Professional Documents
Culture Documents
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).
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]
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.
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.
Kingdom: Protista
Phylum: Apicomplexa
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Toxoplasma
Species: T. gondii
T. gondii
Fig. Stages of Toxoplasma gondii. Scale bar in A-D= 20 µm, in E-G = 10 µm.
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.
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]
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]
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]
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]
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]
• 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:
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:
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.
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.
(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.
• 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:
• 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.
The following are statistics from various sources about hospitalizations and
Toxoplasmosis
Refrence:
1. Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill,
pp. 723–7. ISBN 0838585299.
2. Torda A (2001). "Toxoplasmosis. Are cats really the source?". Aust Fam Physician 30
(8): 743–7. PMID 11681144.
3. Montoya J, Liesenfeld O (2004). "Toxoplasmosis". Lancet 363 (9425): 1965–76.
doi:10.1016/S0140-6736(04)16412-X. PMID 15194258.
4. Jones JL, Kruszon-Moran D, Sanders-Lewis K, Wilson M (2007). "Toxoplasma gondii
infection in the United States, 1999-2004, decline from the prior decade". Am J Trop
Med Hyg 77 (3): 405–10. PMID 17827351.
5. Toxoplasmosis". Centers of Disease Control and Prevention (2004-11-22).
6. North Carolina Department of Agriculture & Consumer Services
7. Sukthana Y (2006). "Toxoplasmosis: beyond animals to humans". TRENDS in
Parisitology 22 (3): 137. doi:10.1016/j.pt.2006.01.007.
8. [http://www.blackwell-synergy.com/doi/abs/10.1111/j.1469-0691.2007.01883.x De
Paschale et al. (2008) Seroprevalence and incidence of Toxoplasma gondii infection in
the Legnano area of Italy Clinical Microbiology and Infection 14 (2), 186–189]
9. "Toxoplasmosis - treatment key research". NAM & aidsmap (2005-11-02).
10. Djurković-Djaković O, Milenković V, Nikolić A, Bobić B, Grujić J (2002). "Efficacy of
atovaquone combined with clindamycin against murine infection with a cystogenic
(Me49) strain of Toxoplasma gondii" (PDF). J Antimicrob Chemother 50 (6): 981–7.
doi:10.1093/jac/dkf251. PMID 12461021.
11. Jaroslav Flegr. Women infected with parasite Toxoplasma have more sons,
Naturwissenschaften, August 2006. full text
12. ^ Berdoy M, Webster J, Macdonald D (2000). Fatal Attraction in Rats Infected with
Toxoplasma gondii. Proceedings of the Royal Society of London, B267:1591-1594.
PMID 11007336
13. "'Cat Box Disease' May Change Human Personality And Lower IQ", The Daily
Telegraph (April 8, 2000).
14. Flegr J, Havlíček J, Kodym P, Malý M, Šmahel Z (2002). "Increased risk of traffic
accidents in subjects with latent toxoplasmosis: a retrospective case-control study". BMC
Infect Dis 2: 11. doi:10.1186/1471-2334-2-11. PMID 12095427.
15. Carl Zimmer, The Loom. A Nation of Neurotics? Blame the Puppet Masters?, 1 Aug.
2006
16. Jaroslav Flegr (Jan 2007). "Effects of Toxoplasma on Human Behaviour". Schizophrenia
Bulletin 33 (3): 757–760. doi:10.1093/schbul/sbl074. PMID 17218612.
17. Yereli K, Balcioglu IC, Ozbilgin A. (Dec 2 2005). "Is Toxoplasma gondii a potential risk
for traffic accidents in Turkey?". Forensic Sci Int. PMID 16332418.
18. ^ "Can a parasite carried by cats change your personality?", The Guardian (September
25, 2003).
19. "Dirt infection link to car crashes", BBC News (August 10, 2002).
20. J. Havlícek, Z. Gašová, A. P. Smith, K. Zvára and J. Flegr, Decrease of psychomotor
performance in subjects with latent ‘asymptomatic’ toxoplasmosis, Parasitology (2001),
122: 515-520
21. "Dangerrrr: cats could alter your personality", Times Online (June 23, 2005).
22. "Can a parasite carried by cats change your personality?", The Guardian (September 25,
2003).
23. Novotná M, Hanusova J, Klose J, Preiss M, Havlicek J, Roubalová K, Flegr J (Jul 6
2004). "Probable neuroimmunological link between Toxoplasma and cytomegalovirus
infections and personality changes in the human host". BMC Infect Dis 5: 54.
doi:10.1186/1471-2334-5-54. PMID 16000166.
24. AAP, SMH Parasite makes men dumb, women sexy, 26 Dec. 2006
25. Kevin Lafferty
26. Torrey EF, Yolken RH (2003). "Toxoplasma gondii and schizophrenia". Emerging
Infect. Dis. 9 (11): 1375–80. PMID 14725265.free full text
27. Lafferty, Kevin D. (2006). "Can the common brain parasite, Toxoplasma gondii,
influence human culture?". Proceedings of the Royal Society B: Biological Sciences 273
(FirstCite Early Online Publishing): 2749. doi:10.1098/rspb.2006.3641
28. Wang H, Wang G, Li Q, Shu C, Jiang M, Guo Y (2006). "Prevalence of Toxoplasma
infection in first-episode schizophrenia and comparison between Toxoplasma-
seropositive and Toxoplasma-seronegative schizophrenia". Acta Psychiatrica
Scandinavica 114 (1): 40–8. doi:10.1111/j.1600-0447.2006.00780.x. PMID 16774660.
29. Jones JL, Kruszon-Moran D, Wilson M, McQuillan G, Navin T, McAuley JB (2001).
"Toxoplasma gondii infection in the United States: seroprevalence and risk factors". Am J
Epidemiol 154 (4): 357–65. doi:10.1093/aje/154.4.357. PMID 11495859.
30. Jones J, Kruszon-Moran D, Wilson M (2003). "Toxoplasma gondii infection in the
United States, 1999-2000". Emerg Infect Dis 9 (11): 1371–4. PMID 14718078.
31. David Adam, Guardian Unlimited. Can a parasite carried by cats change your
personality?, 25 Sep. 2003
32. Toxoplasmosis in the Netherlands by the Laboratory for Diagnoses for Infectious
Diseases and Screening; RIVM Bilthoven
33. Conrad P, Miller M, Kreuder C, James E, Mazet J, Dabritz H, Jessup D, Gulland F, Grigg
M (2005). "Transmission of Toxoplasma: clues from the study of sea otters as sentinels
of Toxoplasma gondii flow into the marine environment". Int J Parasitol 35 (11-12):
1155–68. doi:10.1016/j.ijpara.2005.07.002. PMID 16157341.
34. "17:30-22:00 Treating Disease in the Developing World.". Talk of the Nation Science
Friday. National Public Radio (December 16, 2005).
35. Brahic, Catherine. (2008). The world's most successful bug hits dolphins.
36. Toxoplasma Serology Laboratory: Laboratory Tests For The Diagnosis Of
Toxoplasmosis
37. www.cdc.org
38.