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    Toxoplasmosis

    Classification and external resources

    T. gondii tachyzoites

    ICD-10 B58

    (http://apps.who.int/classifications/icd10/browse/2010/en#/B58)

    ICD-9 130 (http://www.icd9data.com/getICD9Code.ashx?icd9=130)

    DiseasesDB 13208 (http://www.diseasesdatabase.com/ddb13208.htm)

    MedlinePlus000637

    (http://www.nlm.nih.gov/medlineplus/ency/article/000637.htm)

    eMedicine med/2294 (http://www.emedicine.com/med/topic2294.htm)

    MeSH D014123 (http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi?

    field=uid&term=D014123)

    ToxoplasmosisFrom Wikipedia, the free encyclopedia

    Toxoplasmosisis a parasitic

    disease caused by the protozoan

    Toxoplasma gondii.[1]The

    parasite infects most genera ofwarm-blooded animals,

    including humans, but the

    primary host is the felid (cat)

    family. Animals are infected by

    eating infected meat, by

    ingestion of feces of a cat that

    has itself recently been infected,

    and by transmission from

    mother to fetus. Cats are the

    primary source of infection tohuman hosts, although contact

    with raw meat, especially pork,

    is a more significant source of

    human infections in some

    countries. Fecal contamination

    of hands is a significant risk

    factor.[2]

    Nicolle and Manceaux first

    described the organism in 1908,after they observed the parasites

    in the blood, spleen, and liver of

    a North African rodent,

    Ctenodactylus gondii. The

    parasite was named Toxoplasma(arclike form)gondii(after the rodent) in 1909. In 1923, Janku reported

    parasitic cysts in the retina of an infant who had hydrocephalus, seizures, and unilateral microphthalmia.

    Wolf, Cowan, and Paige (19371939) determined these findings represented the syndrome of severe

    congenital T. gondii infection.[2]

    Up to a third of the world's human population is estimated to carry a Toxoplasma infection.[3][4]The

    Centers for Disease Controland Prevention notes the overall seroprevalence in the United States as

    determined with specimens collected by the National Health and Nutritional Examination Survey

    (NHANES) between 1999 and 2004 was found to be 10.8%, with seroprevalence among women of

    childbearing age (15 to 44 years) 11%.[5]Another study placed seroprevalence in the US at 22.5%.[4]The

    same study claimed a seroprevalence of 75% in El Salvador.[4]Official assessment in Great Britain places

    the number of infections at about 350,000 a year.[6]

    During the first few weeks after exposure, the infection typically causes a mild, flu-like illness or no illness.

    Thereafter, the parasite rarely causes any physical symptoms in otherwise healthy adults.[citation needed]However, those with weakened immune systems, such as those with AIDS and pregnant women, may

    become seriously ill, and it can occasionally be fatal.[citation needed]The parasite can cause encephalitis

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    (inflammation of the brain) and neurologic diseases, and can affect the heart, liver, inner ears, and eyes

    (chorioretinitis).[citation needed]Recent research has also linked toxoplasmosis with attention deficit

    hyperactivity disorder, obsessive compulsive disorder, and schizophrenia.[7]Numerous studies found a

    positive correlation between latent toxoplasmosis and suicidal behavior in humans.[8][9][10]

    Contents1 Signs and symptoms

    1.1 Acute toxoplasmosis

    1.2 Latent toxoplasmosis

    1.3 Cutaneous toxoplasmosis

    1.4 Psychiatric disorders

    1.5 Contrary evidence

    2 Diagnosis

    3 Transmission

    3.1 Pregnancy precautions

    3.2 Rodent behavior

    4 Treatment

    4.1 Acute

    4.2 Latent

    5 Epidemiology

    6 History

    7 Society and culture

    7.1 Notable cases

    8 Other animals8.1 Livestock

    8.2 Domestic cats

    8.3 Marine mammals

    9 See also

    10 References

    11 Bibliography

    12 External links

    Signs and symptoms

    Infection has two stages:

