Taxoplasmosis

Disease Type: Parasitic Disease

Common Name: Toxoplasmosis
Causative Agent: Toxoplasma gondii
Disease Discription: Toxoplasmosis is a parasitic disease caused by the protozoan
Toxoplasma gondii.[1] The parasite infects most warm-blooded animals, including
humans, but the primary host is the felid (cat) family. Animals are infected by eating
infected meat, by ingestion of faeces of a cat that has itself recently been infected, or by
transmission from mother to fetus. Cats have been shown as a major reservoir of this
infection.[2]

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

The Centers for Disease Control and Prevention notes that overall seroprevalence in the
United States as determined with specimens collected by the National Health and
Nutritional Assessment Survey (NHANES) between 1999 and 2004 was found to be
10.8%, with seroprevalence among women of childbearing age (15 to 44 years) of 11%.[4]

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

Fig. Congital toxoplasmosis

Causes of Disease:
T. gondii exists in trophozoite forms in the acute stages of infection and in cystic forms
(tissue cysts and oocysts) in the latent stages. In addition to possible fecal-oral
transmission from infected cats, ingestion of tissue cysts in raw or uncooked meat
(heating, drying, or freezing destroys these cysts) can also transmit toxoplasmosis.
However, toxoplasmosis also occurs in vegetarians who aren't exposed to cats, so other
means of transmission may exist. Congenital toxoplasmosis follows transplacental
transmission from a chronically infected mother or one who acquired toxoplasmosis
shortly before or during pregnancy.

Risk Factors:
Pregnancy Risk Factor:

Congenital toxoplasmosis is a special form in which an unborn child is infected via the
placenta. A positive antibody titer indicates previous exposure and immunity and largely
ensures the unborn baby's safety. A simple blood draw at the first pre-natal doctor visit
can determine whether or not the woman has had previous exposure and therefore
whether or not she is at risk. If a woman receives her first exposure to toxoplasmosis
while pregnant, the baby 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 and so are not a danger, but the
risk may be reduced further by having the litterbox emptied daily (oocysts require longer
than a single day to become infective), and by having someone else empty the litterbox.
However, while risks can be minimized, they cannot be eliminated. For pregnant women
with negative antibody titer, indicating no previous exposure to T. gondii, as frequent as
monthly serology testing is advisable as treatment during pregnancy for those women
exposed to T. gondii for 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 (France[9], Austria[9] and Italy[10] being the exceptions) for reasons of cost-
effectiveness and the high number of false positives generated as the disease is so rare (an
example of Bayesian statistics). As invasive prenatal testing incurs some risk to the fetus
(18.5 pregnancy losses per toxoplasmosis case prevented[9]), postnatal or neonatal
screening is preferred. The exceptions are cases where foetal abnormalities are noted, and
thus screening can be targeted.[9]

Some regional screening programmes operate in Germany, Switzerland and Belgium.[10]

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
anti-protozoans, an infection can be very serious in the young.

Transplacental transmission:(a) infection in 1st trimester - incidence of transplacental

infection is low (15%) but disease in neonate is most severe. (b) infection in 3rd trimester
- incidence of transplacental infection is high (65%) but infant is usually asymptomatic at
birth.

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

Fig. Summary of Pathogen and host relationship

Reasearch:
 Taxonoimic Classification:

Kingdom: Protista
Phylum: Apicomplexa
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Toxoplasma
Species: T. gondii

T. gondii

Morphology and toxin production:

Fig. Stages of Toxoplasma gondii. Scale bar in A-D= 20 µm, in E-G = 10 µm.

A. Tachyzoites in impression smear of lung. Note crescent-shaped individual tachyzoites

(arrows), dividing tachyzoites (arrowheads) compared with size of host red blood cells
and leukocytes. Giema stain.
B. Tissue cysts in section of muscle. The tissue cyst wall is very thin (arrow) and
encloses many tiny bradyzoites (arrowheads). Hematoxylin and eosin stain.
C. Tissue cyst separated from host tissue by homogenization of infected brain. Note
tissue cyst wall (arrow) and hundreds of bradyzoites (arrowheads). Unstained.

