Cryptococcosis

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Cryptococcosis
Classification and external resources

Histopathological image of pulmonary cryptococcosis in an immunocompromised host. Alcian blue-PAS stain.

ICD-10

B45.

ICD-9

117.5

DiseasesDB

3213

eMedicine

med/482

MeSH

D003453

Cryptococcosis, or cryptococcal disease, is a potentially fatal fungal disease. It is caused by one of three species; Cryptococcus neoformans, Cryptococcus gattii and Cryptococcus grubii. These were all previously thought to be subspecies of C. neoformans, but have now been identified as distinct species. Cryptococcosis is believed to be acquired by inhalation of the infectious propagule from the environment. Although the exact nature of the infectious propagule is unknown, the leading hypothesis is the basidiospore created through sexual or asexual reproduction.

Contents
[hide]

1 Etiology and Incidence 2 Diagnosis 3 Treatment o 3.1 IRIS in immunocompetent hosts 4 Veterinary cases 5 Additional images 6 References 7 External links

[edit] Etiology and Incidence

Cryptococcosis is a defining opportunistic infection for AIDS. Other conditions which pose an increased risk include certain lymphomas (e.g. Hodgkin's lymphoma), sarcoidosis, and patients on long-term corticosteroid therapy. Distribution is worldwide with pigeon droppings serving as the main source of contamination in populated city centers. The prevalence of cryptococcosis has been increasing over the past 20 years for many reasons, including the increase in incidence of AIDS and the expanded use of immunosuppressive drugs. In humans, C. neoformans causes three types of infections:

Wound or cutaneous cryptococcosis Pulmonary cryptococcosis, and Cryptococcal meningitis.

Cryptococcal meningitis (infection of the meninges, the tissue covering the brain) is believed to result from dissemination of the fungus from either an observed or unappreciated pulmonary infection. Cryptococcus gattii causes infections in immunocompetent people (those having a functioning immune system), but C. neoformans v. grubii, and v. neoformans usually only cause clinically evident infections in persons who have some form of defect in their immune systems (immunocompromised persons). People who have defects in their cellmediated immunity, for example, people with AIDS, are especially susceptible to disseminated cryptococcosis. Cryptococcosis is often fatal, especially if untreated. Although the most common presentation of cryptococcosis is of C. neoformans infection in an immunocompromised person (such as patients with AIDS), the C. gattii is being increasingly recognised as a pathogen in presumptively immunocompetent hosts, especially in Canada and Australia. This may be due to rare exposure and high pathogenicity, or to unrecognised isolated defects in immunity specific to this organism.

[edit] Diagnosis

Symptoms include fever, fatigue, chest pain, dry cough, swelling of abdomen, headache, blurred vision and confusion.[1] Detection of cryptococcal antigen (capsular material) by culture of CSF, sputum and urine provides definitive diagnosis. Blood cultures may be positive in heavy infections. Cryptococcosis can rarely occur in the immunocompetent person without HIV, when it usually goes undiagnosed. Less than 250 cases in all are reported in the medical literature, the majority diagnosed postmortem.[2]

[edit] Treatment
Treatment options in non-AIDS patients who have reduced immune-system function is not well studied. Intravenous Amphotericin B combined with oral flucytosine may be effective. Every attempt should be made to reduce the amount of immunosuppressive medication until the infection is resolved. AIDS patients often have a reduced response to Amphotericin B and flucytosine, therefore after initial treatment as above, oral fluconazole can be used.[1] The decision on when to start treatment for HIV is not yet settled, although one small, under-powered trial suggested that delaying the start of treatment for 10 weeks may be beneficial in avoiding deaths from Immune reconstitution inflammatory syndrome (IRIS).[3]
[edit] IRIS in immunocompetent hosts

The immune reconstitution inflammatory syndrome (IRIS) has been described in immunocompetent hosts who have meningitis caused by C. gattii and C. grubii. Several weeks or even months into appropriate treatment, there is a sudden onset deterioration with worsening meningitis symptoms and progression or development of new neurological symptoms. Magnetic resonance imaging shows increase in the size of brain lesions, and CSF abnormalities (white cell count, protein, glucose) increase. CSF culture is sterile, and there is no increase in CSF cryptococcal antigen titre. The increasing inflammation can cause brain injury or be fatal.[4] [5] [6] The mechanism behind IRIS in cryptococcal meningitis may be local or systemic immunosuppression induced by the cryptococcal infection which resolves as the organism is killed by antifungal treatment. This is associated with increased inflammation as the recovering immune system recognises the fungus. Treatment with systemic corticosteroids during IRIS may be beneficial in preventing death or progressive neurological deterioration. IRIS may be the cause of paradoxically worse outcomes for cryptococcal meningitis in immunocompetent compared with immunocompromised hosts, in whom Cryptococcus neoformans is the usual pathogen.

[edit] Veterinary cases

Cryptococcosis is also seen in cats and occasionally dogs. It is the most common deep fungal disease in cats, usually leading to chronic infection of the nose and sinuses, and skin ulcers. Cats may develop a bump over the bridge of the nose from local tissue inflammation. It can be associated with FeLV infection in cats.[7][8]

[edit] Additional images

[edit] References
1. ^ a b Barron MA and Madinger NE (November 18, 2008). "Opportunistic Fungal Infections, Part 3: Cryptococcosis, Histoplasmosis, Coccidioidomycosis, and Emerging Mould Infections". Infections in Medicine. http://www.consultantlive.com/infection/article/1145625/1404367?pageNumber=1. 2. ^ King JW and Dasgupta A (Jun 15, 2007). "Cryptococcosis". eMedicine. http://emedicine.medscape.com/article/215354-overview. 3. ^ Makadzange AT, Ndhlovu CE, Takarinda K, Reid M, Kurangwa M, Gona P, Hakim JG (2010). "Early versus delayed initiation of antiretroviral therapy for concurrent HIV infection and cryptococcal meningitis in sub-saharan Africa". Clin Infect Dis 50 (11): 15328.|pmid= 20415574} 4. ^ Lane M, McBride J and Archer J "Steroid responsive late deterioration in Cryptococcus neoformans variety gattii meningitis", Neurology 2004;63;713-714 5. ^ Einsiedel L, Gordon DL, and Dyer JR, "Paradoxical inflammatory reaction during treatment of Cryptococcus neoformans var. gattii meningitis in an HIV-seronegative woman", CID 2004;39:e7882 6. ^ Ecevit IZ, Clancy CJ, Schmalfuss IM, and Nguyen MH, "The poor prognosis of central nervous system cryptococcosis among nonimmunosuppressed atients: A call for better disease recognition and evaluation of adjuncts to antifungal therapy", CID 2006;42:14437 7. ^ Deep fungal infections 8. ^ Malik (2003), "Feline Cryptococcosis"

[edit] External links

The Merck Manual Health AtoZ synd/1793 at Who Named It? See pathology video with commentary of brain tissue infested by cryptoccocus neoformans