    Acute toxoplasmosis

    During acute toxoplasmosis, symptoms are often influenza-like: swollen lymph nodes, or muscle aches and

    pains that last for a month or more. Rarely will a human with a fully functioning immune system develop

    severe symptoms following infection. Young children and immunocompromised people, such as thosewith HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an

    organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain (encephalitis) or

    http://en.wikipedia.org/wiki/Encephalitishttp://en.wikipedia.org/wiki/Organ_transplanthttp://en.wikipedia.org/wiki/Chemotherapyhttp://en.wikipedia.org/wiki/Immunodeficiencyhttp://en.wikipedia.org/wiki/Immune_systemhttp://en.wikipedia.org/wiki/Myalgiahttp://en.wikipedia.org/wiki/Lymph_nodehttp://en.wikipedia.org/wiki/Influenzahttp://en.wikipedia.org/wiki/Acute_(medical)http://en.wikipedia.org/wiki/Suicidal_behaviorhttp://en.wikipedia.org/wiki/Correlationhttp://en.wikipedia.org/wiki/Schizophreniahttp://en.wikipedia.org/wiki/Obsessive_compulsive_disorderhttp://en.wikipedia.org/wiki/Attention_deficit_hyperactivity_disorderhttp://en.wikipedia.org/wiki/Wikipedia:Citation_neededhttp://en.wikipedia.org/wiki/Chorioretinitishttp://en.wikipedia.org/wiki/Human_eyehttp://en.wikipedia.org/wiki/Inner_earhttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Neurologic_disease
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    the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either

    of these problems, or with nasal malformations, although these complications are rare in newborns. The

    toxoplasmic trophozoites causing acute toxoplasmosis are referred to as Tachyzoites, and are typically

    found in bodily fluids.

    Swollen lymph nodes are commonly found in the neck or under the chin, followed by the axillae (armpits)

    and the groin. Swelling may occur at different times after the initial infection, persist, and/or recur for

    various times independently of antiparasitic treatment.[11]

    It is usually found at single sites in adults, but inchildren, multiple sites may be more common. Enlarged lymph nodes will resolve within one to two

    months in 60% of cases. However, a quarter of those affected take two to four months to return to normal,

    and 8% take four to six months. A substantial number (6%) do not return to normal until much later.[12]

    Latent toxoplasmosis

    It is easy for a host to become infected with Toxoplasma gondiiand develop toxoplasmosis without

    knowing it. In most immunocompetent people, the infection enters a latent phase, during which only

    bradyzoites are present, forming cysts in nervous and muscle tissue. Most infants who are infected while in

    the womb have no symptoms at birth, but may develop symptoms later in life.[13]

    Cutaneous toxoplasmosis

    While rare, skin lesions may occur in the acquired form of the disease, including roseola and erythema

    multiforme-like eruptions, prurigo-like nodules, urticaria, and maculopapular lesions. Newborns may have

    punctate macules, ecchymoses, or blueberry muffin lesions. Diagnosis of cutaneous toxoplasmosis is

    based on the tachyzoite form of T. gondiibeing found in the epidermis. It is found in all levels of the

    epidermis, is about 6 m by 2 m and bow-shaped, with the nucleus being one-third of its size. It can be

    identified by electron microscopy or by Giemsa staining tissue where the cytoplasm shows blue, thenucleus red.[14]

    Psychiatric disorders

    Studies have shown the toxoplasmosis parasite may affect behavior and may present as or be a causative or

    contributory factor in various psychiatric disorders, such as depression, anxiety, and

    schizophrenia.[15][16][17]In 11 of 19 scientific studies, T. gondiiantibody levels were found to be

    significantly higher in individuals affected by first-incidence schizophrenia than in unaffected persons.

    Individuals with schizophrenia are also more likely to report a clinical history of toxoplasmosis than those

    in the general population.[18]Recent work at the University of Leeds has found the parasite produces an

    enzyme with tyrosine hydroxylase and phenylalanine hydroxylase activity. This enzyme may contribute to

    the behavioral changes observed in toxoplasmosis by altering the production of dopamine, a

    neurotransmitter involved in mood, sociability, attention, motivation, and sleep patterns. Schizophrenia has

    long been linked to dopamine dysregulation.[19]Minocycline, an antibiotic capable of passing the blood-

    brain barrier used for treating toxoplasmosis, has been found to alleviate the symptoms of

    schizophrenia.[20]

    Chronic infection with T. gondiihas traditionally been considered asymptomatic in immunocompetent

    human hosts. However, accumulating evidence suggests latent infection may subtly influence a range ofhuman behaviors and tendencies, and infection may alter the susceptibility to or intensity of a number of

    affective, psychiatric, or neurological disorders.[21]

