Toxoplasmosis Wiki

Toxoplasmosis
Toxoplasmosis is a parasitic disease caused by Toxoplasma

Toxoplasmosis
gondii, an apicomplexan.[3] Infections with toxoplasmosis
usually cause no obvious symptoms in adults.[2] Occasionally,
people may have a few weeks or months of mild, flu-like
illness such as muscle aches and tender lymph nodes.[1] In a
small number of people, eye problems may develop.[1] In
those with a weak immune system, severe symptoms such as
seizures and poor coordination may occur.[1] If a woman
becomes infected during pregnancy, a condition known as
congenital toxoplasmosis may affect the child.[1]
Toxoplasmosis is usually spread by eating poorly cooked food

that contains cysts, exposure to infected cat feces, and from an
T. gondii tachyzoites
infected mother to her baby during pregnancy.[3] Rarely, the
disease may be spread by blood transfusion.[3] It is not Specialty Infectious disease
otherwise spread between people.[3] The parasite is known to Symptoms Often none, during
reproduce sexually only in the cat family.[8] However, it can pregnancy (birth
infect most types of warm-blooded animals, including defects)[1][2]
humans.[8] Diagnosis is typically by testing blood for
Causes Toxoplasma gondii[3]
antibodies or by testing the amniotic fluid in pregnant women
for the parasite's DNA.[4] Risk Eating poorly cooked food,
factors exposure to infected cat
Prevention is by properly preparing and cooking food.[9] feces[3]
Pregnant women are also recommended not to clean cat litter
Diagnostic Blood test, amniotic fluid
boxes or, if they must, to wear gloves and wash their hands
afterwards.[9] Treatment of otherwise healthy people is usually method test[4]
not needed.[5] During pregnancy, spiramycin or Treatment During pregnancy
pyrimethamine/sulfadiazine and folinic acid may be used for spiramycin or
treatment.[5] pyrimethamine/sulfadiazine
and folinic acid[5]
Up to half of the world's population is infected by
toxoplasmosis, but have no symptoms.[7] In the United States, Frequency Up to 50% of people,
approximately 11% of people are infected, while in some 200,000 cases of
areas of the world this is more than 60%.[3] Approximately congenital toxoplasmosis a
200,000 cases of congenital toxoplasmosis occur a year.[6] year[6][7]
Charles Nicolle and Louis Manceaux first described the
organism in 1908.[10] In 1941, transmission during pregnancy from a mother to a baby was confirmed.[10]
There is tentative evidence that infection may affect people's behavior.[11]
Contents
Signs and symptoms
Acute
Latent
Skin
Cause
Parasitology
Transmission
Pregnancy precautions
Diagnosis
Congenital
Treatment
Acute
Latent
Congenital
Epidemiology
History
Society and culture
"Crazy cat-lady"
Notable cases
Other animals
Livestock
Domestic cats
Rodents
Marine mammals
Giant panda
Research
Mental health
Neurological disorders
Traffic accidents
Climate change
See also
References
Bibliography
External links
Signs and symptoms

Infection has three stages:
Acute
Acute toxoplasmosis is often asymptomatic in healthy adults.[12][13] However, symptoms may manifest and
are often influenza-like: swollen lymph nodes, headaches, fever, and fatigue,[14] or muscle aches and pains
that last for a month or more. It is rare for a human with a fully functioning immune system to develop
severe symptoms following infection. People with weakened immune systems are likely to experience
headache, confusion, poor coordination, seizures, lung problems that may resemble tuberculosis or
Pneumocystis jiroveci pneumonia (a common opportunistic infection that occurs in people with AIDS), or
chorioretinitis caused by severe inflammation of the retina (ocular toxoplasmosis).[14] Young children and
immunocompromised people, such as those with 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 the eyes (necrotizing retinochoroiditis).[15] 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 various tissues and body fluids, but rarely in blood or
cerebrospinal fluid.[16]
Swollen lymph nodes are commonly found in the neck or under the chin, followed by the armpits and the
groin. Swelling may occur at different times after the initial infection, persist, and recur for various times
independently of antiparasitic treatment.[17] It is usually found at single sites in adults, but in children,
multiple sites may be more common. Enlarged lymph nodes will resolve within 1–2 months in 60% of
cases. However, a quarter of those affected take 2–4 months to return to normal, and 8% take 4–6 months.
A substantial number (6%) do not return to normal until much later.[18]
Latent
Due to the absence of obvious symptoms,[12][13] hosts easily become infected with T. gondii and develop
toxoplasmosis without knowing it. Although mild, flu-like symptoms occasionally occur during the first
few weeks following exposure, infection with T. gondii produces no readily observable symptoms in
healthy human adults.[7][19] In most immunocompetent people, the infection enters a latent phase, during
which only bradyzoites (in tissue cysts) are present;[20] these tissue cysts and even lesions can occur in the
retinas, alveolar lining of the lungs (where an acute infection may mimic a Pneumocystis jirovecii
infection), heart, skeletal muscle, and the central nervous system (CNS), including the brain.[21] Cysts form
in the CNS (brain tissue) upon infection with T. gondii and persist for the lifetime of the host.[22] Most
infants who are infected while in the womb have no symptoms at birth, but may develop symptoms later in
life.[23]
Reviews of serological studies have estimated that 30–50% of the global population has been exposed to
and may be chronically infected with latent toxoplasmosis, although infection rates differ significantly from
country to country.[7][24][25] This latent state of infection has recently been associated with numerous
disease burdens,[7] neural alterations,[22][24] and subtle gender-dependent behavioral changes in
immunocompetent humans,[26][27] as well as a increased risk of motor vehicle collisions.[28]
Skin
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. gondii being found in the epidermis.[29] It is found in all levels of the
epidermis, is about 6 by 2 μm 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, the
nucleus red.[30]
Cause
Parasitology
In its lifecycle, T. gondii adopts several forms.[31]

