Toxoplasmosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii.The parasite infects most warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by ingestion of faeces of a cat that has itself recently been infected, or by transmission from mother to fetus. Cats have been shown as a major reservoir of this infection, contact with infected undercooked meat seems to be a more important cause of human infection in many countries. Toxoplasmosis manifests as a painless lymphadenopathy in an immunocompetent individual. In patients with AIDS and other immunocompromised conditions, it mainly involves brain and presents with fever and focal neurological symptoms.The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with toxoplasma oocysts excreted in cat feces. ^{[1] [2]}

Toxoplasma gondi was first identified in 1908 by Nicolle and Manceaux. Sabin & Olitsky in 1937 described that toxoplasma was an obligate intracellular parasite and could be passed onto laboratory animals by intracranial, subcutaneous, intraperitoneal inoculation of brain homogenates (The slurry of tissues and cells which result when cell structure has been mechanically disrupted). They have also suggested that ingestion of toxoplasma contaminated tissue can result in toxoplasmosis. In 1937 to 1940, Wolf and Cowen have described necrotic and granulomatous lesions on an autopsy of a 3-day old infant’s brain infected with toxoplasma. They have also reported that the mothers were asymptomatic but carried antibodies against Toxoplasma and the possibility of congenital transmission was expressed. Sabin and Feldman developed a serological test to identify infected individuals by using antibodies specific to toxoplasma, called the Sabin Feldman Dye test. The serological test when used in large population studies showed a high proportion of humans and domestic animals carried antibodies against toxoplasma. Dubley described the life cycle of the parasite in 1970 and established that the cats are the definitive hosts and any warm-blooded animal can be an intermediate host.^{[3][4][5] [6][7][8]}

Toxoplasma gondii is a protozoan parasite that infects most species of warm-blooded animals, including humans, causing the disease toxoplasmosis. Members of the cat family (Felidae) are the only known definitive hosts for the sexual stages of T. gondii and thus are the main reservoirs of infection. Cats become infected with T. gondii by carnivorism . After tissue cysts or oocysts are ingested by the cat, viable organisms are released and invade epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then form oocysts, which are excreted. The unsporulated oocyst takes 1 to 5 days after excretion to sporulate (become infective). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed. Oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C for 10 minutes.^[9]

Toxoplasma gondii is a species of parasitic protozoa in the genus Toxoplasma.^[1]

Toxoplasmosis manifests as a painless lymphadenopathy in an immunocompetent individual. In patients with AIDS and other immunocompromised conditions, it mainly involves brain and presents with fever and focal neurological symptoms. The major differential diagnosis of focal CNS lesions in patients with AIDS is CNS lymphoma, which manifests as multiple enhancing lesions in 40% of cases. Other differentials in the diagnosis of toxoplasmosis include brain abscess, cytomegalovirus, herpes simplex, histoplasmosis, infectious mononucleosis, listeria monocytogenes infection (Listeriosis), lymphoblastic lymphoma, metastatic cancer with unknown primary site.^[10][11][12]

Serologic prevalence data indicate that toxoplasmosis is one of the most common of humans infections throughout the world. Infection is more common in warm climates and at lower altitudes than in cold climates and mountainous regions. High prevalence of infection in France has been related to a preference for eating raw or undercooked meat, while high prevalence in Central America has been related to the frequency of stray cats in a climate favoring survival of oocysts. The overall seroprevalence in the United States as determined with specimens collected by the third National Health and Nutritional Assessment Survey (NHANES III) between 1988 and 1994 was found to be 22.5%, with seroprevalence among women of childbearing age (15 to 44 years) of 15%.

The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with toxoplasma oocysts excreted in cat feces.

Majority of the countries do not follow standard screening for the detection of toxoplasma infection during the antenatal period. Women are tested for antibodies against toxoplasma on their first antenatal visit, and if they are seropositive they are followed up periodically in every trimester to examine the trends in IgG titer levels. All HIV-infected patients should be tested for prior exposure by measuring anti-Toxoplasma IgG. Patients with HIV and CD4+ T lymphocyte counts <100 cells/microliter with detectable anti-Toxoplasma IgG are at risk for reactivation of latent infection and should receive prophylactic treatment. Screening for Toxoplasma is routinely performed for cardiac donors.^[13]