D. Schizont (arrow) with several merozoites (arrowheads) separating from the main
mass. Impression smear of infected cat intestine. Giemsa stain.

E. A male gamete with two flagella (arrows). Impression smear of infected cat intestine.
Giemsa stain.

F. Unsporulated oocyst in fecal float of cat feces. Unstained. Note double layered oocyst
wall (arrow) enclosing a central undivided mass.

G. Sporulated oocyst with a thin oocyst wall (large arrow), 2 sporocysts (arrowheads).
Each sporocyst has 4 sporozoites (small arrow) which are not in complete focus.
Unstained.

Biological modifications of the host

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

Reproductive changes

A recent study [13] has indicated Toxoplasmosis correlates strongly with an increase in
boy births in humans. According to the researchers, depending on the antibody
concentration, the probability of the birth of a boy can increase up to a value of 0.72 ...
which means that for every 260 boys born, 100 girls are born. The study also notes a
mean rate of 0.60 to 0.65 (as opposed to the normal 0.51) for Toxoplasma positive
mothers.

Behavioral changes

It has been found that the parasite has the ability to change the behavior of its host:
infected rats and mice are less fearful of cats — in fact, some of the infected rats seek out
cat-urine-marked areas. This effect is advantageous to the parasite, which will be able to
sexually reproduce if its host is eaten by a cat.[14] The mechanism for this change is not
completely understood, but there is evidence that toxoplasmosis infection raises
dopamine levels and concentrates in the amygdala in infected mice.

The findings of behavioral alteration in rats and mice have led some scientists to
speculate that toxoplasma may have similar effects in humans, even in the latent phase
that had previously been considered asymptomatic. Toxoplasma is one of a number of
parasites that may alter their host's behaviour as a part of their life cycle.[15] The behaviors
observed, if caused by the parasite, are likely due to infection and low-grade encephalitis,
which is marked by the presence of cysts in the brain, which may produce or induce
production of a neurotransmitter, possibly dopamine,[16] therefore acting similarly to
dopamine reuptake inhibitor type antidepressants and stimulants.

Correlations have been found between latent Toxoplasma infections and various
characteristics:[17]

• Decreased novelty-seeking behaviour[18]

• Slower reactions
• Lower rule-consciousness and jealousy (in men)[18]
• More warmth and conscientiousness (in women)[18]

The evidence for behavioral effects on humans is relatively weak. No prospective

research has been done on the topic, e.g., testing people before and after infection to
ensure that the proposed behavior arises only afterwards. Although some researchers
have found potentially important associations with toxoplasma, the causal relationship, if
any, is unknown, e.g., it is possible that these associations merely reflect factors that
predispose certain types of people to infection.

Studies have found that toxoplasmosis is associated with an increased car accident rate,
roughly doubling or tripling the chance of an accident relative to uninfected people.[16][19]
This may be due to the slowed reaction times that are associated with infection.[19] "If our
data are true then about a million people a year die just because they are infected with
toxoplasma," the researcher Jaroslav Flegr told The Guardian.[20] The data shows that the
risk decreases with time after infection, but is not due to age.[16] Ruth Gilbert, medical
coordinator of the European Multicentre Study on Congenital Toxoplasmosis, told BBC
News Online these findings could be due to chance, or due to social and cultural factors
associated with toxoplasma infection.[21]However there is also evidence of a delayed
effect which increases reaction times.[22]

Other studies suggest that the parasite may influence personality. There are claims of
toxoplasma causing antisocial attitudes in men and promiscuity[23] (or even "signs of
higher intelligence"[24] ) in women, and greater susceptibility to schizophrenia and manic
depression in all infected persons.[23] A 2004 study found that toxoplasma "probably
induce[s] a decrease of novelty seeking." [25]

According to Sydney University of Technology infectious disease researcher Nicky

Boulter in an article that appeared in the January/February 2007 edition of Australasian
Science magazine, Toxoplasma infections lead to changes depending on the sex of the
infected person. [26]