Tachyzoites are responsible for acute infection;
they divide rapidly and spread through the tissues
of the body. Tachyzoites are also known as
"tachyzoic merozoites", a descriptive term that
conveys more precisely the parasitological nature
of this stage.[32] After proliferating, tachyzoites
convert into bradyzoites, which are inside latent
intracellular tissue cysts that form mainly in the
muscles and brain. The formation of cysts is in
part triggered by the pressure of the host immune
system.[33] The bradyzoites (also called
"bradyzoic merozoites") are not responsive to
antibiotics. Bradyzoites, once formed, can remain
in the tissues for the lifespan of the host. In a
healthy host, if some bradyzoites convert back
into active tachyzoites, the immune system will
quickly destroy them. However, in
immunocompromised individuals, or in fetuses,
which lack a developed immune system, the
tachyzoites can run rampant and cause significant
neurological damage.[31] Lifecycle of Toxoplasma gondii
The parasite's survival is dependent on a balance

between host survival and parasite proliferation.[33] T. gondii achieves this balance by manipulating the
host's immune response, reducing the host's immune response, and enhancing the parasite's reproductive
advantage.[33] Once it infects a normal host cell, it resists damage caused by the host's immune system, and
changes the host's immune processes.
As it forces its way into the host cell, the parasite forms a parasitophorous vacuole (PV) membrane from the
membrane of the host cell.[2][34] The PV encapsulates the parasite, and is both resistant to the activity of the
endolysosomal system, and can take control of the host's mitochondria and endoplasmic reticulum.[2][34]
When first invading the cell, the parasite releases ROP proteins from the bulb of the rhoptry organelle.[2]
These proteins translocate to the nucleus and the surface of the PV membrane where they can activate
STAT pathways to modulate the expression of cytokines at the transcriptional level, bind and inactivate PV
membrane destroying IRG proteins, among other possible effects.[2][34][35] Additionally, certain strains of
T. gondii can secrete a protein known as GRA15, activating the NF-κB pathway, which upregulates the
pro-inflammatory cytokine IL-12 in the early immune response, possibly leading to the parasite's latent
phase.[2] The parasite's ability to secrete these proteins depends on its genotype and affects its
virulence.[2][35]
The parasite also influences an anti-apoptotic mechanism, allowing the infected host cells to persist and
replicate. One method of apoptosis resistance is by disrupting pro-apoptosis effector proteins, such as BAX
and BAK.[36] To disrupt these proteins, T. gondii causes conformational changes to the proteins, which
prevent the proteins from being transported to various cellular compartments where they initiate apoptosis
events. T. gondii does not, however, cause downregulation of the pro-apoptosis effector proteins.[36]
T. gondii also has the ability to initiate autophagy of the host's cells.[37] This leads to a decrease in healthy,
uninfected cells, and consequently fewer host cells to attack the infected cells. Research by Wang et al finds
that infected cells lead to higher levels of autophagosomes in normal and infected cells.[37] Their research
reveals that T. gondii causes host cell autophagy using a calcium-dependent pathway.[37] Another study
suggests that the parasite can directly affect calcium being released from calcium stores, which are
important for the signalling processes of cells.[36]
The mechanisms above allow T. gondii to persist in a host. Some limiting factors for the toxoplasma is that
its influence on the host cells is stronger in a weak immune system and is quantity-dependent, so a large
number of T. gondii per host cell cause a more severe effect.[38] The effect on the host also depends on the
strength of the host immune system. Immunocompetent individuals do not normally show severe symptoms
or any at all, while fatality or severe complications can result in immunocompromised individuals.[38]
Since the parasite can change the host's immune response, it may also have an effect, positive or negative,
on the immune response to other pathogenic threats.[33] This includes, but is not limited to, the responses to
infections by Helicobacter felis, Leishmania major, or other parasites, such as Nippostrongylus
brasiliensis.[33]
Transmission
Toxoplasmosis is generally transmitted through the mouth when Toxoplasma gondii oocysts or tissue cysts
are accidentally eaten.[39] Congenital transmittance from mother to fetus can also occur.[40] Transmission
may also occur during the solid organ transplant process[41] or hematogenous stem cell transplants.[42]
Oral transmission may occur through:
Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing
Toxoplasma cysts: 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.[43]
Ingestion of unwashed fruit or vegetables that have been in contact with contaminated soil
containing infected cat feces.[44]
Ingestion of cat feces containing oocysts: This can occur through hand-to-mouth contact
following gardening, cleaning a cat's litter box, contact with children's sandpits; the parasite
can survive in the environment for months.[45]
Ingestion of untreated, unfiltered water through direct consumption or utilization of water for
food preparation.[46]
Ingestion of unpasteurized milk and milk products, particularly goat's milk.
Ingestion of raw seafood.
Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by
eating an infected intermediate host that could include mammals (like rodents) or birds. Oocyst shedding
usually starts from the third day after ingestion of infected intermediate hosts, and may continue for weeks.
The oocysts are not infective when excreted. After about a day, the oocyst undergoes a process called
sporulation and becomes potentially pathogenic.[47] In addition to cats, birds and mammals including
human beings are also intermediate hosts of the parasite and are involved in the transmission process.
However the pathogenicity varies with the age and species involved in infection and the mode of
transmission of T. gondii.[48]
Toxoplasmosis may also be transmitted through solid organ transplants. Toxoplasma-seronegative recipients
who receive organs from recently infected Toxoplasma-seropositive donors are at risk. Organ recipients
who have latent toxoplasmosis are at risk of the disease reactivating in their system due to the
immunosuppression occurring during solid organ transplant.[41] Recipients of hematogenous stem cell
transplants may experience higher risk of infection due to longer periods of immunosuppression.[42]
Heart and lung transplants provide the highest risk for toxoplasmosis infection due to the striated muscle
making up the heart,[41] which can contain cysts, and risks for other organs and tissues vary widely.[49]
Risk of transmission can be reduced by screening donors and recipients prior to the transplant procedure
and providing treatment.[49]
Pregnancy precautions
Congenital toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected via the
placenta.[50] Congenital toxoplasmosis is associated with fetal death and miscarriage, and in infants, it is
associated with hydrocephalus, cerebral calcifications and chorioretinitis, leading to encephalopathy and
possibly blindness.[6] 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.[6]
Not much evidence exists around the effect of education before pregnancy to prevent congenital
toxoplasmosis.[51] However educating parents before the baby is born has been suggested to be effective
because it may improve food, personal and pet hygiene.[51] More research is needed to find whether
antenatal education can reduce congenital toxoplasmosis.[51]
For pregnant 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.
gondii for the first time dramatically decreases the risk of passing the parasite to 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.
Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries, for
reasons of cost-effectiveness and the high number of false positives generated; Portugal,[52] France,[53]
Austria,[53] Uruguay,[54] and Italy[55] are notable exceptions, and some regional screening programmes
operate in Germany, Switzerland and Belgium.[55] As invasive prenatal testing incurs some risk to the fetus
(18.5 pregnancy losses per toxoplasmosis case prevented),[53] postnatal or neonatal screening is preferred.
The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.[53]
Pregnant women should avoid handling raw meat, drinking raw milk (especially goat milk) and be advised
to not eat raw or undercooked meat regardless of type.[56] Because of the obvious relationship between
Toxoplasma and cats it is also often advised to avoid exposure to cat feces, and refrain from gardening (cat
feces are common in garden soil) or at least wear gloves when so engaged.[56] Most cats are not actively
shedding oocysts, since they get infected in the first six months of their life, when they shed oocysts for a
short period of time (1–2 weeks.)[57] However, these oocysts get buried in the soil, sporulate and remain
infectious for periods ranging from several months to more than a year.[56] Numerous studies have shown
living in a household with a cat is not a significant risk factor for T. gondii infection,[56][58][59] though
living with several kittens has some significance.[60]
In 2006, a Czech research team[61] 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. gondii had up to a 72% chance of a boy.[62]
Diagnosis
Diagnosis of toxoplasmosis in humans is made by biological,
serological, histological, or molecular methods, or by some
combination of the above.[57] Toxoplasmosis can be difficult to
distinguish from primary central nervous system lymphoma. It
mimics several other infectious diseases so clinical signs are non-
specific and are not sufficiently characteristic for a definite
diagnosis. As a result, the possibility of an alternate diagnosis is
supported by a failed trial of antimicrobial therapy (pyrimethamine,
sulfadiazine, and folinic acid (USAN: leucovorin)), i.e., if the
drugs produce no effect clinically and no improvement on repeat
imaging.
T. gondii may also be detected in blood, amniotic fluid, or

