Editing Toxoplasmosis

{{Short description|Protozoan parasitic disease}}
{{Expert needed|medicine|reason=convoluted logic in first para of diagnosis|date=May 2023}}
{{Infobox medical condition (new)
| name            = Toxoplasmosis
| image           = Toxoplasma gondii tachy.jpg
| caption         = ''T. gondii'' [[tachyzoite]]s
| field           = [[Infectious disease (medical specialty)|Infectious disease]]
| symptoms        = Often none, during [[pregnancy]] (birth defects)<ref name=CDC2015Sym/><ref name=Hunter2012/>
| complications   =
| onset           =
| duration        =
| causes          = ''[[Toxoplasma gondii]]''<ref name=CDC2015Epi/>
| risks           = Eating poorly cooked food, exposure to infected cat feces<ref name=CDC2015Epi/>
| diagnosis       = Blood test, [[amniotic fluid]] test<ref name=CDC2013Diag/>
| differential    =
| prevention      =
| treatment       = During pregnancy [[spiramycin]] or [[pyrimethamine]]/[[sulfadiazine]] and [[folinic acid]]<ref name=CDC2014Tx/>
| medication      =
| prognosis       =
| frequency       = Up to 50% of people, 200,000 cases of congenital toxoplasmosis a year<ref name="TorgersonMastroiacovo2013"/><ref name="Global threat"/>
| deaths          =
}}
<!-- Definition and symptoms -->
'''Toxoplasmosis''' is a [[parasitic disease]] caused by ''[[Toxoplasma gondii]]'', an [[apicomplexan]].<ref name=CDC2015Epi>{{cite web|title=Parasites – Toxoplasmosis (Toxoplasma infection) Epidemiology & Risk Factors|url=https://www.cdc.gov/parasites/toxoplasmosis/epi.html|access-date=22 August 2015|date=March 26, 2015|url-status=live|archive-url=https://web.archive.org/web/20150823023754/http://www.cdc.gov/parasites/toxoplasmosis/epi.html|archive-date=23 August 2015}}</ref> Infections with toxoplasmosis are associated with a variety of neuropsychiatric and behavioral conditions.<ref name=MilneEtAl2020>{{cite journal|vauthors=Milne G, Webster JP, Walker M|journal=Trends in Parasitology|volume=36|issue=12|doi=10.1016/j.pt.2020.08.005|doi-access=free|title=Toxoplasma gondii: An Underestimated Threat?|date=December 2020| pages=959–969 |pmid=33012669|quote=Accumulating evidence suggests that latent infection of Toxoplasma gondii is associated with a variety of neuropsychiatric and behavioral conditions.}}</ref> Occasionally, people may have a few weeks or months of mild, [[flu-like illness]] such as muscle aches and tender [[lymph nodes]].<ref name=CDC2015Sym/> In a small number of people, eye problems may develop.<ref name=CDC2015Sym/> In those with a [[Immunodeficiency|weakened immune system]], severe symptoms such as [[seizure]]s and poor coordination may occur.<ref name=CDC2015Sym/> If a person becomes infected during [[pregnancy]], a condition known as '''congenital toxoplasmosis''' may affect the child.<ref name=CDC2015Sym>{{cite web|title=Parasites – Toxoplasmosis (Toxoplasma infection) Disease|url=https://www.cdc.gov/parasites/toxoplasmosis/disease.html|access-date=22 August 2015|date=July 10, 2014|url-status=live|archive-url=https://web.archive.org/web/20150822052351/http://www.cdc.gov/parasites/toxoplasmosis/disease.html|archive-date=22 August 2015}}</ref>