If left untreated in people with a weakened immune system, such as those infected with HIV, and fetuses, the disease can become seriously ill, and occasionally be fatal. The parasite can cause encephalitis (inflammation of the brain) and neurologic diseases and can affect the heart, liver, and eyes (chorioretinitis). Complications that can develop as a result of toxoplasmosis are mental retardation, seizures, motor difficulties, severe vision loss, hydrocephalus or microcephalus, hearing loss. Prognosis of infection in immunocompromised individual is dependent on the severity of the disease. Severe infection causes death at an early age, asymptomatic infection will present in the 1st or 2nd decade with progressive chorioretinitis with poor prognosis.^[14]

Acquired infection with Toxoplasma in immunocompetent persons is generally an asymptomatic infection. However, 10% to 20% of patients with acute infection may develop cervical lymphadenopathy and/or a flu-like illness. The clinical course is usually benign and self-limited; symptoms usually resolve within a few months to a year. Immunodeficient patients often have central nervous system (CNS) disease but may have retinochoroiditis, or pneumonitis. In patients with AIDS, toxoplasmic encephalitis is the most common cause of intracerebral mass lesions and is thought to be caused by reactivation of chronic infection. Toxoplasmosis in patients being treated with immunosuppressive drugs may be due to either newly acquired or reactivated latent infection.

The most common physical examination findings of toxoplasmosis include painless lymphadenopathy in immunocompetent individuals. Other findings include fever, malaise, myalgias, and a maculopapular skin rash that spares the palms and the soles. In retinochoroiditis examination reveals multiple yellow-white cotton like patches with indistinct margins located in small clusters in the posterior pole.

Toxoplasma infection is diagnosed by the presence of parasite in the fluids such as blood, body fluids, or tissue by DNA amplification, microscopy or by isolation of the organism. The most commonly used diagnostic test is the PCR of the amniotic fluid and a positive test is diagnostic of congenital toxoplasmosis. The most commonly used diagnostic investigation for early detection is the serological detection of antibodies (IgG, IgM and IgA) in the serum. A combination of all the antibodies (IgG, IgM, IgA) is usally employed.^[15]

There are no specific chest x ray findings associated with toxoplasmosis.

Toxoplasmic encephalitis is the most common cause of intracerebral mass lesions and is caused by reactivation of chronic infection. Typically cerebral toxoplasmosis manifest as multiple lesions, with a predilection for the basal ganglia, thalami, and corticomedullary junction. Intracerebral mass lesions can be diagnosed using CT and MRI scan. Findings of CT brain include multiple hypodense regions predominantly in the basal ganglia and at the corticomedullary junction.

On brain MRI, toxoplasmosis is characterized by isointense or hyperintense lesions with surrounding perilesional oedema. Lesions often demonstrate ring enhancement or nodular enhancement

Treatment of immunocompetent adults with lymphadenopathic toxoplasmosis is rarely indicated. Antimalarials and antibiotics are the mainstays of treatment. Treatment for ocular diseases should be based on a complete ophthalmologic evaluation.When a pregnant woman is diagnosed with acute toxoplasmosis, amniocentesis can be used to determine whether the fetus has been infected or not.If the parasite has not yet reached the fetus, spiramycin can help to prevent placental transmission. If the fetus has been infected, the pregnant woman can be treated with pyrimethamine and sulfadiazine, with folinic acid, after the first trimester. Persons with AIDS who develop active toxoplasmosis (usually toxoplasmic enchephalitis) need treatment that must be taken until a significant immunologic improvement is achieved as a result of antiretroviral therapy.

Surgical intervention is not recommended for the management for toxoplasmosis infection.

Effective measures for the primary prevention of toxoplasmosis include general sanitation and food safety steps such as hands should be washed well with soap and water after outdoor activities, especially before you eat or while handing preparation of food. A woman with no previous exposure should avoid handling raw meat, exposure to cat faeces, and gardening (cat faeces are common in garden soil).

Secondary preventive measures are same as of primary preventive.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Toxoplasma gondi was first identified in 1908 by Nicolle and Manceaux. Sabin & Olitsky in 1937 described that toxoplasma was an obligate intracellular parasite and could be passed onto laboratory animals by intracranial, subcutaneous, intraperitoneal inoculation of brain homogenates (The slurry of tissues and cells which results when cell structure has been mechanically disrupted). They have also suggested that ingestion of toxoplasma contaminated tissue can result in toxoplasmosis. In 1937 to 1940, Wolf and Cowen have described necrotic and granulomatous lesions on autopsy of a 3 day old infant’s brain infected with toxoplasma. They have also reported that the mothers were asymptomatic but carried antibodies against toxoplasma and the possibility of congenital transmission was expressed. Sabin and Feldman developed a serological test to identify infected individuals by using antibodies specific to toxoplasma, called the Sabin Feldman Dye test. The serological test when used in large population studies showed a high proportion of humans and domestic animals carried antibodies against toxoplasma. Dubley described the life cycle of the parasite in 1970 and established that the cats are the definitive hosts and any warm blooded animal can be an intermediate host.^{[1][2][3] [4][5][6]}