cerebrospinal fluid by using polymerase chain reaction.[63] T.
gondii may exist in a host as an inactive cyst that would likely
evade detection. MRI: Cerebral toxoplasmosis with
primary involvement in the right
Serological testing can detect T. gondii antibodies in blood serum, occipital lobe (at left and below of the
using methods including the Sabin–Feldman dye test (DT), the image). 48-year-old woman with
indirect hemagglutination assay, the indirect fluorescent antibody AIDS.
assay (IFA), the direct agglutination test, the latex agglutination test
(LAT), the enzyme-linked immunosorbent assay (ELISA), and the
immunosorbent agglutination assay test (IAAT).[57]
The most commonly used tests to measure IgG antibody are the DT, the ELISA, the IFA, and the modified
direct agglutination test.[64] IgG antibodies usually appear within a week or two of infection, peak within
one to two months, then decline at various rates.[64] Toxoplasma IgG antibodies generally persist for life,
and therefore may be present in the bloodstream as a result of either current or previous infection.[65]
To some extent, acute toxoplasmosis infections can be differentiated from chronic infections using an IgG
avidity test, which is a variation on the ELISA. In the first response to infection, toxoplasma-specific IgG
has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG affinity for the
antigen increases. Based on the IgG avidity test, if the IgG in the infected individual has a high affinity, it
means that the infection began three to five months before testing. This is particularly useful in congenital
infection, where pregnancy status and gestational age at time of infection determines treatment.[66]
In contrast to IgG, IgM antibodies can be used to detect acute infection but generally not chronic
infection.[65] The IgM antibodies appear sooner after infection than the IgG antibodies and disappear faster
than IgG antibodies after recovery.[57] In most cases, T. gondii-specific IgM antibodies can first be detected
approximately a week after acquiring primary infection and decrease within one to six months; 25% of
those infected are negative for T. gondii-specific IgM within seven months.[65] However, IgM may be
detectable months or years after infection, during the chronic phase, and false positives for acute infection
are possible.[64] The most commonly used tests for the measurement of IgM antibody are double-sandwich
IgM-ELISA, the IFA test, and the immunosorbent agglutination assay (IgM-ISAGA). Commercial test kits
often have low specificity, and the reported results are frequently misinterpreted.[64]
In 2021, twenty commercial anti-Toxoplasma IgG assays were evaluated in a systematic review, in
comparison with an accepted reference method.[67] Most of them were enzyme-immunoassays, followed
by agglutination tests, immunochromatographic tests, and a Western-Blot assay. The mean sensitivity of
IgG assays ranged from 89.7% to 100% for standard titers and from 13.4% to 99.2% for low IgG titers. A
few studies pointed out the ability of some methods, especially WB to detect IgG early after primary
infection. The specificity of IgG assays was generally high, ranging from 91.3% to 100%; and higher than
99% for most EIA assays. The positive predictive value (PPV) was not a discriminant indicator among
methods, whereas significant disparities (87.5%–100%) were reported among negative predictive values
(NPV), a key-parameter assessing the ability to definitively rule out a Toxoplasma infection in patients at-
risk for opportunistic infections.[67]
Congenital
Recommendations for the diagnosis of congenital toxoplasmosis include: prenatal diagnosis based on
testing of amniotic fluid and ultrasound examinations; neonatal diagnosis based on molecular testing of
placenta and cord blood and comparative mother-child serologic tests and a clinical examination at birth;
and early childhood diagnosis based on neurologic and ophthalmologic examinations and a serologic
survey during the first year of life.[50] During pregnancy, serological testing is recommended at three week
intervals.[68]
Even though diagnosis of toxoplasmosis heavily relies on serological detection of specific anti-Toxoplasma
immunoglobulin, serological testing has limitations. For example, it may fail to detect the active phase of T.
gondii infection because the specific anti-Toxoplasma IgG or IgM may not be produced until after several
weeks of infection. As a result, a pregnant woman might test negative during the active phase of T. gondii
infection leading to undetected and therefore untreated congenital toxoplasmosis.[69] Also, the test may not
detect T. gondii infections in immunocompromised patients because the titers of specific anti-Toxoplasma
IgG or IgM may not rise in this type of patient.
Many PCR-based techniques have been developed to diagnose toxoplasmosis using clinical specimens that
include amniotic fluid, blood, cerebrospinal fluid, and tissue biopsy. The most sensitive PCR-based
technique is nested PCR, followed by hybridization of PCR products.[69] The major downside to these