<!-- Spread, cause and diagnosis-->
Toxoplasmosis is usually spread by eating poorly cooked food that contains [[Microbial cyst|cysts]], by exposure to infected cat feces, or from an infected woman to her baby during pregnancy.<ref name=CDC2015Epi/> Rarely, the disease may be spread by [[blood transfusion]] or other organ transplant.<ref name=CDC2015Epi/> It is not otherwise spread between people.<ref name=CDC2015Epi/><!-- Quote = Toxoplasmosis is not passed from person-to-person, except in instances of parent-to-child (congenital) transmission and blood transfusion or organ transplantation. --> The parasite is only known to reproduce sexually in the [[Felidae|cat family]].<ref name=CDC2015Bio/> However, it can infect most types of [[warm-blooded animals]], including humans.<ref name=CDC2015Bio>{{cite web|title=Parasites – Toxoplasmosis (Toxoplasma infection) Biology|url=https://www.cdc.gov/parasites/toxoplasmosis/biology.html|access-date=22 August 2015|date=March 17, 2015|url-status=live|archive-url=https://web.archive.org/web/20150828061023/http://www.cdc.gov/parasites/toxoplasmosis/biology.html|archive-date=28 August 2015}}</ref> Diagnosis is typically by testing blood for [[antibody|antibodies]] or by testing the [[amniotic fluid]] in a pregnant patient for the parasite's [[DNA]].<ref name=CDC2013Diag>{{cite web|title=Parasites – Toxoplasmosis (Toxoplasma infection) Diagnosis|url=https://www.cdc.gov/parasites/toxoplasmosis/diagnosis.html|access-date=22 August 2015|date=January 10, 2013|url-status=live|archive-url=https://web.archive.org/web/20150822100916/http://www.cdc.gov/parasites/toxoplasmosis/diagnosis.html|archive-date=22 August 2015}}</ref>

<!-- Prevention and treatment -->
Prevention is by properly preparing and cooking food.<ref name=CDC2015Pre/> Pregnant women are also recommended not to clean cat litter boxes or, if they must, to wear gloves and wash their hands afterwards.<ref name=CDC2015Pre>{{cite web|title=Parasites – Toxoplasmosis (Toxoplasma infection) Prevention & Control|url=https://www.cdc.gov/parasites/toxoplasmosis/prevent.html|access-date=22 August 2015|date=January 10, 2013|url-status=live|archive-url=https://web.archive.org/web/20150822103220/http://www.cdc.gov/parasites/toxoplasmosis/prevent.html|archive-date=22 August 2015}}</ref> Treatment of otherwise healthy people is usually not needed.<ref name=CDC2014Tx/> During pregnancy, [[spiramycin]] or [[pyrimethamine]]/[[sulfadiazine]] and [[folinic acid]] may be used for treatment.<ref name=CDC2014Tx>{{cite web|title=Parasites – Toxoplasmosis (Toxoplasma infection) Resources for Health Professionals|url=https://www.cdc.gov/parasites/toxoplasmosis/health_professionals/index.html#tx|access-date=22 August 2015|date=April 14, 2014|url-status=live|archive-url=https://web.archive.org/web/20150913010353/http://www.cdc.gov/parasites/toxoplasmosis/health_professionals/index.html#tx|archive-date=13 September 2015}}</ref>