• In 1908, Nicolle and Manceaux described the parasite in the blood, spleen and liver of a North African rodent–gundi (Ctenodactylus gundi) and named it Leishmania gondii.^[7]
• In 1909, Nicolle and Manceaux renamed the parasite as T.gondii.^[8]
• In 1937, Sabin & Olitsky described that toxoplasma was an obligate intracellular parasite and could be passed onto laboratory animals by intracranial, subcutaneous, intraperitoneal inoculation of brain homogenates (The slurry of tissues and cells which results when cell structure has been mechanically disrupted). They have also suggested that ingestion of toxoplasma contaminated tissue can result in toxoplasmosis.^[6]
• In 1937 to 1940, Wolf and Cowen have described necrotic and granulomatous lesions on autopsy of a 3 day old infant’s brain infected with toxoplasma. They have also reported that the mothers were asymptomatic but carried antibodies against toxoplasma and the possibility of congenital transmission was expressed.^[5]
• In 1940, Pinkerton and Weinman reported the first fatal case of toxoplasmosis in an adult.^[9]
• In 1948, Sabin and Feldman developed a serological test to identify infected individuals by using antibodies specific to toxoplasma, called the Sabin Feldman Dye test. The serological test when used in large population studies showed a high proportion of humans and domestic animals carried antibodies against toxoplasma.^[4]
• In 1965, Desmonts described that ingestion of under-cooked and uncooked meat plays a role in the pathogenesis of toxoplasmosis.^[10]
• In 1970, Dubley described the life cycle of the parasite and established that the cats are the definitive hosts and any warm blooded animal can be an intermediate host.^[1][2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Toxoplasmosis is an opportunistic parasitic infection most commonly seen in AIDS and immunocompromised individuals. Its mostly asymtomatic in immunocompetent individuals. It can be classified into two categories based on the duration of symptoms and organ involvement.^[1]

• Acute: If the duration of symptoms is less than 4-6 weeks
• Chronic: If the symptoms persist for more than 6 weeks.

• Neurotoxoplasmosis (cerebral toxoplasmosis)
• Pulmonary toxoplasmosis
• Occular toxoplasmosis
• Congenital toxoplasmosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Toxoplasma gondii is a protozoan parasite that infects most species of warm blooded animals, including humans, causing the disease toxoplasmosis. Members of the cat family (Felidae) are the only known definitive hosts for the sexual stages of T. gondii and thus are the main reservoirs of infection. Cats become infected with T. gondii by carnivorism . After tissue cysts or oocysts are ingested by the cat, viable organisms are released and invade epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then form oocysts, which are excreted. The unsporulated oocyst takes 1 to 5 days after excretion to sporulate (become infective). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed. Oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C for 10 minutes.^[1]

Toxoplasma gondii is a protozoan parasite that infects most species of warm blooded animals, including humans, causing the disease toxoplasmosis. Members of the cat family (Felidae) are the only known definitive hosts for the sexual stages of T. gondii and thus are the main reservoirs of infection. Cats become infected with T. gondii by carnivorism . After tissue cysts or oocysts are ingested by the cat, viable organisms are released and invade epithelial cells of the small intestine where they undergo an asexual followed by a sexual cycle and then form oocysts, which are excreted. The unsporulated oocyst takes 1 to 5 days after excretion to sporulate (become infective). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed. Oocysts can survive in the environment for several months and are remarkably resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C for 10 minutes.^[2]