[hide]vdeInfectious diseases Mycoses and Mesomycetozoea (B35B49,

110118)
Tinea barbae/Tinea capitis (Kerion) Tinea corporis (Ringworm, Dermatophytid) Tinea cruris Tinea manuum Tinea pedis (Athlete's foot) Tinea unguium/Onychomycosis By (White superficial location onychomycosis Distal subungual onychomycosis Proximal subungual Dermatophyte onychomycosis) (Dermatophytos Tinea corporis is) Ascomycota gladiatorum Tinea faciei Tinea imbricata Tinea incognito Favus Epidermophyton floccosum Microsporum canis Microsporum audouinii Trichophyton By interdigitale/mentagrophy organism tes Trichophyton tonsurans Trichophyton schoenleini Trichophyton rubrum Other Hortaea werneckii (Tinea nigra) Piedraia hortae (Black piedra)

Superficial and cutaneous (dermatomycosi s): Tinea=skin; Piedra (exothrix/ endothrix)=hair

Basidiomyco Malassezia furfur (Tinea versicolor, Pityrosporum ta folliculitis) Trichosporon spp (White piedra) Coccidioides immitis/Coccidioides posadasii (Coccidioidomycosis, Disseminated coccidioidomycosis, Primary cutaneous Dimorphic Onygenale coccidioidomycosis. Ascomycota (yeast+mold s Primary pulmonary ) coccidioidomycosis) Histoplasma capsulatum (Histoplasmosis, Primary cutaneous histoplasmosis, Primary pulmonary

Subcutaneous, systemic, and opportunistic

histoplasmosis, Progressive disseminated histoplasmosis) Histoplasma duboisii (African histoplasmosis) Lacazia loboi (Lobomycosis) Paracoccidioides brasiliensis (Paracoccidioidomycosis ) Blastomyces dermatitidis (Blastomycosis, North American blastomycosis, South American Other blastomycosis) Sporothrix schenckii (Sporotrichosis) Penicillium marneffei (Penicilliosis) Candida albicans (Candidiasis, Oral, Esophageal, Vulvovaginal, Chronic mucocutaneous, Antibiotic candidiasis, Candidal intertrigo, Candidal onychomycosis, Candidal paronychia, Candidid, Diaper candidiasis, Congenital cutaneous Yeast-like candidiasis, Perianal candidiasis, Systemic candidiasis, Erosio interdigitalis blastomycetica) C. glabrata C. tropicalis C. lusitaniae Pneumocystis jirovecii (Pneumocystosis, Pneumocystis pneumonia) Aspergillus (Aspergillosis, Aspergilloma, Allergic bronchopulmonary aspergillosis, Primary cutaneous aspergillosis) Exophiala jeanselmei (Eumycetoma) Fonsecaea Mold-like pedrosoi/Fonsecaea compacta/Phialophora verrucosa (Chromoblastomycosis) Geotrichum candidum (Geotrichosis) Pseudallescheria boydii (Allescheriasis) Basidiomycota Cryptococcus neoformans (Cryptococcosis),

Trichosporon spp (Trichosporonosis) Rhizopus oryzae Mucor indicus Absidia Mucorales corymbifera (Mucormycosis) Syncephalastrum racemosum Zygomycota Basidiobolus ranarum (Zygomycosis) (Basidiobolomycosis) Entomophthorales Conidiobolus (Entomophthoramycosis) coronatus/Conidiobolus incongruus (Conidiobolomycosis) Microsporidia Enterocytozoon bieneusi/Encephalitozoon (Microsporidiosis intestinalis ) Mesomycetozoe a Ungrouped Rhinosporidium seeberi (Rhinosporidiosis)

Alternariosis Fungal folliculitis Fusarium (Fusariosis) Granuloma gluteale infantum Hyalohyphomycosis Otomycosis Phaeohyphomycosis M: MYC fung, clas fung drug (fung) Retrieved from "http://en.wikipedia.org/wiki/Cryptococcosis" Categories: Fungal diseases | Mycosis-related cutaneous conditions
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Toxoplasmosis From Wikipedia, the free encyclopedia Jump to: navigation, search

Toxoplasmosis Classification and external resources

T. gondii tachyzoites ICD-10 ICD-9 DiseasesDB MedlinePlus eMedicine MeSH

B58. 130 13208 000637 med/2294 D014123

Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii.[1] The parasite infects most genera of warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by ingestion of feces of a cat that has itself recently been infected, or by transmission from mother to fetus.

Although cats are often blamed for spreading toxoplasmosis, contact with raw meat is a more significant source of human infections in many countries, and fecal contamination of hands is a greater risk factor.[2] Up to one third of the world's human 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 Examination Survey (NHANES) between 1999 and 2004 was found to be 10.8%, with seroprevalence among women of childbearing age (15 to 44 years) 11%.[4] During the first few weeks post-exposure, the infection typically causes a mild flu-like illness or no illness. Thereafter, the parasite rarely causes any symptoms in otherwise healthy adults. However, those with a weakened immune system, such as AIDS patients or pregnant women, 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, inner ears, and eyes (chorioretinitis).

Contents [hide] 1 Signs and symptoms 1.1 Acute toxoplasmosis 1.2 Latent toxoplasmosis 1.3 Cutaneous toxoplasmosis 1.4 Possible link to psychiatric disorders 2 Diagnosis 3 Transmission 3.1 Pregnancy precautions 4 Treatment 4.1 Acute 4.2 Latent 5 Biological modifications of the host 5.1 Reproductive changes 5.2 Behavioral changes 5.2.1 Toxoplasma's role in schizophrenia 6 Epidemiology

6.1 In humans 6.2 In other animals 7 History 8 Society and culture 8.1 Notable people 8.2 Literature and film 9 See also 10 References 11 External links

[edit] Signs and symptoms Infection has two stages: [edit] 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 or nasal lesions 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 (encephalitis) or the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns. Swollen lymph nodes are more commonly found in the neck followed by axillae and then groin. Swelling may occur at different times after the initial infection, persist, and/or recur for various times independently of antiparasitic treatment.[5] It is usually found at single sites in adults, but in children multiple sites may be more common. Enlarged lymph nodes will resolve within one to two months in 60% of patients. However, a quarter of patients take 24 months to return to normal and 8% take 46 months. A substantial number of patients (6%) do not return to normal until much later.[6] [edit] Latent toxoplasmosis It is easy for a host to become infected with Toxoplasma gondii and develop toxoplasmosis without knowing 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.[7] [edit] Cutaneous toxoplasmosis While rare, skin lesions may occur in the acquired form of the disease, including roseola and erythema multiforme-like eruptions, prurigo-like nodules, urticaria, and maculopapular lesions. Newborns may have punctate macules, ecchymoses, or blueberry muffin lesions. Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of T. gondii being

found in the epidermis. It is found in all levels of the epidermis, is about 6 m by 2 m , bowshaped, 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.[8] [edit] Possible link to psychiatric disorders Studies have been conducted that show the toxoplasmosis parasite may affect behavior and may present as or be a causative or contributory factor in various psychiatric disorders such as depression, anxiety and schizophrenia.[9][10][11] In 11 of 19 scientific studies, T. gondii antibody levels were found to be significantly higher in individuals affected by first-incidence schizophrenia than in unaffected persons. Individuals with schizophrenia are also more likely to report a clinical history of toxoplasmosis than those in the general population.[12] Recent work at the University of Leeds has found that the parasite produces an enzyme with tyrosine hydroxylase and phenylalanine hydroxylase activity. This enzyme may contribute to the behavioral changes observed in toxoplasmosis by altering the production of dopamine, a neurotransmitter involved in mood, sociability, attention, motivation and sleep patterns. Schizophrenia has long been linked to dopamine dysregulation.[13] [edit] Diagnosis

