C.H. and Todd K.S. 1995. Risk factors for transmission of Toxoplasma gondii on swine farms in Illinois. J. Parasitol. 81, 736-741.

 

Weigel R.M., Dubey J.P., Siegel A.M., Hoefling D., Reynolds D., Herr L., Kitron U.D., Shen S.K., Thulliez P., Fayer R. and Todd K.S. 1995. Prevalence of antibodies to Toxoplasma gondii in swine in Illinois in 1992. Am. J. Vet. Med. Assoc. 206: 1747-1751.

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