The study suggests that male carriers have lower IQs, a tendency to achieve a lower level
of education and have shorter attention spans, a greater likelihood of breaking rules and
taking risks, and are more independent, anti-social, suspicious, jealous and morose. It
also suggests that these men are deemed less attractive to women. Women carriers are
suggested to be more outgoing, friendly, more promiscuous, and are considered more
attractive to men compared with non-infected controls. The results are shown to be true
when tested on mice, though it is still inconclusive. A few scientists have suggested that,
if these effects are genuine, prevalence of toxoplasmosis could be a major determinant of
cultural differences.[27][17]

Toxoplasma's role in schizophrenia

The possibility that toxoplasmosis is one cause of schizophrenia has been studied by
scientists since at least 1953. [28] These studies had attracted little attention from U.S.
researchers until they were publicized through the work of prominent psychiatrist and
advocate E. Fuller Torrey. In 2003, Torrey published a review of this literature, reporting
that almost all the studies had found that schizophrenics have elevated rates of
toxoplasma infection.[28] A 2006 paper has even suggested that prevalence of
toxoplasmosis has large-scale effects on national culture. [29] These types of studies are
suggestive but cannot confirm a causal relationship (because of the possibility, for
example, that schizophrenia increases the likelihood of toxoplasma infection rather than
the other way around).[28]

• Acute Toxoplasma infection sometimes leads to psychotic symptoms not unlike

schizophrenia.
• Some anti-psychotic medications that are used to treat schizophrenia, such as
Haloperidol, also stop the growth of Toxoplasma in cell cultures.
• Several studies have found significantly higher levels of Toxoplasma antibodies in
schizophrenia patients compared to the general population.[30]
• Toxoplasma infection causes damage to astrocytes in the brain, and such damage
is also seen in schizophrenia .

History:

The protozoan was first discovered by Nicolle & Manceaux, who in 1908 isolated it from
the African rodent Ctenodactylus gundi, then in 1909 differentiated the disease from
Leishmania and named it Toxoplasmosis gondii [9][5]. The first recorded congenital case
was not until 1923, and the first adult case not until 1940[9]. In 1948, a serological dye test
was created by Sabin & Feldman, which is now the standard basis for diagnostic tests.[38]

Epidemiology:

In humans
The U.S. NHANES (1999-2004) national probability sample found that 10.8% of U.S.
persons 6-49 years of age, and 11.0% of women 15-44 years of age, had Toxoplasma-
specific IgG antibodies, indicating that they had been infected with the organism. [4] This
prevalence has significantly decreased from the NHANES III (1988-1994). [31] [32]

It is estimated that between 30% and 65% of all people worldwide are infected with
Toxoplasmosis. However, there is large variation countries: in France, for example,
around 88% of the population are carriers, probably due to a high consumption of raw
and lightly cooked meat. [33] Germany, the Netherlands and Brazil also have high
prevalences of around 80%, over 80%[34] and 67% respectively. In Britain, about 22% are
carriers, and South Korea's rate is only 4.3%.[17]

Two risk factors for contracting toxoplasmosis are:

• Infants born to mothers who became infected with Toxoplasma for the first time
during or just before pregnancy.
• Persons with severely weakened immune systems, such as those with AIDS.
Illness may result from an acute Toxoplasma infection or reactivation of an
infection that occurred earlier in life.

In other animals

A University of California, Davis study of dead sea otters collected from 1998 to 2004
found that toxoplasmosis was the cause of death for 13% of the animals.[35] Proximity to
freshwater outflows into the ocean were a major risk factor. Ingestion of oocysts from cat
faeces is considered to be the most likely ultimate source.[36] According to an article in the
New Scientist, the parasites have also been found in dolphins and whales. Researchers
Black and Massie believe that anchovies, which travel from estuaries into the open ocean,
may be helping to spread the disease. Michael Grigg of the US National Institute of
Health mentioned that a new type of T. gondii, type X, has been found which is
responsible for the large deaths of sea otters, and may be "poised to sweep the world".[37]

Disease Host: Cat is primary host but human and other animal is secondry host.