Micrograph of a lymph node showing the characteristic changes of toxoplasmosis (scattered epithelioid histiocytes (pale cells), monocytoid cells (top-center of image), large germinal centers (left of image)). H&E stain. Detection of Toxoplasma gondii in human blood samples may be achieved by using the polymerase chain reaction (PCR).[14] Inactive cysts may exist in a host which would evade detection. Toxoplasmosis can't 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. [edit] Transmission

Life cycle of Toxoplasma gondii. 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.[15] Ingestion of contaminated cat feces. This can occur through hand-to-mouth contact following gardening, cleaning a cat's litter box, contact with children's sandpits, or touching leach, and can survive in the environment for over a year. It is, however, susceptible to high temperaturesabove 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.[16] 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[citation needed]. Studies have shown that only about 2% of cats are shedding oocysts at any one time[citation needed], and that oocyst shedding does not recur even after repeated exposure to the parasite[citation needed]. 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.[citation needed] [edit] Pregnancy precautions 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 (Portugal,[17] France,[18] Austria,[18] Uruguay,[19] and Italy[20] being the exceptions) for reasons of cost-effectiveness and the high number of false positives generated. As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented),[18] postnatal or neonatal screening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.[18] Some regional screening programmes operate in Germany, Switzerland and Belgium.[20] Treatment is very important for recently infected pregnant women, to prevent infection of the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in the young. [edit] 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. [edit] Acute 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 used most often for people with HIV/AIDS. Cotrimoxazole combitation of Pyrimethamine and Sulfadiazine in one tablet another option for people with problems like thrombocytopenia. spiramycin an antibiotic 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). [edit] Latent 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.[21] clindamycin an antibiotic which, in combination with atovaquone, seemed to optimally kill cysts in mice.[22] [edit] Biological modifications of the host The parasite itself can cause various effects on the host body, some of which are not fully understood. [edit] Reproductive changes A recent study has indicated toxoplasmosis correlates strongly with an increase in male births in humans.[23] 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 0.608 (as opposed to the normal 0.51) for Toxoplasma-positive mothers. The study explains that this effect may not significantly influence the actual sex ratio of children born in countries with high rates of latent toxoplasmosis infection because "In high-prevalence countries, most women of reproductive age have already been infected for a long time and therefore have only low titres of anti-Toxoplasma antibodies. Our results suggest that lowtitre women have similar sex ratios to Toxoplasma-negative women."[23] [edit] Behavioral changes It has been found that the parasite has the ability to change the behaviour of its host: infected rats and mice are less fearful of catsin fact, some of the infected rats seek out caturine-marked areas. This effect is advantageous to the parasite, which will be able to proliferate as a cat could eat the infected rat and later reproduce.[24] 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.[25] The findings of behavioural 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.[26] 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 human brain, which may produce or induce production of a neurotransmitter, possibly dopamine,[27] therefore acting similarly to dopamine reuptake inhibitor type antidepressants and stimulants. Correlations have been found between latent Toxoplasma infections and various characteristics:[28] Decreased novelty seeking behaviour[29] Slower reactions[30] Lower rule-consciousness and greater jealousy (in men)[29] Promiscuity and greater conscientiousness (in women)[29] The evidence for behavioral effects on humans is controversial (see a collection of research papers at http://natur.cuni.cz/flegr/publ.php).[citation needed] 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, i.e., it is possible that these associations merely reflect factors that predispose certain types of people to infection. However, many of the neurobehavioral symptoms that are postulated to be due to toxoplasmosis correlate to the general function of dopamine in the human brain, and the fact that toxoplasma encodes the dopamine synthetic enzyme tyrosine hydroxylase enzymes makes it likely that neurobehavioral symptoms can result from infection. Studies have found that toxoplasmosis is associated with an increased car accident rate in people with Rh-negative blood. The chance of an accident relative to uninfected people is increased roughly 2.5 times.[27][31][32] This may be due to the slowed reaction times that are associated with infection.[31] "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.[33] The data shows that the

risk decreases with time after infection, but is not due to age.[27] 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.[34] However there is also evidence of a delayed effect which increases reaction times.[35] Other studies suggest that the parasite may influence personality. There are claims of Toxoplasma causing antisocial attitudes in men and promiscuity[36] (or even "signs of higher intelligence"[33] ) in women, and greater susceptibility to schizophrenia and bipolar disorder in all infected persons.[36] A 2004 study found that Toxoplasma "probably induce[s] a decrease of novelty seeking." [37] 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. [38][39] The study suggests that male carriers 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.[28][39][40] [edit] Toxoplasma's role in schizophrenia The possibility that toxoplasmosis is one cause of schizophrenia has been studied by scientists since the year 1953.[41] 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.[41] A 2006 paper has even suggested that prevalence of toxoplasmosis has largescale effects on national culture.[42] 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).[41] Acute Toxoplasma infection sometimes leads to psychotic symptoms not unlike schizophrenia. Several studies have found significantly higher levels of Toxoplasma antibodies in schizophrenia patients compared to the general population.[43] Toxoplasma infection causes damage to astrocytes in the brain, and such damage is also seen in schizophrenia[citation needed]. [edit] Epidemiology [edit] In humans The U.S. NHANES (19992004) national probability sample found that 10.8% of U.S. persons 649 years of age, and 11.0% of women 1544 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 (19881994).[44][45]

It is estimated that between 30% and 65% of all people worldwide are infected with toxoplasmosis.[46] However, there is large variation between countries: in France, for example, around 88% of the population are carriers, probably due to a high consumption of raw and lightly cooked meat. [47] Germany, the Netherlands and Brazil also have high prevalences of around 68%, over 80%[48] and 67% respectively. In Britain about 22% are carriers, and South Korea's rate is 4.3%.[28] 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. [edit] 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.[49] Proximity to freshwater outflows into the ocean was a major risk factor. Ingestion of oocysts from cat faeces is considered to be the most likely ultimate source.[50] According to an article in New Scientist[51] the parasites have 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. [edit] 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 Toxoplasma gondii.[18] The first recorded congenital case was not until 1923, and the first adult case not until 1940.[18] In 1948, a serological dye test was created by Sabin & Feldman, which is now the standard basis for diagnostic tests.[52] [edit] Society and culture [edit] Notable people Arthur Ashe (tennis player) developed neurological problems from toxoplasmosis (and was later found to be HIV-positive).[53] Prince Franois, Count of Clermont (pretender to the Throne of France); his disability has caused him to be overlooked in the line of succession. Leslie Ash (actress) contracted toxoplasmosis in the second month of pregnancy.[54] Sebastian Coe (British middle distance runner)[55] Martina Navrtilov (tennis player) retired from a competition in 1982 with symptoms of a mystery 'virus' that were later found to be due to toxoplasmosis.[56] Louis Wain (artist) was famous for painting cats; he later developed schizophrenia, which some believe was due to toxoplasmosis resulting from his prolonged exposure to cats.[57] [edit] Literature and film Toxoplasmosis is often referenced in Peeps, a 2005 novel by Scott Westerfeld. In the 1996 film Trainspotting, the character Tommy, an HIV+ heroin addict, acquires toxoplasmosis and dies. Toxoplasmosis is referenced in And The Band Played On, a 1993 American television film docudrama directed by Roger Spottiswoode. The teleplay by Arnold Schulman is based on