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    Micrograph of a lymph node showing

    the characteristic changes oftoxoplasmosis (scattered epithelioid

    histiocytes (pale cells), monocytoid

    cells (top-center of image), large

    germinal centers (left of image))

    H&E stain

    Latent T. gondiiinfection in humans has been associated with impaired psychomotor performance,

    enhanced risk-taking personality profiles, and higher incidence of automobile accidents.[21]Moreover,

    correlations have been found between positive antibody titers to T. gondiiand OCD, Parkinsons disease,

    Alzheimers disease, suicide in people with mood disorders, and bipolar disorder.[21]Positive antibody

    titers to T. gondiihave been shown to be not correlative with major depression or dysthymia.[22]

    The most substantial body of evidence linking T. gondiito a neurological disorder involves the potential

    association between schizophrenia and infection with the parasite.[23][24]As of 2013, at least 38 studieshave found a positive correlation between T. gondiiantibody titers and schizophrenia.[21][25]While the

    vast majority of these studies tested people already diagnosed with schizophrenia for T. gondiiantibodies,

    significant associations between T. gondiiand schizophrenia have been found prior to the onset of

    schizophrenia disease symptoms.[23]

    In most of the current studies where positive associations have been found between T. gondiiantibody

    titers and certain behavioral traits or neurological disorders, T. gondiiseropositivity tests are conducted

    after the onset of the examined disease or behavioral trait that is, it is often unclear whether infection with

    the parasite increases the chances of having a certain trait or disorder, or if having a certain trait or disorder

    increases the chances of becoming infected with the parasite.[26]

    Groups of individuals with certain behavioral traits or neurological

    disorders may share certain behavioral tendencies that increase the

    likelihood of exposure to and infection with T. gondii as a result,

    it is difficult to confirm causal relationships between T. gondii

    infections and associated neurological disorders or behavioral

    traits.[26]

    Contrary evidence

    Toxoplasma gondiiis beneficial to mice with Alzheimer's disease.[27]Murine analogues to the Comt, DRD4andDAT1human

    genes also exist, and these genes are related to Alzheimer's

    disease.[28]DAT1, for example, encodes the neural membranes

    through which dopamine returns to the cell.DAT1gene mutations

    are responsible for too rapid dopamine uptake, which results in

    deficiency in extracellular dopamine. Since T. gondiiproduces

    dopamine, it has a potential to overcome these gene-related

    disorders also in humans, mainly because the mechanisms

    encoded by Comt, DRD4, andDAT1are both murine and human.

    Too fast DAT1 dopamine uptake is related to other neurological

    disorders [29][30]which can potentially benefit from T. gondii

    dopamine synthesis. It is an interesting open question whether

    mammals with DAT1 polymorphisms are genetically better

    adapted to T. gondii infection.

    Examples of genetic factors in Parkinson's disease areLRRK2mutations Gly2019Ser, I2020T, and others.

    Some evidence indicates exposure to pesticides causes Parkinson's disease[31]The disease presents when

    80% of the neurons that produce dopamine in the substantia nigra die. This shortage of dopamine could becompensated by T. gondii, which is known to produce dopamine.

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    Lifecycle of Toxoplasma gondii

    Diagnosis

    Toxoplasmosis can be difficult to distinguish from primary central nervous system lymphoma, and as a

    result, the diagnosis is made by a trial of therapy (pyrimethamine, sulfadiazine, and folinic acid (USAN:

    leucovorin)), followed by a brain biopsy if the drugs produce no effect clinically and no improvement on

    repeat imaging.

    Detection of T. gondiiin human blood samples may also be achieved by using the polymerase chainreaction.[32]Inactive cysts may exist in a host which would evade detection.

    Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected by Toxoplasmahave

    characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B

    cells, and scattered epithelioid histiocytes.