Disease Transmission:

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. Oocysts 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.[7]
 • Ingestion of contaminated cat faeces. This can occur through hand-to-mouth
contact following gardening, cleaning a cat's litter box, contact with children's
sandpits, or touching anything that has come into contact with cat faeces.
• Drinking water contaminated with Toxoplasma.
• Transplacental infection in utero.
• Receiving an infected organ transplant or blood transfusion, although this is
extremely rare.[7]

The cyst form of the parasite is extremely hardy, capable of surviving exposure to
freezing down to −12 degrees Celsius (10 degrees Fahrenheit), moderate temperatures
and chemical disinfectants such as bleach, and can survive in the environment for over a
year. It is, however, susceptible to high temperatures—above 66 degrees Celsius (150
degrees Fahrenheit), and is thus killed by thorough cooking, and would be killed by 24
hours in a typical domestic freezer.[8]

Cats excrete the pathogen in their faeces for a number of weeks after contracting the
disease, generally by eating an infected rodent. Even then, cat faeces are not generally
contagious for the first day or two after excretion, after which the cyst 'ripens' and
becomes potentially pathogenic. Studies have shown that only about 2% of cats are
shedding oocysts at any one time, and that oocyst shedding does not recur even after
repeated exposure to the parasite. Although the pathogen has been detected on the fur of
cats, it has not been found in an infectious form, and direct infection from handling cats is
generally believed to be very rare.
Members of the cat family (Felidae) are the only known definitive hosts for the sexual
stages of T. gondii and thus are the main reservoirs of infection. Cats become infected
with T. gondii by carnivorism . After tissue cysts or oocysts are ingested by the cat,
viable organisms are released and invade epithelial cells of the small intestine where they
undergo an asexual followed by a sexual cycle and then form oocysts, which are
excreted. The unsporulated oocyst takes 1 to 5 days after excretion to sporulate (become
infective). Although cats shed oocysts for only 1 to 2 weeks, large numbers may be
shed. Oocysts can survive in the environment for several months and are remarkably
resistant to disinfectants, freezing, and drying, but are killed by heating to 70°C for 10
minutes.
Human infection may be acquired in several ways: A) ingestion of undercooked infected
meat containing Toxoplasma cysts ; B) ingestion of the oocyst from fecally
contaminated hands or food ; C) organ transplantation or blood transfusion; D)
transplacental transmission; E) accidental inoculation of tachyzoites. The parasites form
tissue cysts, most commonly in skeletal muscle, myocardium, and brain; these cysts may
remain throughout the life of the host.
Signs and symptoms of disease:

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, a patient with a fully
functioning immune system may develop eye damage from toxoplasmosis. Young
children and immunocompromised patients, 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 or the eyes. Only
a small percentage of infected newborn babies have serious eye or brain damage at birth.

Latent toxoplasmosis

Most patients who become infected with Toxoplasma gondii and develop toxoplasmosis
do not know it. In most immunocompetent patients, 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.[5]

Diagnosis:
Detection of Toxoplasma gondii in human blood samples may be achieved by using the
polymerase chain reaction (PCR).[6] Inactive cysts may exist in a host which would evade
detection.

Diagnosis of toxoplasmosis in humans is made by biologic, serologic, histologic, or

molecular methods, or by some combination of the above. Clinical signs of
toxoplasmosis are non-specific and are not sufficiently characteristic for a definite
diagnosis. Toxoplasmosis in fact mimics several other infectious diseases.

Detection of T. gondii antibody in patients may aid diagnosis. There are numerous
serologic procedures available for detection of humoral antibodies; these include the
Sabin-Feldman dye test, the indirect hemagglutination assay, the indirect fluorescent
antibody assay (IFA), the direct agglutination test, the latex agglutination test (LAT), the
enzyme-linked immunoabsorbent assay (ELISA), and the immunoabsorbent agglutination
assay test (IAAT). The IFA, IAAT and ELISA have been modified to detect IgM
antibodies. The IgM antibodies appear sooner after infection than the IgG antibodies and
the IgM antibodies disappear faster than IgG antibodies after recovery.