• The only known definitive hosts for Toxoplasma gondii are members of family Felidae (domestic cats and their relatives).
• T gondii has 2 distinct life cycles.
• The sexual cycle occurs only in cats, the definitive host.
• The asexual cycle occurs in other mammals (including humans) and various strains of birds.
• Unsporulated oocysts are shed in the cat’s feces.
• Although oocysts are usually only shed for 1-2 weeks, large numbers may be shed.
• Oocysts take 1-5 days to sporulate in the environment and become infective.
• Intermediate hosts in nature (including birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts.
• Oocysts transform into tachyzoites shortly after ingestion.
• These tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites.
• Cats become infected after consuming intermediate hosts harboring tissue cysts.
• Cats may also become infected directly by ingestion of sporulated oocysts.
• Animals bred for human consumption and wild game may also become infected with tissue cysts after ingestion of sporulated oocysts in the environment.
• Humans can become infected by any of several routes:
  • Eating undercooked meat of animals harboring tissue cysts.
  • Consuming food or water contaminated with cat feces or by contaminated environmental samples (such as fecal-contaminated soil or changing the litter box of a pet cat).
  • Blood transfusion or organ transplantation.
  • Transplacentally from mother to fetus.
• In the human host, the parasites form tissue cysts, most commonly in skeletal muscle, myocardium, brain, and eyes; these cysts may remain throughout the life of the host.
• Diagnosis is usually achieved by serology, although tissue cysts may be observed in stained biopsy specimens.
• Diagnosis of congenital infections can be achieved by detecting T. gondii DNA in amniotic fluid using molecular methods such as PCR .

• Infection can occur by ingestion of oocysts following the handling of contaminated soil or cat litter or through the consumption of contaminated water or food sources (eg, unwashed garden vegetables).
• Transmission of tachyzoites to the fetus can occur via the placenta following primary maternal infection.
• Rarely, infection by tachyzoites occurs from ingestion of unpasteurized milk or by direct entry into the bloodstream through a blood transfusion or laboratory accident.
• Transmission can also occur via ingestion of tissue cysts (bradyzoites) in undercooked or uncooked meat or through transplantation of an organ that contains tissue cysts.

• They are transported via the lymphatics and are disseminated hematogenously throughout the tissues.

The time between exposure to the parasite and symptom development is 1 – 2 weeks.

The three infective stages of T. gondii include:^[3]

• Tachyzoite: It is the rapidly dividing and invasive form and can invade any vertebrate cell type
• Bradyzoite: These are the result of conversion from tachyzoites, they are slowly diving form and are present as tissue cysts, which can remain in the host throughout the lifetime in the muscles.
• Sporozoite: It is the environmental form present in the oocysts

• The initial step of invasion is attachment of the tachyzoite to the host cell membrane. A set of proteins help in the adherence and penetration of the host cell membrane, these proteins also enhance the growth and virulence of the parasite.^[4]
• In the host cell the parasite forms a vacuole where it divides for 6 to 9 cycles after which the parasites are released into the circulation. It is an active process dependent on the increase in intracellular calcium stores.

• Acute infection with tachyzoites in the blood stream during pregnancy, a possibility of transplacental infection is present.^[5]
• The tachyzoites colonize in the placenta and can cross the barrier to reach the fetus in 30% of cases leading to the disease.^[6]
• The frequency of transmission of the tachyzoites to the fetus is related to the gestational age, with low transmission rates in the first trimester (10-15%) and highest transmission rates in the third trimester (60-90%). However the disease is more severe if the infection is acquired early in the pregnancy.^[7]
• The factors influencing the transfer of tachyzoites to the fetus is not well understood.

The parasite itself can cause various effects on the host body, some of which are not fully understood.

• A recent study ^[8] has indicated Toxoplasmosis correlates strongly with an increase in boy births in humans.

• According to the researchers, depending on the antibody concentration, the probability of the birth of a boy can increase up to a value of 0.72 … which means that for every 260 boys born, 100 girls are born.
• The study also notes a mean rate of 0.60 to 0.65 (as opposed to the normal 0.51) for Toxoplasma-positive mothers.

• It has been found that the parasite has the ability to change the behavior of its host^[9]
• The mechanism for this change is not completely understood, but there is evidence that toxoplasmosis infection raises dopamine levels.
• The behaviors observed, if caused by the parasite, are likely due to infection and low-grade encephalitis, which is marked by the presence of cysts in the brain, which may produce or induce production of a neurotransmitter, possibly dopamine, therefore acting similarly to dopamine reuptake inhibitor type antidepressants and stimulants.^[10]
  • Decreased novelty-seeking behaviour ^[11]
  • Slower reactions
  • Lower rule-consciousness and jealousy (in men) ^[11]
  • More warmth and conscientiousness (in women) ^[11]
• Studies have found that toxoplasmosis is associated with an increased car accident rate, roughly doubling or tripling the chance of an accident relative to uninfected people.^[12][13]
• This may be due to the slowed reaction times that are associated with infection.^[13] “If our data are true then about a million people a year die just because they are infected with toxoplasma,” the researcher Jaroslav Flegr told The Guardian.^[14]
• The data shows that the risk decreases with time after infection, but is not due to age.^[12][15]
• However there is also evidence of a delayed effect which increases reaction times.^[16]
• Other studies suggest that the parasite may influence personality. There are claims of toxoplasma causing antisocial attitudes in men and promiscuity.^[17]
• Even signs of higher intelligence in women, and greater susceptibility to schizophrenia and manic depression in all infected persons.^[18][17][19]