the best-selling 1987 non-fiction book And the Band Played On: Politics, People, and the AIDS Epidemic by Randy Shilts. Toxoplasmosis is referred to at the end of the British TV series Doc Martin, Series 4, Episode 6: "MidWife Crisis", first broadcast on 25 October 2009. This was in relation to eating roadkill, including "Badger Burgers". Toxoplasmosis is referred to in one episode of the first season of House M.D. Toxoplasmosis was the subject of a controversial story line in the early years of the American television soap opera "All My Children" (1973-1974) in which a then-teenage Erica Kane (Susan Lucci) developed a nearly fatal case of Toxoplasmosis after an abortion. It was later explained to have been caused by the changing of a cat litter box. The effects of Toxoplasmosis on human behavior is central to the plot of Kitty Kitty, a film directed by Michael Medaglia in 2011. [edit] See also List of parasites (human) List of cutaneous conditions [edit] References ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 7237. ISBN 0838585299. ^ Torda A (2001). "Toxoplasmosis. Are cats really the source?". Aust Fam Physician 30 (8): 7437. PMID 11681144. ^ Montoya J, Liesenfeld O (2004). "Toxoplasmosis". Lancet 363 (9425): 196576. doi:10.1016/S0140-6736(04)16412-X. PMID 15194258. ^ a b 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): 40510. PMID 17827351. ^ Paul M (1 July 1999). "Immunoglobulin G avidity in diagnosis of toxoplasmic lymphadenopathy and ocular toxoplasmosis". Clin. Diagn. Lab. Immunol. 6 (4): 5148. PMID 10391853. PMC 95718. http://cvi.asm.org/cgi/pmidlookup?view=long&pmid=10391853. ^ "Lymphadenopathy". Btinternet.com. http://www.btinternet.com/~ukneqas.parasitologyscheme/Toxoplasma_Scheme/Teaching_I nformation/_Lymphadenopathy/_lymphadenopathy.html. Retrieved 2010-07-28. ^ Randall Parker: Humans Get Personality Altering Infections From Cats. September 30, 2003 ^ Klaus, Sidney N.; Shoshana Frankenburg, and A. Damian Dhar (2003). "Chapter 235: Leishmaniasis and Other Protozoan Infections". In Freedberg et al. Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ISBN 0-07-138067-1. ^ Kar N, Misra B.Toxoplasma seropositivity and depression: a case report. BMC Psychiatry. 2004 Feb 5;4:1.PMID 15018628 ^ Henriquez SA, Brett R, Alexander J, Pratt J, Roberts CW.Neuropsychiatric disease and Toxoplasma gondii infection. Neuroimmunomodulation. 2009;16(2):122-33. Epub 2009 Feb 11.PMID 19212132 ^ name="newscientist.com">http://www.newscientist.com/article/mg20427301.600-3schizophrenia.html ^ redOrbit:Researchers Link Parasites To Schizophrenia. March 19, 2009

^ Science Daily: Toxoplasmosis Parasite May Trigger Schizophrenia And Bipolar Disorders. March 11, 2009 ^ Ho-Yen DO, Joss AW, Balfour AH, Smyth ET, Baird D, Chatterton JM (October 1992). "Use of the polymerase chain reaction to detect Toxoplasma gondii in human blood samples". J. Clin. Pathol. 45 (10): 9103. doi:10.1136/jcp.45.10.910. PMID 1430262. PMC 495065. http://jcp.bmj.com/cgi/pmidlookup?view=long&pmid=1430262. ^ "Toxoplasmosis". Centers of Disease Control and Prevention. 2004-11-22. http://www.dpd.cdc.gov/DPDx/HTML/Toxoplasmosis.htm. ^ North Carolina Department of Agriculture & Consumer Services ^ Circular Normativa sobre Cuidados Pr-Concepcionais - Direco-Geral de Sade ^ a b c d e f Sukthana Y (March 2006). "Toxoplasmosis: beyond animals to humans". Trends Parasitol. 22 (3): 13742. doi:10.1016/j.pt.2006.01.007. PMID 16446116. http://linkinghub.elsevier.com/retrieve/pii/S1471-4922(06)00023-7. ^ [1] ^ a b M. De Paschale, C. Agrappi, P. Clerici, P. Mirri, M. T. Manco, S. Cavallari and E. F. Vigan: Seroprevalence and incidence of Toxoplasma gondii infection in the Legnano area of Italy. Clinical Microbiology and Infection Volume 14 Issue 2 (2007), Pages 186 - 189. ^[dead link]"Toxoplasmosis - treatment key research". NAM & aidsmap. 2005-11-02. http://www.aidsmap.com/en/docs/659BAD5D-332A-4F8D-9F93-8D0F470B2D32.asp. ^ Djurkovi-Djakovi O, Milenkovi V, Nikoli A, Bobi B, Gruji 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): 9817. doi:10.1093/jac/dkf251. PMID 12461021. http://jac.oxfordjournals.org/cgi/reprint/50/6/981.pdf. ^ a b Kankov S, Sulc J, Nouzov K, Fajfrlk K, Frynta D, Flegr J (February 2007). "Women infected with parasite Toxoplasma have more sons". Naturwissenschaften 94 (2): 1227. doi:10.1007/s00114-006-0166-2. PMID 17028886. http://www.natur.cuni.cz/~flegr/pdf/toxosons.pdf. ^ Berdoy M, Webster JP, Macdonald DW (August 2000). "Fatal attraction in rats infected with Toxoplasma gondii". Proc. Biol. Sci. 267 (1452): 15914. doi:10.1098/rspb.2000.1182. PMID 11007336. PMC 1690701. http://journals.royalsociety.org/openurl.asp?genre=article&issn=09628452&volume=267&issue=1452&spage=1591. ^ "TOXO A Conversation With Robert Sapolsky". Edge. http://www.edge.org/3rd_culture/sapolsky09/sapolsky09_index.html#video. Retrieved 2010-07-28. ^ "'Cat Box Disease' May Change Human Personality And Lower IQ". The Daily Telegraph. April 8, 2000. ^ a b c Flegr J, Havlek J, Kodym P, Mal M, mahel 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. ^ a b c Carl Zimmer, The Loom. A Nation of Neurotics? Blame the Puppet Masters?, 1 Aug. 2006 ^ a b c Jaroslav Flegr (January 2007). "Effects of Toxoplasma on Human Behaviour". Schizophrenia Bulletin 33 (3): 757760. doi:10.1093/schbul/sbl074. PMID 17218612.