The finding of antibodies to T. gondii in one serum sample only establishes that the host
has been infected at some time in the past. It is best to collect 2 samples from the same
individual, the second collected 2 to 4 weeks after the first. A 16-fold higher antibody
titer in the second sample indicates an acute infection. A high antibody titer sometimes
persists for months after infection. A rise in antibody titer may not be associated with
clinical symptoms, for as indicated earlier, most infections in humans are asymptomatic.
The fact that titers persist in infected people after clinical recovery complicates the
interpretation of the results of serological tests. Establishing recency of infection in
pregnancy is of clinical importance with respect to medical intervention to minimize
damage to the fetus, and there is no one test that can achieve this at the present time.
Toxoplasma gondii can be isolated from patients by inoculation of laboratory animals and
tissue cultures with secretions, excretions, body fluids, tissues taken by biopsy, and
tissues with macroscopic lesions taken postmortem. Using such specimens, one may not
only attempt isolation of T. gondii, but one may search for T. gondii microscopically
using traditional histochemical stains or by immunohistochemical staining of parasites
with fluorescent or other types of labeled T. gondii. Recent studies have shown that
monoplex and multiplex PCR can be useful for specifically identifying T. gondii (using
the B1 gene as the target sequence) from tissue biopsies, cerebrospinal fluid, vitreous
from patients with undiagnosed uveitis, fetal blood, and amniotic fluid.

Treatment:

Treatment is often only recommended for people with serious health problems, because
the disease is most serious when one's immune system is weak.

Medications that are prescribed for acute Toxoplasmosis are:

• Pyrimethamine — an antimalarial medication.

• Sulfadiazine — an antibiotic used in combination with pyrimethamine to treat
toxoplasmosis.
• clindamycin — an antibiotic. This is used most often for people with HIV/AIDS.
• spiramycin — another antibiotic. This is used most often for pregnant women to
prevent the infection of their child.

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

In people with latent toxoplasmosis, the cysts are immune to these treatments, as the
antibiotics do not reach the bradyzoites in sufficient concentration.

Medications that are prescribed for latent Toxoplasmosis are:

• atovaquone — an antibiotic that has been used to kill Toxoplasma cysts inside
AIDS patients. [11]
• clindamycin — an antibiotic which, in combination with atovaquone, seemed to
optimally kill cysts in mice.[12]

However, in latent infections successful treatment is not guaranteed, and some subspecies
exhibit resistance.

Prevention of disease:

Methods of prevention of Toxoplasmosis mentioned in various sources includes those

listed below. This prevention information is gathered from various sources, and may be
inaccurate or incomplete. None of these methods guarantee prevention of
Toxoplasmosis.

• Avoid cats
• Avoid cat feces
• Avoid soil or garden areas possibly contaminated by cat feces
• Avoid children's sandpits
• Test to determine immunity to toxoplasmosis
• Wash hands after cat exposure
• Wash hands after cleaning cat litter
• Get someone else to clean cat litter if you are pregnant
• Cook meat thorougly - rare cases are caught from (non-cat) raw meat.

Geographical Distribution:

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

Disease Statistics:
Prevalance of Toxoplasmosis:

More than 60 million people in the United States probably are infected with the
Toxoplasma parasite, but very few have symptoms because the immune system usually
keeps the parasite from causing illness.

Hospitalization statistics for Toxoplasmosis:

The following are statistics from various sources about hospitalizations and
Toxoplasmosis

• .0006% (79) of hospital consultant episodes were for toxoplasmosis in

England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
• 87% of hospital consultant episodes for required hospital admission in
England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
 • 43% of hospital consultant episodes for toxoplasmosis were for men in
England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
• 57% of hospital consultant episodes for toxoplasmosis were for women in
England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
• 39% of hospital consultant episodes for required emergency hospital
admission in England 2002-03 (Hospital Episode Statistics, Department of
Health, England, 2002-03)
• 9.3 days was the mean length of stay in hospitals for toxoplasmosis in
England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
• 3 days was the median length of stay in hospitals for toxoplasmosis in
England 2002-03 (Hospital Episode Statistics, Department of Health, England,
2002-03)
• 36 was the mean age of patients hospitalised for toxoplasmosis in England
2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03)
• 86% of hospital consultant episodes for toxoplasmosis occurred in 15-59
year olds in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
• 1% of hospital consultant episodes for toxoplasmosis occurred in people
over 75 in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
• 22% of hospital consultant episodes for toxoplasmosis were single day
episodes in England 2002-03 (Hospital Episode Statistics, Department of Health,
England, 2002-03)
• 0.0008% (413) of hospital bed days were for toxoplasmosis in England
2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03)

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