techniques is that they are time-consuming and do not provide quantitative data.[69]
Real-time PCR is useful in pathogen detection, gene expression and regulation, and allelic discrimination.
This PCR technique utilizes the 5' nuclease activity of Taq DNA polymerase to cleave a nonextendible,
fluorescence-labeled hybridization probe during the extension phase of PCR.[69] A second fluorescent dye,
e.g., 6-carboxy-tetramethyl-rhodamine, quenches the fluorescence of the intact probe.[69] The nuclease
cleavage of the hybridization probe during the PCR releases the effect of quenching resulting in an increase
of fluorescence proportional to the amount of PCR product, which can be monitored by a sequence
detector.[69]
Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected by Toxoplasma have
characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B
cells, and scattered epithelioid histiocytes.
The classic triad of congenital toxoplasmosis includes: chorioretinitis, hydrocephalus, and intracranial
arteriosclerosis.[70] Other consequences include sensorineural deafness, seizures, and intellectual
disability.[71]
Congenital toxoplasmosis may also impact a child's hearing. Up to 30% of newborns have some degree of
sensorineural hearing loss.[72] The child's communication skills may also be affected. A study published in
2010 looked at 106 patients, all of whom received toxoplasmosis treatment prior to 2.5 months. Of this
group, 26.4% presented with language disorders.[73]
Treatment
Treatment is recommended for people with serious health problems, such as people with HIV whose CD4
counts are under 200 cells/mm3 . Trimethoprim/sulfamethoxazole is the drug of choice to prevent
toxoplasmosis, but not for treating active disease. A 2012 study shows a promising new way to treat the
active and latent form of this disease using two endochin-like quinolones.[74]
Acute
The medications prescribed for acute toxoplasmosis are the following:
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.
Clindamycin[75]
Spiramycin — 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).
If infected during pregnancy, spiramycin is recommended in the first and early second trimesters while
pyrimethamine/sulfadiazine and leucovorin is recommended in the late second and third trimesters.[76]
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 Toxoplasma cysts inside AIDS
patients[77]
Clindamycin — an antibiotic that, in combination with atovaquone, seemed to optimally kill
cysts in mice[78]
Congenital
When a pregnant woman is diagnosed with acute toxoplasmosis, amniocentesis can be used to determine
whether the fetus has been infected or not. When a pregnant woman develops acute toxoplasmosis, the
tachyzoites have approximately a 30% chance of entering the placental tissue, and from there entering and
infecting the fetus. As gestational age at the time of infection increases, the chance of fetal infection also
increases.[31]
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. They are treated after the first trimester because pyrimethamine has an
antifolate effect, and lack of folic acid can interfere with fetal brain formation and cause
thrombocytopaenia.[79] Infection in earlier gestational stages correlates with poorer fetal and neonatal
outcomes, particularly when the infection is untreated.[80]
Newborns who undergo 12 months of postnatal anti-toxoplasmosis treatment have a low chance of
sensorineural hearing loss.[81] Information regarding treatment milestones for children with congenital
toxoplasmosis have been created for this group.[82]
Epidemiology
T. gondii infections occur throughout the world, although infection rates differ significantly by country.[25]
For women of childbearing age, a survey of 99 studies within 44 countries found the areas of highest
prevalence are within Latin America (about 50–80%), parts of Eastern and Central Europe (about 20–
60%), the Middle East (about 30–50%), parts of Southeast Asia (about 20–60%), and parts of Africa (about
20–55%).[25]
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 12–49 years of age were seropositive for IgG antibodies
against T. gondii, down from 14.1% as measured in the NHANES 1988–1994.[83] In the 1999–2004
survey, 7.7% of US-born and 28.1% of foreign-born women 15–44 years of age were T. gondii
seropositive.[83] A trend of decreasing seroprevalence has been observed by numerous studies in the
United States and many European countries.[25] Toxoplasma gondii is considered the second leading cause
of foodborne-related deaths and the fourth leading cause of foodborne-related hospitalizations in the United
States.[84]
The protist responsible for toxoplasmosis is T. gondii. There are three major types of T. gondii responsible
for the patterns of Toxoplasmosis throughout the world. There are types I, II, and III. These three types of
T. gondii have differing effects on certain hosts, mainly mice and humans due to their variation in
genotypes.[85]
Type I: virulent in mice and humans, seen in people with AIDS.