    Transmission

    Transmission may occur through:

    Ingestion of raw or partly cooked meat, especially pork, lamb,

    or venison containing Toxoplasmacysts: Infection prevalence

    in countries where undercooked meat is traditionally eaten

    has been related to this transmission method. Tissue cysts

    may also be ingested during hand-to-mouth contact after

    handling undercooked meat, or from using knives, utensils, or

    cutting boards contaminated by raw meat.[33]

    Ingestion of contaminated cat feces: This can occur through

    hand-to-mouth contact following gardening, cleaning a cat's

    litter box, contact with children's sandpits, or touching a

    leech the parasite can survive in the environment for over a

    year.[34]

    Cats excrete the pathogen in their feces for a number of weeks after

    contracting the disease, generally by eating an infected rodent. Even

    then, cat feces are not generally contagious for the first day or two after excretion, after which the cyst

    'ripens' and becomes potentially pathogenic.[35]

    Pregnancy precautions

    Congenital toxoplasmosis is a special form in which an unborn fetus is infected via the placenta. A positive

    antibody titer indicates previous exposure and immunity, and largely ensures the unborn fetus' safety. A

    simple blood draw at the first prenatal doctor visit can determine whether or not a woman has had previous

    exposure and therefore whether or not she is at risk. If a woman receives her first exposure to T. gondii

    while pregnant, the fetus is at particular risk. A woman with no previous exposure should avoid handling

    raw meat, exposure to cat feces, and gardening (cat feces are common in garden soil). Most cats are not

    actively shedding oocysts, so are not a danger, but the risk may be reduced further by having the litter box

    emptied daily (oocysts require longer than a single day to become infective), and by having someone else

    empty the litter box. However, while risks can be minimized, they cannot be eliminated. For pregnant

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    women with negative antibody titers, indicating no previous exposure to T. gondii, serology testing as

    frequent as monthly is advisable as treatment during pregnancy for those women exposed to T. gondiifor

    the first time decreases dramatically the risk of passing the parasite to the fetus.

    Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries

    (Portugal,[36]France,[37]Austria,[37]Uruguay,[38]and Italy[39]being the exceptions) for reasons of cost-

    effectiveness and the high number of false positives generated. As invasive prenatal testing incurs some

    risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented),[37]

    postnatal or neonatalscreening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening

    can be targeted.[37]

    Some regional screening programmes operate in Germany, Switzerland and Belgium.[39]

    Treatment is very important for recently infected pregnant women, to prevent infection of the fetus. Since a

    baby's immune system does not develop fully for the first year of life, and the resilient cysts that form

    throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in

    the young.

    In 2006, a Czech research team discovered women with high levels of toxoplasmosis antibodies were

    significantly more likely to have baby boys than baby girls. In most populations, the birth rate is around

    51% boys, but women infected with T. gondiihad up to a 72% chance of a boy.[40]

    Rodent behavior

    Infection with T. gondiihas been shown to alter the behavior of mice and rats in ways thought to increase

    the rodents chances of being preyed upon by cats.[23][41][42]Infected rodents show a reduction in their

    innate aversion to cat odors while uninfected mice and rats will generally avoid areas marked with cat

    urine or with cat body odor, this avoidance is reduced or eliminated in infected animals. [23][42][43]

    Moreover, some evidence suggests this loss of aversion may be specific to feline odors: when given a

    choice between two predator odors (cat or mink), infected rodents show a significantly stronger preference

    to cat odors than do uninfected controls.[44][45]

    T. gondii-infected rodents show a number of behavioral changes beyond altered responses to cat odors.

    Rats infected with the parasite show increased levels of activity and decreased neophobic behavior.[41][46]

    Similarly, infected mice show alterations in patterns of locomotion and exploratory behavior during

    experimental tests. These patterns include traveling greater distances, moving at higher speeds, accelerating

    for longer periods of time, and showing a decreased pause-time when placed in new arenas. [47]Infectedrodents have also been shown to have differences in traditional measures of anxiety, such as elevated plus

    mazes, open field arenas, and social interaction tests.[47][48]

    Treatment

    Treatment is often only recommended for people with serious health problems, such as people with HIV

    whose CD4 counts are under 200, because the disease is most serious when one's immune system is weak.

    Trimethoprim/sulfamethoxazole is the drug of choice to prevent toxoplasmosis, but not for treating active

    disease.

    Acute

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    The medications prescribed for acute toxoplasmosis are:

    Pyrimethamine an antimalarial medication

    Sulfadiazine an antibiotic used in combination with pyrimethamine to treat toxoplasmosis

    Combination therapy is usually given with folic acid supplements to reduce incidence of

    thrombocytopaenia.

    Combination therapy is most useful in the setting of HIV.