• The study suggests that male carriers have lower intelligence quotient(IQ)s, a tendency to achieve a lower level of education and have shorter attention spans, a greater likelihood of breaking rules and taking risks, and are more independent, anti-social, suspicious, jealous and morose.
• It also suggests that these men are deemed less attractive to women.
• Women carriers are suggested to be more outgoing, friendly, more promiscuous, and are considered more attractive to men compared with non-infected controls.

• The possibility that toxoplasmosis is one cause of schizophrenia has been studied by scientists since at least 1953.^[20]
• These studies had attracted little attention from U.S. researchers until they were publicized through the work of prominent psychiatrist and advocate E. Fuller Torrey.
• In 2003, Torrey published a review of this literature, reporting that almost all the studies had found that schizophrenics have elevated rates of toxoplasma infection.^[20]
• A 2006 paper has even suggested that prevalence of toxoplasmosis has large-scale effects on national culture.^[21]
• These types of studies are suggestive but cannot confirm a causal relationship (because of the possibility, for example, that schizophrenia increases the likelihood of toxoplasma infection rather than the other way around).^[20]
• Acute Toxoplasma infection sometimes leads to psychotic symptoms not unlike schizophrenia.
• Some anti-psychotic medications that are used to treat schizophrenia, such as Haloperidol, also stop the growth of Toxoplasma in cell cultures.
• Several studies have found significantly higher levels of Toxoplasma antibodies in schizophrenia patients compared to the general population.^[22]
• Toxoplasma infection causes damage to astrocytes in the brain, and such damage is also seen in schizophrenia.

• T.gondii has tropism for central nervous system and mostly affects the brain and eye. Areas of necrosis and granulomatous lesions in the brain can be demonstrated on autopsy.^[23]

• In patients with toxoplasmosis, microscopy of the lesions demonstrate periaqueductal and periventricular vasculitis with necrosis.^[24][25]
• Fetal tissue and placenta can demonstrate t.gondii cysts with the Wright-Giemsa stain and also with immunoperoxidase staining using t.gondii–specific antibodies.^[26]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Toxoplasma gondii is a species of parasitic protozoa in the genus Toxoplasma.^[1] The definitive host of T. gondii is the cat, but the parasite can be carried by the vast majority of warm-blooded animals, including humans. Toxoplasmosis, the disease of which T. gondii is the causative agent, is usually minor and self-limiting but can have serious or even fatal effects on a fetus whose mother first contracts the disease during pregnancy or on an immunocompromised human or cat.

The life cycle of T. gondii has two phases. The sexual part of the life cycle (coccidia like) takes place only in members of the Felidae family (domestic and wild cats), which makes these animals the parasite’s primary host. The asexual part of the life cycle can take place in any warm-blooded animal, like other mammals (including felines) and birds.

In the intermediate hosts (including felines), the parasite invades cells, forming intracellular so-called parasitophorous vacuoles containing bradyzoites, the slowly replicating form of the parasite.^[2] Vacuoles form tissue cysts mainly within the muscles and brain. Since they are within cells, the host’s immune system does not detect these cysts. Resistance to antibiotics varies, but the cysts are very difficult to eradicate entirely. Within these vacuoles T. gondii propagates by a series of binary fissions until the infected cell eventually bursts and tachyzoites are released. Tachyzoites are the motile, asexually reproducing form of the parasite. Unlike the bradyzoites, the free tachyzoites are usually efficiently cleared by the host’s immune response, although some manage to infect cells and form bradyzoites, thus maintaining the infection.

Tissue cysts are ingested by a cat (e.g., by feeding on an infected mouse). The cysts survive passage through the stomach of the cat and the parasites infect epithelial cells of the small intestine where they undergo sexual reproduction and oocyst formation. Oocysts are shed with the feces. Animals and humans that ingest oocysts (e.g., by eating unwashed vegetables etc.) or tissue cysts in improperly cooked meat become infected. The parasite enters macrophages in the intestinal lining and is distributed via the blood stream throughout the body.