Type II: non-virulent in mice, virulent in humans (mostly Europe and North America), seen in
people with AIDS.
Type III: non-virulent in mice, virulent mainly in animals but seen to a lesser degree in
humans as well.
Current serotyping techniques can only separate type I or III from type II parasites.[86]
Because the parasite poses a particular threat to fetuses when it is contracted during pregnancy,[87] much of
the global epidemiological data regarding T. gondii comes from seropositivity tests in women of
childbearing age. Seropositivity tests look for the presence of antibodies against T. gondii in blood, so while
seropositivity guarantees one has been exposed to the parasite, it does not necessarily guarantee one is
chronically infected.[88]
History
Toxoplasma gondii was first described in 1908 by Nicolle and Manceaux in Tunisia, and independently by
Splendore in Brazil.[10] Splendore reported the protozoan in a rabbit, while Nicolle and Manceaux
identified it in a North African rodent, the gundi (Ctenodactylus gundi).[39] In 1909 Nicolle and Manceaux
differentiated the protozoan from Leishmania.[10] Nicolle and Manceaux then named it Toxoplasma gondii
after the curved shape of its infectious stage (Greek root 'toxon'= bow).[10]
The first recorded case of congenital toxoplasmosis was in 1923, but it was not identified as caused by T.
gondii.[39] Janků (1923) described in detail the autopsy results of an 11-month-old boy who had presented
to hospital with hydrocephalus. The boy had classic marks of toxoplasmosis including chorioretinitis
(inflammation of the choroid and retina of the eye).[39] Histology revealed a number of "sporocytes",
though Janků did not identify these as T. gondii.[39]
It was not until 1937 that the first detailed scientific analysis of T. gondii took place using techniques
previously developed for analyzing viruses.[10] In 1937 Sabin and Olitsky analyzed T. gondii in laboratory
monkeys and mice. Sabin and Olitsky showed that T. gondii was an obligate intracellular parasite and that
mice fed T. gondii-contaminated tissue also contracted the infection.[10] Thus Sabin and Olitsky
demonstrated T. gondii as a pathogen transmissible between animals.
T. gondii was first described as a human pathogen in 1939 at Babies Hospital in New York City.[10][89]
Wolf, Cowen and Paige identified T. gondii infection in an infant girl delivered full-term by Caesarean
section.[39] The infant developed seizures and had chorioretinitis in both eyes at three days. The infant then
developed encephalomyelitis and died at one month of age. Wolf, Cowen and Paige isolated T. gondii from
brain tissue lesions. Intracranial injection of brain and spinal cord samples into mice, rabbits and rats
produced encephalitis in the animals.[10] Wolf, Cowen and Page reviewed additional cases and concluded
that T. gondii produced recognizable symptoms and could be transmitted from mother to child.[39]
The first adult case of toxoplasmosis was reported in 1940 with no neurological signs. Pinkerton and
Weinman reported the presence of Toxoplasma in a 22-year-old man from Peru who died from a
subsequent bacterial infection and fever.[39]
In 1948, a serological dye test was created by Sabin and Feldman based on the ability of the patient's
antibodies to alter staining of Toxoplasma.[10][90] The Sabin Feldman Dye Test is now the gold standard
for identifying Toxoplasma infection.[10]
Transmission of Toxoplasma by eating raw or undercooked meat was demonstrated by Desmonts et al. in
1965 Paris.[10] Desmonts observed that the therapeutic consumption of raw beef or horse meat in a
tuberculosis hospital was associated with a 50% per year increase in Toxoplasma antibodies.[10] This
means that more T. gondii was being transmitted through the raw meat.
In 1974, Desmonts and Couvreur showed that infection during the first two trimesters produces most harm
to the fetus, that transmission depended on when mothers were infected during pregnancy, that mothers
with antibodies before pregnancy did not transmit the infection to the fetus, and that spiramycin lowered the
transmission to the fetus.[39]
Toxoplasma gained more attention in the 1970s with the rise of immune-suppressant treatment given after
organ or bone marrow transplants and the AIDS epidemic of the 1980s.[10] Patients with lowered immune
system function are much more susceptible to disease.
Society and culture
"Crazy cat-lady"
"Crazy cat-lady syndrome" is a term coined by news organizations to describe scientific findings that link
the parasite Toxoplasma gondii to several mental disorders and behavioral problems.[91][92] The suspected
correlation between cat ownership in childhood and later development of schizophrenia suggested that
further studies were needed to determine a risk factor for children;[93] however, later studies showed that T.
gondii was not a causative factor in later psychoses.[94] Researchers also found that cat ownership does not
strongly increase the risk of a T. gondii infection in pregnant women.[56][95]
The term crazy cat-lady syndrome draws on both stereotype and popular cultural reference. It was
originated as instances of the aforementioned afflictions were noted amongst the populace. A cat lady is a
cultural stereotype of a woman who compulsively hoards and dotes upon cats. The biologist Jaroslav Flegr
is a proponent of the theory that toxoplasmosis affects human behaviour.[96][97]
Notable cases
Tennis player Arthur Ashe developed neurological problems from toxoplasmosis (and was
later found to be HIV-positive).[98]
Actor Merritt Butrick was HIV-positive and died from toxoplasmosis as a result of his already-
weakened immune system.[99]
Pedro Zamora, reality television personality and HIV/AIDS activist, was diagnosed with
toxoplasmosis as a result of his immune system being weakened by HIV.[100][101]
Prince François, Count of Clermont, pretender to the throne of France had congenital
toxoplasmosis; his disability caused him to be overlooked in the line of succession.
Actress Leslie Ash contracted toxoplasmosis in the second month of pregnancy.[102]
British middle-distance runner Sebastian Coe contracted toxoplasmosis in 1983, which was
probably transmitted by a cat while he trained in Italy.[103][104]
Tennis player Martina Navratilova suffered from toxoplasmosis during the 1982 US
Open.[105]
Other animals
Although T. gondii has the capability of infecting virtually all
warm-blooded animals, susceptibility and rates of infection vary
widely between different genera and species.[108][109] Rates of
infection in populations of the same species can also vary widely
due to differences in location, diet, and other factors.
Although infection with T. gondii has been noted in several species

