Neglected Parasitic Infections in the United States: Toxoplasmosis

0 Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention , 1600 Clifton Road, NE , Mailstop A-06, Atlanta, GA 30333 1 Monica E. Parise, and Anthony E. Fiore Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention , Atlanta, Georgia Toxoplasma gondii is a leading cause of severe foodborne illness in the United States. Population-based studies have found T. gondii infection to be more prevalent in racial/ethnic minority and socioeconomically disadvantaged groups. Soil contaminated with cat feces, undercooked meat, and congenital transmission are the principal sources of infection. Toxoplasmosis-associated illnesses include congenital neurologic and ocular disease; acquired illness in immunocompetent persons, most notably ocular disease; and encephalitis or disseminated disease in immunosuppressed persons. The association of T. gondii infection with risk for mental illness is intriguing and requires further research. Reduction of T. gondii in meat, improvements in hygiene and food preparation practices, and reduction of environmental contamination can prevent toxoplasmosis, but more research is needed on how to implement these measures. In addition, screening and treatment may help prevent toxoplasmosis or reduce the severity of disease in some settings. - Toxoplasmosis is an infection caused by the protozoan parasite Toxoplasma gondii. Cats are the definitive host in which the organism can complete its sexual cycle. Cats usually shed the environmentally resistant oocyst form of the organism in their feces for 12 weeks after a new infection, although in specific situations related to strain types, co-infection with Cystoisospora felis (syn. Isospora felis), and immunosuppression, repeat shedding is possible.1 Sporulation is required for oocysts to become infectious and occurs within 15 days in the environment. Sporulated oocysts are quite hardy; they can remain infective in a moist environment for a year or more.1 Once ingested by humans or any other warm-blooded animal, the parasite transforms into a tissue-infective stage in the intestine, migrates through the intestinal wall, and is carried via the blood to other tissues including the central nervous system. Humans are accidental hosts and can be infected through a variety of exposures. Food-borne transmission occurs with ingestion of raw or undercooked meat containing the parasite in tissue cysts (usually pork, lamb, goat, or wild game meat, although beef and field-raised chickens have been implicated in epidemiologic studies),2 or through ingestion of food, soil, or water contaminated by cat feces (for example, from eating unwashed fruits and vegetables, gardening, or cleaning a cats litter box). Mother-to-child transmission typically occurs when a pregnant woman is newly infected during, or just prior to, her pregnancy. The organism can also be transmitted when a previously uninfected person receives an organ or blood transfusion from an infected donor. The proportion of human T. gondii infections acquired by eating meat containing infective cysts versus ingesting oocysts from cat feces contamination is not known for a representative sample of the general population. However, ingestion of oocysts from cat feces/soil and ingestion of tissue cysts in meat both are significant contributors to the disease burden in humans, although oocysts have recently been shown to play an important role.35 Modern confinement production has decreased T. gondii contamination of meat but there is concern that a new trend in the production of free-range raised animals for meat could increase the risk of contamination.2 Three principal clonal T. gondii genotypes were originally detected, primarily in isolates from the United States and Europe. However, more recently using sequence-based technology 15 haplogroups that define 6 major clades have been described,6 and the new paradigm is that many atypical genotypes differ in pathogenicity and transmissibility from typical genotypes.7 Research supports the concept that T. gondii genotype may be related to disease severity.810 However, there is relatively little information about T. gondii genotypes infecting asymptomatic persons, and in general, the clinical implications of T. gondii strains are incompletely understood. CLINICAL MANIFESTATIONS A self-limited or mild illness characterized by fever, malaise and lymphadenopathy is often seen after T. gondii infection, but many infections are subclinical. However, regardless of initial symptoms, a chronic infection is established, and immunosuppression, such as occurs with advanced human immunodeficiency virus disease or use of immunosuppressive medications in cancer treatment or after organ transplant, can result in disease reactivation and severe morbidity including neurologic involvement, or mortality. In those with advanced human immunodeficiency virusrelated immunosuppression, encephalitis is a common manifestation unless long-term prophylactic medication is taken. Congenital infection can cause pregnancy loss (miscarriage or stillbirth) or severe disease in the newborn, including developmental delays, blindness, and epilepsy.11 However, many newborns with congenital toxoplasmosis are asymptomatic at birth. Nevertheless, even if asymptomatic at birth, illness will develop in many infected infants later in their life, most often ocular disease, but also neurologic symptoms and developmental disabilities.11 For example, 82% of congenitally infected children (9 of 11, including 4 who received treatment) were shown to have ocular lesions by age 20 in one small prospective series.12 Other studies confirm the risk for severe illness among congenitally infected children but have found a somewhat lower risk in treated children. For example, in a group of 127 treated children followed-up to 16 years in France, ocular lesions were present in 18.9%.13 In another series of 130 treated children followed-up 12 years in France, ocular involvement was found in 30%,14 and in a third series of French adults (median age = 22 years) who had congenital toxoplasmosis that was treated pre- and post-natally, 59% had ocular lesions but only 13% had reduced vision.15 A comparison of cohorts of children with congenital toxoplasmosis in Brazil with those in Europe found that T. gondii causes more severe ocular disease in congenitally infected children in Brazil.9 The authors suggested that the increased frequency and severity of ocular disease in Brazil compared with that in Europe may be caused by more virulent type 1 and atypical strains found there.9 In general, infants born to women who were infected with T. gondii more than a few weeks before conception are not at risk for congenital infection, although congenital infection from women with chronic T. gondii infection has occurred with reactivation in immunosuppression or with infection by atypical genotypes.7 Al (...truncated)