    ClindamycinSpiramycin an antibiotic used most often for pregnant women to prevent the infection of their

    children

    (other antibiotics, such as minocycline, have seen some use as a salvage therapy).

    Latent

    In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not

    reach the bradyzoites in sufficient concentration.

    The medications prescribed for latent toxoplasmosis are:

    Atovaquone an antibiotic that has been used to kill Toxoplasmacysts inside AIDS patients[49]

    Clindamycin an antibiotic which, in combination with atovaquone, seemed to optimally kill cysts

    in mice[50]

    Epidemiology

    T. gondiiinfections occur throughout the world, although infection rates differ significantly by country.[51]

    For women of childbearing age, a survey of 99 studies within 44 countries found the areas of highest

    prevalence are within Latin America (about 5080%), parts of Eastern and Central Europe (about 20

    60%), the Middle East (about 30-50%), parts of Southeast Asia (about 2060%), and parts of Africa (about

    2055%).[51]

    In the United States, data from the National Health and Nutrition Examination Survey (NHANES) from

    1999 to 2004 found 9.0% of US-born persons 1249 years of age were seropositive for IgG antibodies

    against T. gondii, down from 14.1% as measured in the NHANES 19881994.[52]In the 19992004

    survey, 7.7% of US-born and 28.1% of foreign-born women 1544 years of age were T. gondii

    seropositive.[52]A trend of decreasing seroprevalence has been observed by numerous studies in the

    United States and many European countries.[51]

    Because the parasite poses a particular threat to fetuses when it is contracted during pregnancy, [53]much

    of the global epidemiological data regarding T. gondiicomes from seropositivity tests in women of

    childbearing age. Seropositivity tests look for the presence of antibodies against T. gondiiin blood, so

    while seropositivity guarantees one has been exposed to the parasite, it does not necessarily guarantee one

    is chronically infected.[54]

    History

    http://en.wikipedia.org/wiki/Epidemiologicalhttp://en.wikipedia.org/wiki/Seroprevalencehttp://en.wikipedia.org/wiki/Antibodieshttp://en.wikipedia.org/wiki/IgGhttp://en.wikipedia.org/wiki/Seropositivehttp://en.wikipedia.org/wiki/National_Health_and_Nutrition_Examination_Surveyhttp://en.wikipedia.org/wiki/United_Stateshttp://en.wikipedia.org/wiki/Africahttp://en.wikipedia.org/wiki/Southeast_Asiahttp://en.wikipedia.org/wiki/Middle_Easthttp://en.wikipedia.org/wiki/Central_Europehttp://en.wikipedia.org/wiki/Eastern_Europehttp://en.wikipedia.org/wiki/Latin_Americahttp://en.wikipedia.org/wiki/Atovaquonehttp://en.wikipedia.org/wiki/Clindamycinhttp://en.wikipedia.org/wiki/AIDShttp://en.wikipedia.org/wiki/Atovaquonehttp://en.wikipedia.org/wiki/Bradyzoitehttp://en.wikipedia.org/wiki/Salvage_therapyhttp://en.wikipedia.org/wiki/Minocyclinehttp://en.wikipedia.org/wiki/Spiramycinhttp://en.wikipedia.org/wiki/Clindamycinhttp://en.wikipedia.org/wiki/Thrombocytopaeniahttp://en.wikipedia.org/wiki/Antibiotichttp://en.wikipedia.org/wiki/Sulfadiazinehttp://en.wikipedia.org/wiki/Antimalarial_medicationhttp://en.wikipedia.org/wiki/Pyrimethamine
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    The T. gondiiprotozoan was first discovered by Nicolle and Manceaux, who in 1908 isolated it from the

    African rodent Ctenodactylus gundi, then in 1909 differentiated the organism fromLeishmaniaand named

    it Toxoplasma gondii.[37]The first recorded congenital case was not until 1923, and the first adult case not

    until 1940.[37]In 1948, a serological dye test was created by Sabin and Feldman, which is now the

    standard basis for diagnostic tests.[55]

    Society and cultureNotable cases

    Arthur Ashe (tennis player) developed neurological problems from toxoplasmosis (and was later

    found to be HIV-positive).[56]

    Merritt Butrick (actor) was HIV positive and died from toxoplasmosis as a result of his already

    weakened immune system.[57]