<!-- Epidemiology and history -->
Up to half of the world's population is infected by ''T.&nbsp;gondii'', but have no symptoms.<ref name="Global threat">{{cite journal | vauthors = Flegr J, Prandota J, Sovičková M, Israili ZH | title = Toxoplasmosis—a global threat. Correlation of latent toxoplasmosis with specific disease burden in a set of 88 countries | journal = PLOS ONE | volume = 9 | issue = 3 | pages = e90203 | date = March 2014 | pmid = 24662942 | pmc = 3963851 | doi = 10.1371/journal.pone.0090203 | quote = Toxoplasmosis is becoming a global health hazard as it infects 30–50% of the world human population.| bibcode = 2014PLoSO...990203F | doi-access = free }}</ref> In the United States, approximately 11% of people have been infected, while in some areas of the world this is more than 60%.<ref name=CDC2015Epi/> Approximately 200,000 cases of congenital toxoplasmosis occur a year.<ref name="TorgersonMastroiacovo2013">{{cite journal |last1=Torgerson |first1=Paul R |last2=Mastroiacovo |first2=Pierpaolo |year=2013 |title=The global burden of congenital toxoplasmosis: a systematic review |journal=Bulletin of the World Health Organization |volume=91 |issue=7 |pages=501–508 |doi=10.2471/BLT.12.111732 |pmc=3699792 |pmid=23825877 }}</ref> [[Charles Nicolle]] and [[Louis Manceaux]] first described the organism in 1908.<ref name=Ferguson_2009/> In 1941, transmission during pregnancy from a pregnant woman to her baby was confirmed.<ref name=Ferguson_2009>{{cite journal | author = Ferguson DJ | title = ''Toxoplasma gondii'': 1908–2008, homage to Nicolle, Manceaux and Splendore | journal = Memórias do Instituto Oswaldo Cruz | volume = 104 | issue = 2 | pages = 133–48 | year = 2009 | pmid = 19430635 | doi = 10.1590/S0074-02762009000200003| doi-access = free | hdl = 1807/57623 | hdl-access = free }}</ref> There is tentative evidence that otherwise asymptomatic infection may affect people's behavior.<ref>{{cite journal |last1=Tyebji |first1=S |last2=Seizova |first2=S |last3=Hannan |first3=AJ |last4=Tonkin |first4=CJ |title=Toxoplasmosis: A pathway to neuropsychiatric disorders. |journal=Neuroscience and Biobehavioral Reviews |date=January 2019 |volume=96 |pages=72–92 |doi=10.1016/j.neubiorev.2018.11.012 |pmid=30476506|s2cid=53726244 }}</ref>
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== Signs and symptoms ==
Infection has three stages:

=== Acute ===
Acute toxoplasmosis is often asymptomatic in healthy adults.<ref name="Dupont_2012">{{cite journal |vauthors=Dupont CD, Christian DA, Hunter CA | title = Immune response and immunopathology during toxoplasmosis | journal = Seminars in Immunopathology | volume = 34 | issue = 6 | pages = 793–813 | year = 2012 | pmid = 22955326 | pmc = 3498595 | doi = 10.1007/s00281-012-0339-3 }}</ref><ref name=Dubey2008/> However, symptoms may manifest and are often [[influenza]]-like: swollen [[lymph node]]s, headaches, fever, and fatigue,<ref name="The Mayo Clinic_2015">{{cite web | title = toxoplasmosis | website = [[Mayo Clinic]] | url = http://www.mayoclinic.org/diseases-conditions/toxoplasmosis/basics/symptoms/con-20025859 | url-status = live | archive-url = https://web.archive.org/web/20150908012728/http://www.mayoclinic.org/diseases-conditions/toxoplasmosis/basics/symptoms/con-20025859 | archive-date = 2015-09-08 }}</ref> or [[myalgia|muscle aches]] and pains that last for a month or more. It is rare for a human with a fully functioning [[immune system]] to develop severe symptoms following infection. People with weakened immune systems are likely to experience headache, confusion, poor coordination, seizures, lung problems that may resemble tuberculosis or ''Pneumocystis jirovecii'' pneumonia (a common opportunistic infection that occurs in people with AIDS), or chorioretinitis caused by severe inflammation of the retina (ocular toxoplasmosis).<ref name="The Mayo Clinic_2015"/> Young children and [[Immunodeficiency|immunocompromised]] people, such as those with HIV/AIDS, those taking certain types of [[chemotherapy]], or those who have recently received an [[organ transplant]], may develop severe toxoplasmosis. This can cause damage to the brain ([[encephalitis]]) or the eyes ([[Toxoplasmic chorioretinitis|necrotizing retinochoroiditis]]).<ref name="Jones_2001">{{cite journal |vauthors=Jones JL, Kruszon-Moran D, Wilson M, McQuillan G, Navin T, McAuley JB | title = ''Toxoplasma gondii'' infection in the United States: seroprevalence and risk factors | journal = American Journal of Epidemiology | volume = 154 | issue = 4 | pages = 357–65 | year = 2001 | pmid = 11495859 | doi = 10.1093/aje/154.4.357 | doi-access = free }}</ref> Infants infected via [[Vertically transmitted infection|placental transmission]] may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns. The toxoplasmic [[trophozoite]]s causing acute toxoplasmosis are referred to as [[tachyzoites]], and are typically found in various tissues and body fluids, but rarely in blood or cerebrospinal fluid.<ref>{{cite book |doi=10.1016/B978-0-443-06668-9.50102-2 |date=2006 |isbn=978-0-443-06668-9 |last1=Schwartzman |first1=Joseph D. |last2=Maguire |first2=James H. |title=Tropical Infectious Diseases |chapter=Systemic Coccidia (Toxoplasmosis) |publisher=Elsevier |quote=Tachyzoites are found in all organs in acute infection, most prominently in muscle, including heart, and in the liver, spleen, lymph nodes, and the CNS. }}</ref>