^ Hollie V Thomas, Daniel Rh Thomas, Roland L Salmon, Glyn Lewis and Andy P Smith (October 2004). "Toxoplasma and coxiella infection and psychiatric morbidity: A retrospective cohort analysis". BMC Psychiatry 4:32: 32. doi:10.1186/1471-244X-4-32. PMID 15491496. ^ a b Yereli K, Balcioglu IC, Ozbilgin A. (December 2 2005). "Is Toxoplasma gondii a potential risk for traffic accidents in Turkey?". Forensic Sci Int 163 (1-2): 347. doi:10.1016/j.forsciint.2005.11.002. PMID 16332418. ^ Flegr J, Klose J, Novotn M, Berenreitterov M, Havlcek J (2009). "Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study". BMC Infect. Dis. 9: 72. doi:10.1186/1471-2334-9-72. PMID 19470165. PMC 2692860. http://www.biomedcentral.com/1471-2334/9/72. ^ a b Adam, David (September 25, 2003). "Can a parasite carried by cats change your personality?". London: The Guardian. http://www.guardian.co.uk/life/thisweek/story/0,12977,1048642,00.html. Retrieved May 25, 2010. ^ "Dirt infection link to car crashes". BBC News. August 10, 2002. http://news.bbc.co.uk/1/hi/health/2176548.stm. ^ Havlcek J, Gasov ZG, Smith AP, Zvra K, Flegr J (May 2001). "Decrease of psychomotor performance in subjects with latent 'asymptomatic' toxoplasmosis". Parasitology 122 (Pt 5): 51520. doi:10.1017/S0031182001007624. PMID 11393824. ^ a b "Dangerrrr: cats could alter your personality". Times Online. June 23, 2005. http://www.libertypost.org/cgi-bin/readart.cgi?ArtNum=99546. ^ Novotn M, Hanusova J, Klose J, Preiss M, Havlicek J, Roubalov K, Flegr J (July 6 2004). "Probable neuroimmunological link between Toxoplasma and cytomegalovirus infections and personality changes in the human host". BMC Infect Dis 5: 54. doi:10.1186/1471-2334-554. PMID 16000166. ^ AAP, SMH Parasite makes men dumb, women sexy, 26 Dec. 2006 ^ a b "Cat Parasite Affects Everything We Feel and Do". ABC News. August 9, 2006. http://a.abcnews.com/Technology/DyeHard/Story?id=2288095. Retrieved 2009-05-06. ^ Kevin Lafferty ^ a b c Torrey EF, Yolken RH (2003). "Toxoplasma gondii and schizophrenia". Emerging Infect. Dis. 9 (11): 137580. PMID 14725265. free full text ^ 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. ISSN 0962-8452 (Paper) 1471-2954 (Online). PMID 17015323. PMC 1635495. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1635495/. ^ 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): 408. doi:10.1111/j.1600-0447.2006.00780.x. PMID 16774660. ^ 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): 35765. doi:10.1093/aje/154.4.357. PMID 11495859.

^ Jones J, Kruszon-Moran D, Wilson M (2003). "Toxoplasma gondii infection in the United States, 1999-2000". Emerg Infect Dis 9 (11): 13714. PMID 14718078. http://www.cdc.gov/ncidod/EID/vol9no11/03-0098.htm. [dead link] ^ Tenter AM, Heckeroth AR, Weiss LM (2000). "Toxoplasma gondii: from animals to humans". Int J Parasitol 30 (12-13): 121758. doi:10.1016/S0020-7519(00)00124-7. PMID 11113252. ^ David Adam, Guardian Unlimited. Can a parasite carried by cats change your personality?, 25 Sep. 2003 ^ Toxoplasmosis in the Netherlands by the Laboratory for Diagnoses for Infectious Diseases and Screening; RIVM Bilthoven ^ 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): 115568. doi:10.1016/j.ijpara.2005.07.002. PMID 16157341. ^ 17:30-22:00 "Treating Disease in the Developing World.". Talk of the Nation Science Friday. National Public Radio. December 16, 2005. http://www.npr.org/templates/story/story.php?storyId=5058325 17:30-22:00. ^ http://www.newscientist.com/article/mg20427301.600-3-schizophrenia.html ^ Toxoplasma Serology Laboratory: Laboratory Tests For The Diagnosis Of Toxoplasmosis ^ Arthur Ashe, Tennis Star, is Dead at 49 New York Times (02/08/93) ^ "Pregnancy superfoods revealed". BBC News. January 10, 2001. http://news.bbc.co.uk/1/hi/health/1109818.stm. Retrieved May 25, 2010. ^ "Olympics bid Coes finest race". The Times (London). June 26, 2005. http://www.timesonline.co.uk/tol/sport/article537461.ece. Retrieved May 25, 2010. ^ Sonja Matthee: Parasite of the month: Toxoplasma gondii. November 16, 1998. ^ "Topic 33. Coccidia and Cryptosporidium spp.". Biology 625: Animal Parasitology. Kent State Parasitology Lab. October 24, 2005. http://www.kstate.edu/parasitology/classes/625protozoa33.html. Retrieved 2006-10-14. Includes a list of famous victims. [edit] External links Parts of this article are taken from the public domain CDC factsheet: Toxoplasmosis Toxoplasmosis at Merck Manual of Diagnosis and Therapy Professional Edition Health Protection Agency (HPA), UK: Toxoplasmosis.

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Toxoplasmosis
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Toxoplasmosis
Classification and external resources

T. gondii tachyzoites

ICD-10

B58.

ICD-9

130

DiseasesDB

13208

MedlinePlus

000637

eMedicine

med/2294

MeSH

D014123

Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii.[1] The parasite infects most genera of warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by ingestion of feces of a cat that has itself recently been infected, or by transmission from mother to fetus. Although cats are often blamed for spreading toxoplasmosis, contact with raw meat is a more significant source of human infections in many countries, and fecal contamination of hands is a greater risk factor.[2] Up to one third of the world's human 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 Examination Survey (NHANES) between 1999 and 2004 was found to be 10.8%, with seroprevalence among women of childbearing age (15 to 44 years) 11%.[4] During the first few weeks post-exposure, the infection typically causes a mild flu-like illness or no illness. Thereafter, the parasite rarely causes any symptoms in otherwise healthy adults. However, those with a weakened immune system, such as AIDS patients or pregnant women, 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, inner ears, and eyes (chorioretinitis).