Acute stage toxoplasma infections can be asymptomatic, but often gives flu-like symptoms in the early acute stages, and like flu can become, in very rare cases, fatal. The acute stage fades in a few days to months, leading to the latent stage. Latent infection is normally asymptomatic; however, in the case of immunocompromised patients (such as those infected with HIV or transplant recipients on immunosuppressive therapy), toxoplasmosis can develop. The most notable manifestation of toxoplasmosis in immunocompromised patients is toxoplasmic encephalitis, which can be deadly. If infection with T. gondii occurs for the first time during pregnancy, the parasite can cross the placenta, possibly leading to hydrocephalus, intracranial calcification, and chorioretinitis, with the possibility of spontaneous abortion or intrauterine death.

T. gondii infections have the ability to change the behavior of rats and mice, making them drawn to rather than fearful of the scent of cats. This effect is advantageous to the parasite, which will be able to sexually reproduce if its host is eaten by a cat. ^[3] The infection is almost surgical in its precision, as it does not impact a rat’s other fears such as the fear of open spaces or of unfamiliar smelling food. There has been speculation that human behavior may also be affected in some ways, and correlations have been found between latent Toxoplasma infections and various characteristics such as decreased novelty-seeking behavior, slower reactions, feelings of insecurity, and neuroticism.^[4]

Several independent pieces of evidence point towards a possible role of Toxoplasma infection in some cases of schizophrenia and paranoia, but this theory does not seem to account for many cases.^[5] A recent study has indicated toxoplasmosis is also correlated strongly with an increase in boy births in humans, leading to an alteration of the human sex ratio.^[6] According to the researchers, “depending on the antibody concentration, the probability of the birth of a boy can increase up to a value of 0.72 … which means that for every 260 boys born, 100 girls are born.” The study also notes a mean rate of 0.60 to 0.65 (as opposed to the normal 0.51) for Toxoplasma positive mothers.

Other possible behavior modifications are suggested by a study suggesting that people not infected with the parasite found women with toxoplasma more attractive than women who don’t have toxoplasma. ^[7]

The prevalence of human infection by Toxoplasma varies greatly between countries. Factors that influence infection rates include diet (prevalence is possibly higher where there is a preference for less-cooked meat) and proximity to cats.

To read about guidelines for prevention and treatment of Toxoplasma gondii Infections in HIV-Infected Adults and Adolescents, click here.

• Toxoplasma images, from CDC’s DPDx, in the public domain

[[Category:Infectious disease]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Toxoplasmosis manifests as a painless lymphadenopathy in an immunocompetent individual. In patients with AIDS and other immunocompromised conditions, it mainly involves brain and presents with fever and focal neurological symptoms. The major differential diagnosis of focal CNS lesions in patients with AIDS is CNS lymphoma, which manifests as multiple enhancing lesions in 40% of cases. Other differentials in the diagnosis of toxoplasmosis include brain abscess, cytomegalovirus, herpes simplex, histoplasmosis, infectious mononucleosis, listeria monocytogenes infection (Listeriosis), lymphoblastic lymphoma, metastatic cancer with unknown primary site.^[1][2][3]

Toxoplasmosis manifests as a painless lymphadenopathy in an immunocompetent individual. In patients with AIDS and other immunocompromised conditions, it mainly involves brain and presents with fever and focal neurological symptoms. The major differential diagnosis of focal CNS lesions in patients with AIDS is CNS lymphoma, which manifests as multiple enhancing lesions in 40% of cases. Other differentials in the diagnosis of toxoplasmosis include brain abscess, cytomegalovirus, herpes simplex, histoplasmosis, infectious mononucleosis, listeria monocytogenes infection (Listeriosis), lymphoblastic lymphoma, metastatic cancer with unknown primary site.^[1][2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [3]

Serologic prevalence data indicate that toxoplasmosis is one of the most common human infections throughout the world. Infection is more common in warm climates and at lower altitudes than in cold climates and mountainous regions. High prevalence of infection in France has been related to a preference for eating raw or undercooked meat, while high prevalence in Central America has been related to the frequency of stray cats in a climate favoring survival ofoocysts. The overall seroprevalence in the United States as determined with specimens collected by the third National Health and Nutritional Assessment Survey (NHANES III) between 1988 and 1994 was found to be 22.5%, with seroprevalence among women of childbearing age (15 to 44 years) of 15%.