    Prince Franois, Count of Clermont (pretender to the throne of France) his disability caused him to

    be overlooked in the line of succession.Leslie Ash (actress) contracted toxoplasmosis in the second month of pregnancy.[58]

    Sebastian Coe (British middle distance runner)[59]

    Martina Navratilova suffered from toxoplasmosis during the 1982 US Open.[60]

    Louis Wain (artist) was famous for painting cats he later developed schizophrenia, which some

    believe was due to toxoplasmosis resulting from his prolonged exposure to cats.[61]

    Jaroslav Flegr (biologist) is a proponent of the theory that toxoplasmosis affects human behavior. [62]

    Other animals

    Although T. gondiihas the capability of infecting virtually all warm-blooded animals, susceptibility and

    rates of infection vary widely between different genera and species. [63]Rates of infection in populations of

    the same species can also vary widely due to differences in location, diet, and other factors.

    Livestock

    Among livestock, pigs, sheep, and goats have the highest rates of chronic T. gondii infection.[64]The

    prevalence of T. gondiiin meat-producing animals varies widely both within and between countries,[64]

    and rates of infection have been shown to be dramatically influenced by varying farming and managementpractices.[65]For instance, animals kept outdoors or in free-ranging environments are more at risk of

    infection than animals raised indoors or in commercial confinement operations.[65][66]

    In the United States, the percentage of pigs harboring viable parasites has been measured (via bioassay in

    mice or cats) to be as high as 92.7% and as low as 0%, depending on the farm or herd. [66]Surveys of

    seroprevalence (T. gondiiantibodies in blood) are more common, and such measurements are indicative of

    the high relative seroprevlance in pigs across the world.[67]Along with pigs, sheep and goats are among

    the most commonly infected livestock of epidemiological significance for human infection.[64]Prevalence

    of viable T. gondiiin sheep tissue has been measured (via bioassay) to be as high as 78% in the United

    States,[68]and a 2011 survey of goats intended for consumption in the United States found a

    seroprevalence of 53.4%.[69]

    http://en.wikipedia.org/wiki/Bioassayhttp://en.wikipedia.org/wiki/Factory_farminghttp://en.wikipedia.org/wiki/Free_rangehttp://en.wikipedia.org/wiki/Livestockhttp://en.wikipedia.org/wiki/Specieshttp://en.wikipedia.org/wiki/Generahttp://en.wikipedia.org/wiki/Jaroslav_Flegrhttp://en.wikipedia.org/wiki/Louis_Wainhttp://en.wikipedia.org/wiki/1982_US_Open_%E2%80%93_Women%27s_Singleshttp://en.wikipedia.org/wiki/Martina_Navratilovahttp://en.wikipedia.org/wiki/Sebastian_Coehttp://en.wikipedia.org/wiki/Leslie_Ashhttp://en.wikipedia.org/wiki/Throne_of_Francehttp://en.wikipedia.org/wiki/Prince_Fran%C3%A7ois,_Count_of_Clermonthttp://en.wikipedia.org/wiki/Merritt_Butrickhttp://en.wikipedia.org/wiki/Arthur_Ashehttp://en.wikipedia.org/wiki/Serologicalhttp://en.wikipedia.org/wiki/Congenitalhttp://en.wikipedia.org/wiki/Toxoplasma_gondiihttp://en.wikipedia.org/wiki/Leishmaniahttp://en.wiktionary.org/wiki/differentiatehttp://en.wikipedia.org/wiki/Gundi
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    Due to a lack of exposure to the outdoors, chickens raised in large-scale indoor confinement operations are

    not commonly infected with T. gondii.[65]Free-ranging or backyard-raised chickens are much more

    commonly infected.[65]A survey of free-ranging chickens in the United States found its prevalence to be

    17%100%, depending on the farm.[70]Because chicken meat is generally cooked thoroughly before

    consumption, poultry is not generally considered to be a significant risk factor for human T. gondii

    infection.[71]

    Although cattle and buffalo can be infected with T. gondii, the parasite is generally eliminated or reducedto undetectable levels within a few weeks following exposure.[65]Tissue cysts are rarely present in buffalo

    meat or beef, and meat from these animals is considered to be low-risk for harboring viable

    parasites.[64][66]