Contents
[hide]

1 Signs and symptoms o 1.1 Acute toxoplasmosis o 1.2 Latent toxoplasmosis o 1.3 Cutaneous toxoplasmosis o 1.4 Possible link to psychiatric disorders 2 Diagnosis 3 Transmission o 3.1 Pregnancy precautions 4 Treatment o 4.1 Acute o 4.2 Latent 5 Biological modifications of the host o 5.1 Reproductive changes o 5.2 Behavioral changes 5.2.1 Toxoplasma's role in schizophrenia 6 Epidemiology o 6.1 In humans o 6.2 In other animals 7 History 8 Society and culture o 8.1 Notable people o 8.2 Literature and film 9 See also 10 References 11 External links

[edit] Signs and symptoms

Infection has two stages:
[edit] 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 or nasal lesions 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 (encephalitis) or the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns.

Swollen lymph nodes are more commonly found in the neck followed by axillae and then groin. Swelling may occur at different times after the initial infection, persist, and/or recur for various times independently of antiparasitic treatment.[5] It is usually found at single sites in adults, but in children multiple sites may be more common. Enlarged lymph nodes will resolve within one to two months in 60% of patients. However, a quarter of patients take 24 months to return to normal and 8% take 46 months. A substantial number of patients (6%) do not return to normal until much later.[6]
[edit] Latent toxoplasmosis

It is easy for a host to become infected with Toxoplasma gondii and develop toxoplasmosis without knowing 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.[7]
[edit] Cutaneous toxoplasmosis

While rare, skin lesions may occur in the acquired form of the disease, including roseola and erythema multiforme-like eruptions, prurigo-like nodules, urticaria, and maculopapular lesions. Newborns may have punctate macules, ecchymoses, or blueberry muffin lesions. Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of T. gondii being found in the epidermis. It is found in all levels of the epidermis, is about 6 m by 2 m , bowshaped, 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.[8]
[edit] Possible link to psychiatric disorders

Studies have been conducted that show the toxoplasmosis parasite may affect behavior and may present as or be a causative or contributory factor in various psychiatric disorders such as depression, anxiety and schizophrenia.[9][10][11] In 11 of 19 scientific studies, T. gondii antibody levels were found to be significantly higher in individuals affected by first-incidence schizophrenia than in unaffected persons. Individuals with schizophrenia are also more likely to report a clinical history of toxoplasmosis than those in the general population.[12] Recent work at the University of Leeds has found that the parasite produces an enzyme with tyrosine hydroxylase and phenylalanine hydroxylase activity. This enzyme may contribute to the behavioral changes observed in toxoplasmosis by altering the production of dopamine, a neurotransmitter involved in mood, sociability, attention, motivation and sleep patterns. Schizophrenia has long been linked to dopamine dysregulation.[13]

[edit] Diagnosis

Micrograph of a lymph node showing the characteristic changes of toxoplasmosis (scattered epithelioid histiocytes (pale cells), monocytoid cells (top-center of image), large germinal centers (left of image)). H&E stain.

Detection of Toxoplasma gondii in human blood samples may be achieved by using the polymerase chain reaction (PCR).[14] Inactive cysts may exist in a host which would evade detection. Toxoplasmosis can't 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.

[edit] Transmission

Life cycle of Toxoplasma gondii.

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.[15] Ingestion of contaminated cat feces. This can occur through hand-to-mouth contact following gardening, cleaning a cat's litter box, contact with children's sandpits, or touching leach, and can survive in the environment for over a year. It is, however, susceptible to high temperaturesabove 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.[16]

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[citation needed]. Studies have shown that only about 2% of cats are shedding oocysts at any one time[citation needed], and that oocyst shedding does not recur even after repeated exposure to the parasite[citation needed]. 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.[citation needed]
[edit] Pregnancy precautions

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 (Portugal,[17] France,[18] Austria,[18] Uruguay,[19] and Italy[20] being the exceptions) for reasons of cost-effectiveness and the high number of false positives generated. As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented),[18] postnatal or neonatal screening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.[18] Some regional screening programmes operate in Germany, Switzerland and Belgium.[20]

Treatment is very important for recently infected pregnant women, to prevent infection of the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in the young.

[edit] 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.
[edit] Acute

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 used most often for people with HIV/AIDS. Cotrimoxazole combitation of Pyrimethamine and Sulfadiazine in one tablet another option for people with problems like thrombocytopenia. spiramycin an antibiotic 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).
[edit] Latent

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.[21] clindamycin an antibiotic which, in combination with atovaquone, seemed to optimally kill cysts in mice.[22]

[edit] Biological modifications of the host

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

A recent study has indicated toxoplasmosis correlates strongly with an increase in male births in humans.[23] 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 0.608 (as opposed to the normal 0.51) for Toxoplasma-positive mothers. The study explains that this

effect may not significantly influence the actual sex ratio of children born in countries with high rates of latent toxoplasmosis infection because "In high-prevalence countries, most women of reproductive age have already been infected for a long time and therefore have only low titres of anti-Toxoplasma antibodies. Our results suggest that low-titre women have similar sex ratios to Toxoplasma-negative women."[23]
[edit] Behavioral changes

It has been found that the parasite has the ability to change the behaviour of its host: infected rats and mice are less fearful of catsin fact, some of the infected rats seek out cat-urinemarked areas. This effect is advantageous to the parasite, which will be able to proliferate as a cat could eat the infected rat and later reproduce.[24] 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.[25] The findings of behavioural 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.[26] 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 human brain, which may produce or induce production of a neurotransmitter, possibly dopamine,[27] therefore acting similarly to dopamine reuptake inhibitor type antidepressants and stimulants. Correlations have been found between latent Toxoplasma infections and various characteristics:[28]

Decreased novelty seeking behaviour[29] Slower reactions[30] Lower rule-consciousness and greater jealousy (in men)[29] Promiscuity and greater conscientiousness (in women)[29]

The evidence for behavioral effects on humans is controversial (see a collection of research papers at http://natur.cuni.cz/flegr/publ.php).[citation needed] 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, i.e., it is possible that these associations merely reflect factors that predispose certain types of people to infection. However, many of the neurobehavioral symptoms that are postulated to be due to toxoplasmosis correlate to the general function of dopamine in the human brain, and the fact that toxoplasma encodes the dopamine synthetic enzyme tyrosine hydroxylase enzymes makes it likely that neurobehavioral symptoms can result from infection. Studies have found that toxoplasmosis is associated with an increased car accident rate in people with Rh-negative blood. The chance of an accident relative to uninfected people is increased roughly 2.5 times.[27][31][32] This may be due to the slowed reaction times that are associated with infection.[31] "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.[33] The data shows that the

risk decreases with time after infection, but is not due to age.[27] 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.[34] However there is also evidence of a delayed effect which increases reaction times.[35] Other studies suggest that the parasite may influence personality. There are claims of Toxoplasma causing antisocial attitudes in men and promiscuity[36] (or even "signs of higher intelligence"[33] ) in women, and greater susceptibility to schizophrenia and bipolar disorder in all infected persons.[36] A 2004 study found that Toxoplasma "probably induce[s] a decrease of novelty seeking." [37] 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. [38][39] The study suggests that male carriers 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.[28][39][40] [edit] Toxoplasma's role in schizophrenia The possibility that toxoplasmosis is one cause of schizophrenia has been studied by scientists since the year 1953.[41] 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.[41] A 2006 paper has even suggested that prevalence of toxoplasmosis has largescale effects on national culture.[42] 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).[41]

Acute Toxoplasma infection sometimes leads to psychotic symptoms not unlike schizophrenia. Several studies have found significantly higher levels of Toxoplasma antibodies in schizophrenia patients compared to the general population.[43] Toxoplasma infection causes damage to astrocytes in the brain, and such damage is also seen in schizophrenia[citation needed].