• It is estimated that 25 to 30% of the world’s population is infected with toxoplasma.^[1]
• In United States 89% of women in the childbearing age are susceptible to have an acute infection and at risk for transmitting the parasite to the baby if the primary infection occurs during the gestational period.^[2]
• In United States the age adjusted seroprevalence rate is 22.5%. There is significant variation in the distribution with highest prevalence reported in the North-eastern states and lowest in the western states.^[3]
• In countries such as North America, Northern Europe and in Sahelian countries of Africa low seroprevalences of 10% to 30% are observed. In countries of Central and Southern Europe, tropical African countries and Latin America the seroprevalence is around 30 to 50%. This shows the variation within the countries and as well as between the countries.^[4]

• In United States, toxoplasmosis affects 1.1 million people every year.^[5]
• Congenital toxoplasmosis affects 500 to 4000 new borns every year.^[6][7]

• The U.S. NHANES (2004-2005) national probability sample found that 33.1% of U.S. persons above 12 years of age had Toxoplasma-specific IgG antibodies, indicating that they had been infected with the organism.
• This prevalence has significantly increased from the 1999-2000 data.^[8]

• In NHANES 1999–2000, the T. gondii antibody prevalence was higher among non-Hispanic black persons than non-Hispanic white persons.
• This finding may reflect immigration patterns from countries with higher rates of T. gondii infection or soil exposure and culinary practices among these different populations.
• The seroprevalence among persons born outside the United States tended to be higher in NHANES 1999–2000 than in NHANES III, and the percentage of persons born outside the United States tended to be higher in NHANES 1999–2000 than NHANES III, but these findings were not statistically significant.
• Clearly, in both NHANES III and NHANES 1999–2000 the seroprevalence is higher among persons not born in the United States than in U.S.-born persons.
• The NHANES 1999–2000 sample population is not large enough to stratify racial/ethnic groups by foreign-birth status and obtain accurate estimates; however, in a multivariate analysis reported previously that used NHANES III data, being born outside the United States was a significant risk factor for T. gondii seropositivity.
• However, race/ethnicity did not increase risk (using white non-Hispanic persons as the reference group).

• There was found to be an overall T. gondii IgG antibody prevalence of 15.8% among persons 12–49 years of age in 1999–2000, indicating that approximately 1 in 6 persons in this age group was infected with T. gondii.
• No significant changes in T. gondii seroprevalence occurred between 1988–1994 and 1999–2000 for the U.S. population as a whole or for any of the subgroups we examined.
• It was speculated that changes in meat production with lower levels of T. gondiiin meat might result in a reduction in the prevalence of T. gondii infection in the population.
• Perhaps the time was not sufficient for changes in meat production and consumption habits to have had an impact, or perhaps the expected declines in T. gondii infection occurred before NHANES III.
• The prevalence of T. gondii infection declined in U.S. military recruits, when 1965 data were compared with 1989 data and in countries in Europe, such as France and Belgium, during similar periods.
• Predicting future trends in T. gondii prevalence in the United States is difficult because we do not have a national estimate of what proportion of T. gondii infections are attributable to undercooked meat exposure or to cat feces, soil, or water exposure.
• A large European case-control study that examined these factors showed that undercooked meat accounted for the largest portion of risk for T. gondii infection (30%–63%, depending on location).
• However, until researchers examine the risk factors for T. gondii infection in a case-control study throughout the United States, the most important U.S. risk factors and how to best focus preventive education messages will not be determined.
• NHANES gives representative estimates of prevalence for the U.S. population but is not designed to evaluate local T. gondii prevalence levels.
• Studies have indicated that T. gondii prevalence varies greatly in the United States; this local variation is most likely related to culinary practices, the ability of oocysts to survive in different climates, and the levels of immigration from areas of the world in which T. gondii infection is highly endemic.
• Nevertheless, NHANES produces useful surveillance data for tracking T. gondii prevalence over time in the United States. We will continue to monitor trends in this nationally representative survey.^{[9] [10]}

• It is estimated that between 30% and 65% of all people worldwide are infected with Toxoplasmosis.
• However, there is large variation countries: in France, for example, around 88% of the population are carriers, probably due to a high consumption of raw and lightly cooked meat.^[11]
• Germany, the Netherlands and Brazil also have high prevalences of around 80%, over 80%^[12] and 67% respecti ely. In Britain, about 22% are carriers, and South Korea’s rate is only 4.3%.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with toxoplasma oocysts excreted in cat feces.