of Asian primates, seroprevalence of T. gondii antibodies were
found for the first time in toque macaques (Macaca sinica) that are
endemic to the island of Sri Lanka.[110]
Australian marsupials are particularly susceptible to

toxoplasmosis. [111] Wallabies, koalas, wombats, pademelons and
small dasyurids can be killed by it, with eastern barred bandicoots
typically dying within about 3 weeks of infection.[112]
Toxoplasma gondii infects virtually
all warm-blooded animals; these
It is estimated that 23% of wild swine worldwide are seropositive
tachyzoites were found in a bird[106]
for T. gondii.[113] Seroprevalence varies across the globe with the
highest seroprevalence in North America (32%) and Europe (26%)
and the lowest in Asia (13%) and South America (5%).[113]
Geographical regions located at higher latitudes and regions that
experience warmer, humid climates are associated with increased
seroprevalence of T. gondii among wild boar.[113] Wild boar
infected with T. gondii pose a potential health risk for humans who
consume their meat.[113]
Livestock
Among livestock, pigs,[114][115][116] sheep[117] and goats have

Toxoplasma gondii in the lung of a
the highest rates of chronic T. gondii infection.[118] The prevalence
Giant panda.[107] Arrow:
of T. gondii in meat-producing animals varies widely both within
macrophages containing tachyzoites
and among countries,[118] and rates of infection have been shown
to be dramatically influenced by varying farming and management
practices.[13] 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.[13][44]
Pigs
Worldwide, the percentage of pigs harboring viable parasites has been measured to be 3-71.43%[116] and in
the United States, (via bioassay in mice or cats) to be as high as 92.7% and as low as 0%, depending on the
farm or herd.[44] Surveys of seroprevalence (T. gondii antibodies in blood) are more common, and such
measurements are indicative of the high relative seroprevalence in pigs across the world.[119] Neonatal
piglets have been found to suffer the entire range of severity, including progression to stillbirth.[120][114]: 95
This was especially demonstrated in the foundational Thiptara et al 2006, reporting a litter birth of three
stillborns and six live in Thailand. This observation has been relevant not only to that country but to
toxoplasmosis control in porciculture around the world.[121][114]: 95 [116]
Sheep
Along with pigs, sheep and goats are among the most commonly infected livestock of epidemiological
significance for human infection.[118] Prevalence of viable T. gondii in sheep tissue has been measured (via
bioassay) to be as high as 78% in the United States,[122] and a 2011 survey of goats intended for
consumption in the United States found a seroprevalence of 53.4%.[123]
Chickens
Due to a lack of exposure to the outdoors, chickens raised in large-scale indoor confinement operations are
not commonly infected with T. gondii.[13] Free-ranging or backyard-raised chickens are much more
commonly infected.[13] A survey of free-ranging chickens in the United States found its prevalence to be
17–100%, depending on the farm.[124] 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.[125]
Cattle
Although cattle and buffalo can be infected with T. gondii, the parasite is generally eliminated or reduced to
undetectable levels within a few weeks following exposure.[13] 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.[118][44]
Horses
Horses are considered resistant to chronic T. gondii infection.[13] 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.[44][126]
Domestic cats
In 1942, the first case of feline toxoplasmosis was diagnosed and reported in a domestic cat in Middletown,
NY.[127] The investigators isolated oocysts from feline feces and found that the oocysts could be infectious
for up to 12 months in the environment.[128]
The seroprevalence of T. gondii in domestic cats, worldwide has been estimated to be around 30–40%[129]
and exhibits significant geographical variation. In the United States, no official national estimate has been
made, but local surveys have shown levels varying between 16% and 80%.[129] A 2012 survey of 445
purebred pet cats and 45 shelter cats in Finland found an overall seroprevalence of 48.4%,[130] while a
2010 survey of feral cats from Giza, Egypt found a seroprevalence rate of 97.4%.[131] Another survey from
Colombia recorded seroprevalence of 89.3%,[132] whereas a Chinese (Guangdong) study found just a
2.1% prevalence.[133]
T. gondii infection rates in domestic cats vary widely depending on the cats' diets and lifestyles.[134] Feral
cats that hunt for their food are more likely to be infected than domestic cats, and naturally also depends on
the prevalence of T. gondii-infected prey such as birds and small mammals.[135]
Most infected cats will shed oocysts only once in their lifetimes, for a period of about one to two
weeks.[129] This shedding can release millions of oocysts, each capable of spreading and surviving for
months.[129] An estimated 1% of cats at any given time are actively shedding oocysts.[13]
It is difficult to control the cat population with the infected oocysts due to lack of an effective vaccine. This
remains a challenge in most cases and the programs that are readily available are questionable in
efficacy.[136]
Rodents
Infection with T. gondii has been shown to alter the behavior of mice and rats in ways thought to increase
the rodents' chances of being preyed upon by cats.[137][138][139] 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.[137][139][140]
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.[141][142]
In rodents, T. gondii–induced behavioral changes occur through epigenetic remodeling in neurons