[[Swollen lymph node]]s are commonly found in the neck or under the chin, followed by the armpits and the groin. Swelling may occur at different times after the initial infection, persist, and recur for various times independently of antiparasitic treatment.<ref>{{cite journal | author = Paul M | title = Immunoglobulin G Avidity in Diagnosis of Toxoplasmic Lymphadenopathy and Ocular Toxoplasmosis | journal = Clin. Diagn. Lab. Immunol. | volume = 6 | issue = 4 | pages = 514–8 | date = 1 July 1999 | pmid = 10391853 | pmc = 95718 | doi = 10.1128/CDLI.6.4.514-518.1999 }}</ref> It is usually found at single sites in adults, but in children, multiple sites may be more common. Enlarged lymph nodes will resolve within 1–2 months in 60% of cases. However, a quarter of those affected take 2–4 months to return to normal, and 8% take 4–6 months. A substantial number (6%) do not return to normal until much later.<ref>{{cite web |url=http://ukneqasmicro.org.uk/parasitology/images/pdf/ToxoplasmaSerology/Immunocompetent/Lymphadenopathy.pdf |title=Lymphadenopathy |publisher=UK Neqas Micro |access-date=2016-04-12 |url-status=live |archive-url=https://web.archive.org/web/20160424213931/http://ukneqasmicro.org.uk/parasitology/images/pdf/ToxoplasmaSerology/Immunocompetent/Lymphadenopathy.pdf |archive-date=2016-04-24 }}</ref>

===Latent===
Due to the absence of obvious symptoms,<ref name=Dupont_2012 /><ref name=Dubey2008 /> hosts easily become infected with ''T.&nbsp;gondii'' and develop toxoplasmosis without knowing it. Although mild, flu-like symptoms occasionally occur during the first few weeks following exposure, infection with ''T.&nbsp;gondii'' produces no readily observable symptoms in healthy human adults.<ref name="Global threat" /><ref name=CDCdisease>{{cite web|title=CDC Parasites – Toxoplasmosis (Toxoplasma infection) – Disease|url=https://www.cdc.gov/parasites/toxoplasmosis/disease.html|access-date=12 March 2013|url-status=live|archive-url=https://web.archive.org/web/20130307193139/http://www.cdc.gov/parasites/toxoplasmosis/disease.html|archive-date=7 March 2013}}</ref> In most [[immunocompetent]] people, the infection enters a latent phase, during which only [[bradyzoite]]s ([[Toxoplasma gondii#Formation of tissue cysts|in tissue cysts]]) are present;<ref name="Dubey_2006">{{cite journal |vauthors=Dubey JP, Hodgin EC, Hamir AN | title = Acute fatal toxoplasmosis in squirrels (''Sciurus carolensis'') with bradyzoites in visceral tissues | journal = The Journal of Parasitology | volume = 92 | issue = 3 | pages = 658–9 | year = 2006 | pmid = 16884019 | doi = 10.1645/GE-749R.1 | s2cid = 20384171 }}</ref> these tissue cysts and even lesions can occur in the [[retina]]s, [[Pulmonary alveolus|alveolar]] lining of the lungs (where an acute infection may mimic a ''[[Pneumocystis jirovecii]]'' infection), heart, skeletal muscle, and the [[central nervous system]] (CNS), including the brain.<ref name="Nawaz Khan_2015">{{EMedicine|article|344706|CNS Toxoplasmosis Imaging}}</ref> Cysts form in the CNS ([[nervous tissue|brain tissue]]) upon infection with ''T.&nbsp;gondii'' and persist for the lifetime of the host.<ref name="TG CNS review" /> Most infants who are infected while in the womb have no symptoms at birth, but may develop symptoms later in life.<ref name="futurepundit.com">Randall Parker: [http://www.futurepundit.com/archives/001675.html Humans Get Personality Altering Infections From Cats] {{webarchive|url=https://web.archive.org/web/20051217220821/http://www.futurepundit.com/archives/001675.html |date=2005-12-17 }}. September 30, 2003</ref>