[edit] Epidemiology

[edit] In humans

The U.S. NHANES (19992004) national probability sample found that 10.8% of U.S. persons 649 years of age, and 11.0% of women 1544 years of age, had Toxoplasmaspecific IgG antibodies, indicating that they had been infected with the organism.[4] This prevalence has significantly decreased from the NHANES III (19881994).[44][45] It is estimated that between 30% and 65% of all people worldwide are infected with toxoplasmosis.[46] However, there is large variation between countries: in France, for example, around 88% of the population are carriers, probably due to a high consumption of raw and lightly cooked meat. [47] Germany, the Netherlands and Brazil also have high prevalences of around 68%, over 80%[48] and 67% respectively. In Britain about 22% are carriers, and South Korea's rate is 4.3%.[28] 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.

[edit] 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.[49] Proximity to freshwater outflows into the ocean was a major risk factor. Ingestion of oocysts from cat faeces is considered to be the most likely ultimate source.[50] According to an article in New Scientist[51] the parasites have 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.

[edit] 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 Toxoplasma gondii.[18] The first recorded congenital case was not until 1923, and the first adult case not until 1940.[18] In 1948, a serological dye test was created by Sabin & Feldman, which is now the standard basis for diagnostic tests.[52]

[edit] Society and culture

[edit] Notable people

Arthur Ashe (tennis player) developed neurological problems from toxoplasmosis (and was later found to be HIV-positive).[53] Prince Franois, Count of Clermont (pretender to the Throne of France); his disability has caused him to be overlooked in the line of succession. Leslie Ash (actress) contracted toxoplasmosis in the second month of pregnancy.[54]

Sebastian Coe (British middle distance runner)[55] Martina Navrtilov (tennis player) retired from a competition in 1982 with symptoms of a mystery 'virus' that were later found to be due to toxoplasmosis.[56] Louis Wain (artist) was famous for painting cats; he later developed schizophrenia, which some believe was due to toxoplasmosis resulting from his prolonged exposure to cats.[57]

[edit] Literature and film

Toxoplasmosis is often referenced in Peeps, a 2005 novel by Scott Westerfeld. In the 1996 film Trainspotting, the character Tommy, an HIV+ heroin addict, acquires toxoplasmosis and dies. Toxoplasmosis is referenced in And The Band Played On, a 1993 American television film docudrama directed by Roger Spottiswoode. The teleplay by Arnold Schulman is based on the best-selling 1987 non-fiction book And the Band Played On: Politics, People, and the AIDS Epidemic by Randy Shilts. Toxoplasmosis is referred to at the end of the British TV series Doc Martin, Series 4, Episode 6: "MidWife Crisis", first broadcast on 25 October 2009. This was in relation to eating roadkill, including "Badger Burgers". Toxoplasmosis is referred to in one episode of the first season of House M.D. Toxoplasmosis was the subject of a controversial story line in the early years of the American television soap opera "All My Children" (1973-1974) in which a then-teenage Erica Kane (Susan Lucci) developed a nearly fatal case of Toxoplasmosis after an abortion. It was later explained to have been caused by the changing of a cat litter box. The effects of Toxoplasmosis on human behavior is central to the plot of Kitty Kitty, a film directed by Michael Medaglia in 2011.

[edit] See also

List of parasites (human) List of cutaneous conditions

[edit] References
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8. ^ Klaus, Sidney N.; Shoshana Frankenburg, and A. Damian Dhar (2003). "Chapter 235: Leishmaniasis and Other Protozoan Infections". In Freedberg et al. Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ISBN 0-07-138067-1. 9. ^ Kar N, Misra B.Toxoplasma seropositivity and depression: a case report. BMC Psychiatry. 2004 Feb 5;4:1.PMID 15018628 10. ^ Henriquez SA, Brett R, Alexander J, Pratt J, Roberts CW.Neuropsychiatric disease and Toxoplasma gondii infection. Neuroimmunomodulation. 2009;16(2):122-33. Epub 2009 Feb 11.PMID 19212132 11. ^ name="newscientist.com">http://www.newscientist.com/article/mg20427301.600-3schizophrenia.html 12. ^ redOrbit:Researchers Link Parasites To Schizophrenia. March 19, 2009 13. ^ Science Daily: Toxoplasmosis Parasite May Trigger Schizophrenia And Bipolar Disorders. March 11, 2009 14. ^ Ho-Yen DO, Joss AW, Balfour AH, Smyth ET, Baird D, Chatterton JM (October 1992). "Use of the polymerase chain reaction to detect Toxoplasma gondii in human blood samples". J. Clin. Pathol. 45 (10): 9103. doi:10.1136/jcp.45.10.910. PMID 1430262. PMC 495065. http://jcp.bmj.com/cgi/pmidlookup?view=long&pmid=1430262. 15. ^ "Toxoplasmosis". Centers of Disease Control and Prevention. 2004-11-22. http://www.dpd.cdc.gov/DPDx/HTML/Toxoplasmosis.htm. 16. ^ North Carolina Department of Agriculture & Consumer Services 17. ^ Circular Normativa sobre Cuidados Pr-Concepcionais - Direco-Geral de Sade 18. ^ a b c d e f Sukthana Y (March 2006). "Toxoplasmosis: beyond animals to humans". Trends Parasitol. 22 (3): 13742. doi:10.1016/j.pt.2006.01.007. PMID 16446116. http://linkinghub.elsevier.com/retrieve/pii/S1471-4922(06)00023-7. 19. ^ [1] 20. ^ a b M. De Paschale, C. Agrappi, P. Clerici, P. Mirri, M. T. Manco, S. Cavallari and E. F. Vigan: Seroprevalence and incidence of Toxoplasma gondii infection in the Legnano area of Italy. Clinical Microbiology and Infection Volume 14 Issue 2 (2007), Pages 186 - 189. 21. ^[dead link]"Toxoplasmosis - treatment key research". NAM & aidsmap. 2005-11-02. http://www.aidsmap.com/en/docs/659BAD5D-332A-4F8D-9F93-8D0F470B2D32.asp. 22. ^ Djurkovi-Djakovi O, Milenkovi V, Nikoli A, Bobi B, Gruji 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): 9817. doi:10.1093/jac/dkf251. PMID 12461021. http://jac.oxfordjournals.org/cgi/reprint/50/6/981.pdf. 23. ^ a b Kankov S, Sulc J, Nouzov K, Fajfrlk K, Frynta D, Flegr J (February 2007). "Women infected with parasite Toxoplasma have more sons". Naturwissenschaften 94 (2): 1227. doi:10.1007/s00114-006-0166-2. PMID 17028886. http://www.natur.cuni.cz/~flegr/pdf/toxosons.pdf. 24. ^ Berdoy M, Webster JP, Macdonald DW (August 2000). "Fatal attraction in rats infected with Toxoplasma gondii". Proc. Biol. Sci. 267 (1452): 15914. doi:10.1098/rspb.2000.1182. PMID 11007336. PMC 1690701. http://journals.royalsociety.org/openurl.asp?genre=article&issn=09628452&volume=267&issue=1452&spage=1591. 25. ^ "TOXO A Conversation With Robert Sapolsky". Edge. http://www.edge.org/3rd_culture/sapolsky09/sapolsky09_index.html#video. Retrieved 2010-07-28. 26. ^ "'Cat Box Disease' May Change Human Personality And Lower IQ". The Daily Telegraph. April 8, 2000.