associated with observed behaviors;[143][144] for example, it modifies epigenetic methylation to induce
hypomethylation of arginine vasopressin-related genes in the medial amygdala to greatly decrease predator
aversion.[143][144] Similar epigenetically-induced behavioral changes have also been observed in mouse
models of addiction, where changes in the expression of histone-modifying enzymes via gene knockout or
enzyme inhibition in specific neurons produced alterations in drug-related behaviors.[145][146][147]
Widespread histone–lysine acetylation in cortical astrocytes appears to be another epigenetic mechanism
employed by T. gondii.[148][149]
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.[150]
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.[151] Infected
rodents have also been shown to have lower anxiety, using traditional models such as elevated plus mazes,
open field arenas, and social interaction tests.[151][152]
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.[153] Proximity to freshwater outflows into the
ocean was a major risk factor. Ingestion of oocysts from cat feces is considered to be the most likely
ultimate source.[154] Surface runoff containing wild cat feces and litter from domestic cats flushed down
toilets are possible sources of oocysts.[155][156] These same sources may have also introduced the
toxoplasmosis infection to the endangered Hawaiian monk seal.[157] Infection with the parasite has
contributed to the death of at least four Hawaiian monk seals.[157] A Hawaiian monk seal's infection with
T. gondii was first noted in 2004.[158] The parasite's spread threatens the recovery of this highly
endangered pinniped. The parasites have been found in dolphins and whales.[159][160] Researchers Black
and Massie believe anchovies, which travel from estuaries into the open ocean, may be helping to spread
the disease.[161]
Giant panda
Toxoplasma gondii has been reported as the cause of death of a giant panda kept in a zoo in China, who
died in 2014 of acute gastroenteritis and respiratory disease.[107] Although seemingly anecdotal, this report
emphasizes that all warm-blooded species are likely to be infected by T. gondii, including endangered
species such as the giant panda.
Research
Chronic infection with T. gondii has traditionally been considered asymptomatic in people with normal
immune function.[162] Some evidence suggests latent infection may subtly influence a range of human
behaviors and tendencies, and infection may alter the susceptibility to or intensity of a number of
psychiatric or neurological disorders.[163][162]
In most of the current studies where positive correlations have been found between T. gondii antibody titers
and certain behavioral traits or neurological disorders, T. gondii seropositivity 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.[164] 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.[164]
Mental health
Some evidence links T. gondii to schizophrenia.[162] Two 2012

