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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
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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
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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/Gundi8/14/2019 Toxoplasmosis - Wikipedia, the free encyclopedia.pdf
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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_meat8/14/2019 Toxoplasmosis - Wikipedia, the free encyclopedia.pdf
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The T.Gondii Host/Pathogen interactome (http://www.polygenicpathways.co.uk/tgondii.htm)
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Bibliography
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.
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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"
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