Reviews of [[Serology|serological]] studies have estimated that 30–50% of the global population has been exposed to and may be chronically infected with latent toxoplasmosis, although infection rates differ significantly from country to country.<ref name="Global threat"/><ref name="TG Neuronal review" /><ref name="Pappas_2009"/> This latent state of infection has recently been associated with numerous [[disease burden]]s,<ref name="Global threat" /> neural alterations,<ref name="TG CNS review">{{cite journal | vauthors = Blanchard N, Dunay IR, Schlüter D | title = Persistence of ''Toxoplasma gondii'' in the central nervous system: a fine-tuned balance between the parasite, the brain and the immune system | journal = Parasite Immunology | volume = 37 | issue = 3 | pages = 150–158 | year = 2015 | pmid = 25573476 | doi = 10.1111/pim.12173 | s2cid = 1711188 | quote = The seroprevalence of T. gondii in humans varies between 10 and 70% worldwide, depending on the region and increases significantly with age. Upon infection, the parasites persist as intraneuronal cysts in the central nervous system (CNS) for the lifetime of the host (1, Figure 1). Until recently, parasite persistence in healthy individuals was regarded as clinically asymptomatic. However, in the last decade, several reports have indicated that chronic cerebral toxoplasmosis may impact on the behaviour of its host (2).| doi-access = free }}</ref><ref name="TG Neuronal review">{{cite journal | vauthors = Parlog A, Schlüter D, Dunay IR | title = ''Toxoplasma gondii''-induced neuronal alterations | journal = Parasite Immunology | volume = 37 | issue = 3 | pages = 159–170 | date  = March 2015 | pmid = 25376390 | doi = 10.1111/pim.12157 | quote = The zoonotic pathogen ''Toxoplasma gondii'' infects over 30% of the human population. The intracellular parasite can persist lifelong in the CNS within neurons modifying their function and structure, thus leading to specific behavioural changes of the host.&nbsp;...  Furthermore, investigations of the human population have correlated ''Toxoplasma'' seropositivity with changes in neurological functions; however, the complex underlying mechanisms of the subtle behavioural alteration are still not fully understood. The parasites are able to induce direct modifications in the infected cells, for example by altering dopamine metabolism, by functionally silencing neurons as well as by hindering apoptosis.| hdl = 10033/346575 | s2cid = 17132378 }}</ref> and subtle sex-dependent behavioral changes in immunocompetent humans,<ref name="Cook2015 primary source">{{cite journal |last1=Cook |first1=Thomas B. |last2=Brenner |first2=Lisa A. |last3=Cloninger |first3=C. Robert |last4=Langenberg |first4=Patricia |last5=Igbide |first5=Ajirioghene |last6=Giegling |first6=Ina |last7=Hartmann |first7=Annette M. |last8=Konte |first8=Bettina |last9=Friedl |first9=Marion |last10=Brundin |first10=Lena |last11=Groer |first11=Maureen W. |last12=Can |first12=Adem |last13=Rujescu |first13=Dan |last14=Postolache |first14=Teodor T. |title='Latent' infection with Toxoplasma gondii: Association with trait aggression and impulsivity in healthy adults |journal=Journal of Psychiatric Research |date=January 2015 |volume=60 |pages=87–94 |doi=10.1016/j.jpsychires.2014.09.019 |pmid=25306262 }}</ref><ref name="TG behavioral effects review">{{cite journal | vauthors = Hurley RA, Taber KH | title = Latent ''Toxoplasmosis gondii'': emerging evidence for influences on neuropsychiatric disorders | journal = Journal of Neuropsychiatry and Clinical Neurosciences | volume = 24 | issue = 4 | pages = 376–83 | year = 2012 | pmid = 23224444 | doi = 10.1176/appi.neuropsych.12100234 | quote = Nine of eleven studies using the Cattell's 16-Personality Factor self-report questionnaire found significant and consistent results for both genders. Seropositive men overall had lower regard for rules and higher vigilance (suspicious, jealous, rigid/inflexible) than seronegative men. In contrast, seropositive women had greater regard for rules and higher warmth than seronegative women. Both seropositive genders were more anxious than matched healthy-comparison subjects.&nbsp;...  Behavioral observations and interviews were completed to ascertain whether the gender differences found in self-report measures were replicated by objective measures. Seropositive men scored significantly lower than seronegative men on Self-Control, Clothes Tidiness, and Relationships. The differences were less impressive for the seropositive women, with only trends toward higher scores on Self-Control and Clothes Tidiness as compared with seronegative women. The authors view the study results as objective confirmation that ''T. gondii'' presence can change a human host's behaviors.}}</ref> as well as an increased risk of motor vehicle collisions.<ref>{{cite journal |last1=Gohardehi |first1=S |last2=Sharif |first2=M |last3=Sarvi |first3=S |last4=Moosazadeh |first4=M |last5=Alizadeh-Navaei |first5=R |last6=Hosseini |first6=SA |last7=Amouei |first7=A |last8=Pagheh |first8=A |last9=Sadeghi |first9=M |last10=Daryani |first10=A |title=The potential risk of toxoplasmosis for traffic accidents: A systematic review and meta-analysis. |journal=Experimental Parasitology |date=August 2018 |volume=191 |pages=19–24 |doi=10.1016/j.exppara.2018.06.003 |pmid=29906469|s2cid=49234104 }}</ref>