meta-analyses found that the rates of antibodies to T. gondii in
people with schizophrenia were 2.7 times higher than in
controls.[165][166] T. gondii antibody positivity was therefore
considered an intermediate risk factor in relation to other known
risk factors.[165] Cautions noted include that the antibody tests do
not detect toxoplasmosis directly, most people with schizophrenia
do not have antibodies for toxoplasmosis, and publication bias
might exist.[166] While the majority of these studies tested people
already diagnosed with schizophrenia for T. gondii antibodies,
associations between T. gondii and schizophrenia have been found
prior to the onset of schizophrenia symptoms.[137] Sex differences
in the age of schizophrenia onset may be explained in part by a
second peak of T. gondii infection incidence during ages 25–30 in
females only.[167] Although a mechanism supporting the
association between schizophrenia and T. gondii infection is
Micrograph of a lymph node showing
unclear, studies have investigated a molecular basis of this
the characteristic changes of
correlation.[167] Antipsychotic drugs used in schizophrenia appear
toxoplasmosis (scattered epithelioid
to inhibit the replication of T. gondii tachyzoites in cell culture.[137] histiocytes (pale cells), monocytoid
Supposing a causal link exists between T. gondii and cells (top-center of image), large
schizophrenia, studies have yet to determine why only some germinal centers (left of image)) H&E
individuals with latent toxoplasmosis develop schizophrenia; some stain
plausible explanations include differing genetic susceptibility,
parasite strain differences, and differences in the route of the
acquired T. gondii infection.[168]
Correlations have also been found between antibody titers to T. gondii and OCD, suicide in people with
mood disorders including bipolar disorder.[163][169] Positive antibody titers to T. gondii appear to be
uncorrelated with major depression or dysthymia.[170] Although there is a correlation between T. gondii
and many psychological disorders, the underlying mechanism is unclear. A 2016 study of 236 persons with
high levels of Toxoplasmosis antibodies found that "there was little evidence that T. gondii was related to
increased risk of psychiatric disorder, poor impulse control, personality aberrations or neurocognitive
impairment".[171]
Neurological disorders
Latent infection has been linked to Parkinson's disease and Alzheimer's disease.[163]
Individuals with multiple sclerosis show infection rates around 15% lower than the general public.[172]
Traffic accidents
Latent T. gondii infection in humans has been associated with a higher risk of automobile accidents,[173]
potentially due to impaired psychomotor performance or enhanced risk-taking personality profiles.[163]
Climate change
Climate change has been reported to affect the occurrence, survival, distribution and transmission of T.
gondii.[174] T. gondii has been identified in the Canadian arctic, a location that was once too cold for its
survival.[175] Higher temperatures increase the survival time of T. gondii.[174] More snowmelt and
precipitation can increase the amount of T. gondii oocysts that are transported via river flow.[174] Shifts in
bird, rodent, and insect populations and migration patterns can impact the distribution of T. gondii due to
their role as reservoir and vector.[174] Urbanization and natural environmental degradation are also
suggested to affect T. gondii transmission and increase risk of infection.[174]
See also
Toxoplasmic chorioretinitis
TORCH infection
Pyrimethamine
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studies have investigated the effects of AMPH on gene regulation (Table 1), current data
suggest that AMPH acts at multiple levels to alter histone/DNA interaction and to recruit
transcription factors which ultimately cause repression of some genes and activation of other
genes. Importantly, some studies have also correlated the epigenetic regulation induced by
AMPH with the behavioral outcomes caused by this drug, suggesting therefore that
epigenetics remodeling underlies the behavioral changes induced by AMPH. If this proves
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Parts of this article are taken from the public domain CDC factsheet: Toxoplasmosis (ht
tps://www.cdc.gov/toxoplasmosis/)
Bibliography
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Perspectives and Methods (https://books.google.com/books?id=yTUkJEphM_IC). Academic
Press. ISBN 978-0-08-047501-1. Retrieved 12 March 2013.
Dubey, J. P. (2016). Toxoplasmosis of Animals and Humans (https://books.google.com/book
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9237-0. OCLC 423572366 (https://www.worldcat.org/oclc/423572366). ISBN 1-4200-9236-7
ISBN 9781420092363
Dubey JP, Lindsay DS, Speer CA (April 1998). "Structures of Toxoplasma gondii
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Jaroslav Flegr (2011). Pozor, Toxo! (http://www.academia.cz/pozor-toxo.html). Academia,
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External links
How a cat-borne parasite infects humans (http://news.nationalgeographic.com/news/2013/0
1/220113-sneaky-cat-parasite-takes-over-human-brains-science/) (National Geographic)
Toxoplasmosis (http://www.merck.com/mmpe/sec14/ch186/ch186h.html) at Merck Manual of
Diagnosis and Therapy Professional Edition
Toxoplasmosis (https://www.gov.uk/guidance/toxoplasmosis) at Health Protection Agency
(HPA), United Kingdom
Pictures of Toxoplasmosis (https://web.archive.org/web/20130113220407/http://rad.usuhs.ed
u/medpix/medpix.html?mode=image_finder&action=search&srchstr=toxoplasmosis#top)
Medical Image Database
Video-Interview (https://www.youtube.com/watch?v=m3x3TMdkGdQ) with Professor Robert
Sapolsky on Toxoplasmosis and its effect on human behavior (24:27 min)
"Toxoplasmosis" (https://medlineplus.gov/toxoplasmosis.html). MedlinePlus. U.S. National
Library of Medicine.
Classification ICD-10: B58 (http D
s://icd.who.int/brow
se10/2019/en#/B5
8) · ICD-9-CM: 130
(http://www.icd9dat
a.com/getICD9Cod
e.ashx?icd9=130) ·
MeSH: D014123 (h
ttps://www.nlm.nih.
gov/cgi/mesh/2015/
MB_cgi?field=uid&t
erm=D014123) ·
DiseasesDB:
13208 (http://www.
diseasesdatabase.
com/ddb13208.ht
m)
External MedlinePlus:
resources 000637 (https://ww
w.nlm.nih.gov/medli
neplus/ency/article/
000637.htm) ·
eMedicine:
med/2294 (https://e
medicine.medscap
e.com/med/2294-o
verview) · Patient
UK: Toxoplasmosis
(https://patient.info/
doctor/toxoplasmos
is)
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Toxoplasmosis

Toxoplasmosis is a parasitic disease caused by Toxoplasma

Toxoplasmosis is usually spread by eating poorly cooked food

Signs and symptoms

In its lifecycle, T. gondii adopts several forms.[31]

The parasite's survival is dependent on a balance

Oral transmission may occur through:

T. gondii may also be detected in blood, amniotic fluid, or

The medications prescribed for acute toxoplasmosis are the following:

Pyrimethamine — an antimalarial medication

The medications prescribed for latent toxoplasmosis are:

Type I: virulent in mice and humans, seen in people with AIDS.

Society and culture

Although infection with T. gondii has been noted in several species

Australian marsupials are particularly susceptible to

Among livestock, pigs,[114][115][116] sheep[117] and goats have

In rodents, T. gondii–induced behavioral changes occur through epigenetic remodeling in neurons

Some evidence links T. gondii to schizophrenia.[162] Two 2012

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