    Horses are considered resistant to chronic T. gondii infection.[65]However, viable cells have been isolated

    from US horses slaughtered for export, and severe human toxoplasmosis in France has been

    epidemiologically linked to the consumption of horse meat.[66]

    Domestic cats

    The seroprevalence of T. gondiiin domestic cats, worldwide, has been estimated to be around 3040%.[72]

    In the United States, no official national estimate has been made, but local surveys have shown levels

    varied between 16% and 80%.[72]A 2012 survey of 445 purebred pet cats and 45 shelter cats in Finland

    found an overall seroprevalence of 48.4%.[73]A 2010 survey of feral cats from Giza, Egypt, found an

    overall seroprevalence of 97.4%.[74]

    T. gondiiinfection rates in domestic cats vary widely depending on the cats' diets and lifestyles.[75]Feral

    cats that hunt for their food are more likely to be infected than domestic cats. The prevalence of T. gondii

    in cat populations depends on the availability of infected birds and small mammals,[76]but often this prey

    is abundant.

    Most infected cats will shed oocysts only once in their lifetimes, for a period of about one to two

    weeks.[72]Although this period of shedding is quite transient, millions of oocysts can be shed, with each

    oocyst capable of spreading and surviving for months.[72]An estimated 1% of cats at any given time are

    actively shedding oocysts.[65]

    Marine mammals

    A University of California, Davis study of dead sea otters collected from 1998 to 2004 found

    toxoplasmosis was the cause of death for 13% of the animals.[77]Proximity to freshwater outflows into the

    ocean was a major risk factor. Ingestion of oocysts from cat faeces is considered to be the most likely

    ultimate source.[78]Surface runoff containing wild cat faeces and litter from domestic cats flushed down

    toilets are possible sources of oocysts.[79]The parasites have been found in dolphins and whales.[17]

    Researchers Black and Massie believe anchovies, which travel from estuaries into the open ocean, may be

    helping to spread the disease.

    See also

    TORCH infection

    http://en.wikipedia.org/wiki/TORCH_complexhttp://en.wikipedia.org/wiki/Surface_runoffhttp://en.wikipedia.org/wiki/Oocystshttp://en.wikipedia.org/wiki/Sea_otterhttp://en.wikipedia.org/wiki/University_of_California,_Davishttp://en.wikipedia.org/wiki/Mammalshttp://en.wikipedia.org/wiki/Feral_cathttp://en.wikipedia.org/wiki/Giza,_Egypthttp://en.wikipedia.org/wiki/Finlandhttp://en.wikipedia.org/wiki/Purebredhttp://en.wikipedia.org/wiki/Domestic_cathttp://en.wikipedia.org/wiki/Horse_meat
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    The T.Gondii Host/Pathogen interactome (http://www.polygenicpathways.co.uk/tgondii.htm)

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    Louis M Weiss Kami Kim (28 April 2011). Toxoplasma Gondii: The Model Apicomplexan.

    Perspectives and Methods(http://books.google.com/books?id=yTUkJEphM_IC). Academic Press.

    ISBN 978-0-08-047501-1. Retrieved 12 March 2013.

    J. P. Dubey (15 April 2010). Toxoplasmosis of Animals and Humans, Second Edition

    (http://books.google.com/books?id=5Nm7t5p9APAC). CRC Press. ISBN 978-1-4200-9237-0.

    Retrieved 12 March 2013.

    External links

    Toxoplasmosis (http://www.merck.com/mmpe/sec14/ch186/ch186h.html)at Merck Manual of

    Diagnosis and Therapy Professional Edition

    Toxoplasmosis

    (http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733799638) atHealth Protection Agency (HPA), United Kingdom

    Pictures of Toxoplasmosis (http://rad.usuhs.edu/medpix/medpix.html?

    mode=image_finder&action=search&srchstr=toxoplasmosis#top) Medical Image Database

    Video-Interview (http://www.youtube.com/watch?v=m3x3TMdkGdQ) with Professor Robert

    Sapolsky on Toxoplasmosis and its affect on human behavior. (24:27 min)

    Retrieved from "http://en.wikipedia.org/w/index.php?title=Toxoplasmosis&oldid=566312154"

    Categories: Cat diseases Apicomplexa Protozoal diseases Zoonoses Mind-altering parasites

    Parasitic infestations, stings, and bites of the skin Poultry diseases Health issues in pregnancy

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