27. ^ a b c Flegr J, Havlek J, Kodym P, Mal M, mahel 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. 28. ^ a b c Carl Zimmer, The Loom. A Nation of Neurotics? Blame the Puppet Masters?, 1 Aug. 2006 29. ^ a b c Jaroslav Flegr (January 2007). "Effects of Toxoplasma on Human Behaviour". Schizophrenia Bulletin 33 (3): 757760. doi:10.1093/schbul/sbl074. PMID 17218612. 30. ^ Hollie V Thomas, Daniel Rh Thomas, Roland L Salmon, Glyn Lewis and Andy P Smith (October 2004). "Toxoplasma and coxiella infection and psychiatric morbidity: A retrospective cohort analysis". BMC Psychiatry 4:32: 32. doi:10.1186/1471-244X-4-32. PMID 15491496. 31. ^ a b Yereli K, Balcioglu IC, Ozbilgin A. (December 2 2005). "Is Toxoplasma gondii a potential risk for traffic accidents in Turkey?". Forensic Sci Int 163 (1-2): 347. doi:10.1016/j.forsciint.2005.11.002. PMID 16332418. 32. ^ Flegr J, Klose J, Novotn M, Berenreitterov M, Havlcek J (2009). "Increased incidence of traffic accidents in Toxoplasma-infected military drivers and protective effect RhD molecule revealed by a large-scale prospective cohort study". BMC Infect. Dis. 9: 72. doi:10.1186/1471-2334-9-72. PMID 19470165. PMC 2692860. http://www.biomedcentral.com/1471-2334/9/72. 33. ^ a b Adam, David (September 25, 2003). "Can a parasite carried by cats change your personality?". London: The Guardian. http://www.guardian.co.uk/life/thisweek/story/0,12977,1048642,00.html. Retrieved May 25, 2010. 34. ^ "Dirt infection link to car crashes". BBC News. August 10, 2002. http://news.bbc.co.uk/1/hi/health/2176548.stm. 35. ^ Havlcek J, Gasov ZG, Smith AP, Zvra K, Flegr J (May 2001). "Decrease of psychomotor performance in subjects with latent 'asymptomatic' toxoplasmosis". Parasitology 122 (Pt 5): 51520. doi:10.1017/S0031182001007624. PMID 11393824. 36. ^ a b "Dangerrrr: cats could alter your personality". Times Online. June 23, 2005. http://www.libertypost.org/cgi-bin/readart.cgi?ArtNum=99546. 37. ^ Novotn M, Hanusova J, Klose J, Preiss M, Havlicek J, Roubalov K, Flegr J (July 6 2004). "Probable neuroimmunological link between Toxoplasma and cytomegalovirus infections and personality changes in the human host". BMC Infect Dis 5: 54. doi:10.1186/1471-2334-554. PMID 16000166. 38. ^ AAP, SMH Parasite makes men dumb, women sexy, 26 Dec. 2006 39. ^ a b "Cat Parasite Affects Everything We Feel and Do". ABC News. August 9, 2006. http://a.abcnews.com/Technology/DyeHard/Story?id=2288095. Retrieved 2009-05-06. 40. ^ Kevin Lafferty 41. ^ a b c Torrey EF, Yolken RH (2003). "Toxoplasma gondii and schizophrenia". Emerging Infect. Dis. 9 (11): 137580. PMID 14725265.free full text 42. ^ 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. ISSN 0962-8452 (Paper) 1471-2954 (Online). PMID 17015323. PMC 1635495. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1635495/. 43. ^ 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): 408. doi:10.1111/j.1600-0447.2006.00780.x. PMID 16774660.

44. ^ 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): 35765. doi:10.1093/aje/154.4.357. PMID 11495859. 45. ^ Jones J, Kruszon-Moran D, Wilson M (2003). "Toxoplasma gondii infection in the United States, 1999-2000". Emerg Infect Dis 9 (11): 13714. PMID 14718078. http://www.cdc.gov/ncidod/EID/vol9no11/03-0098.htm.[dead link] 46. ^ Tenter AM, Heckeroth AR, Weiss LM (2000). "Toxoplasma gondii: from animals to humans". Int J Parasitol 30 (12-13): 121758. doi:10.1016/S0020-7519(00)00124-7. PMID 11113252. 47. ^ David Adam, Guardian Unlimited. Can a parasite carried by cats change your personality?, 25 Sep. 2003 48. ^ Toxoplasmosis in the Netherlands by the Laboratory for Diagnoses for Infectious Diseases and Screening; RIVM Bilthoven 49. ^ 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): 115568. doi:10.1016/j.ijpara.2005.07.002. PMID 16157341. 50. ^ 17:30-22:00 "Treating Disease in the Developing World.". Talk of the Nation Science Friday. National Public Radio. December 16, 2005. http://www.npr.org/templates/story/story.php?storyId=5058325 17:30-22:00. 51. ^ http://www.newscientist.com/article/mg20427301.600-3-schizophrenia.html 52. ^ Toxoplasma Serology Laboratory: Laboratory Tests For The Diagnosis Of Toxoplasmosis 53. ^ Arthur Ashe, Tennis Star, is Dead at 49 New York Times (02/08/93) 54. ^ "Pregnancy superfoods revealed". BBC News. January 10, 2001. http://news.bbc.co.uk/1/hi/health/1109818.stm. Retrieved May 25, 2010. 55. ^ "Olympics bid Coes finest race". The Times (London). June 26, 2005. http://www.timesonline.co.uk/tol/sport/article537461.ece. Retrieved May 25, 2010. 56. ^ Sonja Matthee: Parasite of the month: Toxoplasma gondii. November 16, 1998. 57. ^ "Topic 33. Coccidia and Cryptosporidium spp.". Biology 625: Animal Parasitology. Kent State Parasitology Lab. October 24, 2005. http://www.kstate.edu/parasitology/classes/625protozoa33.html. Retrieved 2006-10-14. Includes a list of famous victims.

[edit] External links

Parts of this article are taken from the public domain CDC factsheet: Toxoplasmosis Toxoplasmosis at Merck Manual of Diagnosis and Therapy Professional Edition Health Protection Agency (HPA), UK: Toxoplasmosis. [show]vdeInfectious diseases Parasitic disease: protozoan infection:

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