The major risk factors for acquiring the infection is consuming raw meat and ingestion of food contaminated with toxoplasma oocysts excreted in cat feces.
The risk factors which predispose pregnant women for primary infection include: ^[1]

• Consumption of raw oysters and clams^[2]
• Eating undercooked meat which includes pork, beef and lamb^[3]
• Drinking unpasteurized goat’s milk^[4]
• Exposure to kitten litter
• Working with meat^[5]
• Low socioeconomic status^[5]
• Poor Hygiene^[5]
• Drinking unfiltered water^[5]
• Immunocompromised state

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Majority of the countries do not follow standard screening for the detection of toxoplasma infection during the antenatal period. Women are tested for antibodies aganist toxoplasma on their first antenatal visit, and if they are seropositive they are followed up periodically in every trimester to examine the trends in IgG titer levels. All HIV-infected patients should be tested for prior exposure by measuring anti-Toxoplasma IgG. Patients with HIV and CD4+ T lymphocyte counts <100 cells/microliter with detectable anti-Toxoplasma IgG are at risk for reactivation of latent infection and should receive prophylactic treatment. Screening for toxoplasma is routinely performed for cardiac donors.^[1]

• Majority of the countries do not follow standard screening for the detection of toxoplasma infection during the antenatal period.
• In countries such as France, Austria, Brazil standard screening is followed during the antenatal period for detecton of toxoplasmosis .^[2]
• Women are tested for antibodies aganist toxoplasma on their first antenatal visit, and if they are seropositive they are followed up periodically in every trimester to examine the trends in IgG titer levels.^[1]
• Women who seroconvert during gestation, fetal testing by amniocentesis and fetal blood sampling is recommended to identify the infection status in the fetus.

• All HIV-infected patients should be tested for prior exposure by measuring anti-Toxoplasma IgG.
• If previously seronegative and if the patient is unable to take trimethoprim/sulfamethoxazole for Pneumocystis jiroveci prophylaxis, serology should be repeated when the CD4+ T lymphocyte count nears 100 cells/microliter.
• Patients with HIV and CD4+ T lymphocyte counts <100 cells/microliter with detectable anti-Toxoplasma IgG are at risk for reactivation of latent infection and should receive prophylactic treatment.

• Screening for Toxoplasma is routinely performed for cardiac donors.
• Prophylaxis is indicated for patients who have detectable anti-Toxoplasma IgG or who are recipients of hearts from seropositive donors.
• All recipients of allogeneic hematopoietic stem cell transplants should have baseline anti-Toxoplasma IgG testing.
• Seropositive recipients with active graft versus host disease (GVHD) or with a history of toxoplasmic chorioretinitis should receive prophylaxis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

If left untreated in people with a weakened immune system, such as those infected with HIV, and fetuses, the disease can become seriously ill, and occasionally be fatal. The parasite can cause encephalitis (inflammation of the brain) and neurologic diseases and can affect the heart, liver, and eyes (chorioretinitis). Complications that can develop as a result of toxoplasmosis are mental retardation, seizures, motor difficulties, severe vision loss, hydrocephalus or microcephalus, hearing loss. Prognosis of infection in immunocompromised individual is dependent on the severity of the disease. Severe infection causes death at an early age, asymptomatic infection will present in the 1st or 2nd decade with progressive chorioretinitis with poor prognosis.^[1]

During the first few weeks, the infection typically causes a mild flu-like illness or no illness. After the first few weeks of infection have passed, the parasite rarely causes any symptoms in otherwise healthy adults. If left untreated in people with a weakened immune system, such as those infected with HIV, and fetuses, the disease can become seriously ill, and occasionally be fatal. The parasite can cause encephalitis (inflammation of the brain) and neurologic diseases and can affect the heart, liver, and eyes (chorioretinitis).

Complications that can develop as a result of toxoplasmosis are

• Mental retardation
• Seizures
• Motor difficulties
• Severe vision loss
• Hydrocephalus or microcephalus
• hearing loss.^[1]

• Seizures
• Encephalitis
• Blindness

• Blindness

• The prognosis toxoplasmosis infection in an immunocompetent patient is good without treatment.
• Prognosis of infection in immunocompromised individual and congenital toxoplasmosis is dependent on the severity of the disease. Severe infection causes death at an early age, asymptomatic infection at birth will present in the 1st or 2nd decade with progressive chorioretinitis with poor prognosis.

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