===Skin===
While rare, skin lesions may occur in the acquired form of the disease, including [[roseola]] and [[erythema]] multiforme-like eruptions, [[prurigo]]-like nodules, [[urticaria]], and [[Maculopapular rash|maculopapular lesions]]. Newborns may have punctate macules, [[ecchymoses]], or "blueberry muffin" lesions.

Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of ''T.&nbsp;gondii'' being found in the [[Epidermis (skin)|epidermis]].<ref>{{cite journal |last1=Zimmermann |first1=Stefan |last2=Hadaschik |first2=Eva |last3=Dalpke |first3=Alexander |last4=Hassel |first4=Jessica C. |last5=Ajzenberg |first5=Daniel |last6=Tenner-Racz |first6=Klara |last7=Lehners |first7=Nicola |last8=Kapaun |first8=Annette |last9=Schnitzler |first9=Paul |title=Varicella-Like Cutaneous Toxoplasmosis in a Patient with Aplastic Anemia |journal=Journal of Clinical Microbiology |date=April 2013 |volume=51 |issue=4 |pages=1341–1344 |doi=10.1128/JCM.02851-12 |pmid=23390283 |pmc=3666818 }}</ref> It is found in all levels of the epidermis, is about 6 by 2''&nbsp;''μm and bow-shaped, with the nucleus being one-third of its size. It can be identified by electron microscopy or by [[Giemsa stain]]ing tissue where the cytoplasm shows blue, the nucleus red.<ref>{{Fitzpatrick 6|235}}</ref>

== Cause ==
[[File:Toxoplasma gondii Life cycle PHIL 3421 lores.png|thumb|upright=1.5|Lifecycle of ''Toxoplasma gondii'']]

===Parasitology===
In its lifecycle, ''T. gondii'' adopts several forms.<ref name="Robert-GangneuxDarde2012"/> [[Tachyzoites]] are responsible for acute infection; they divide rapidly and spread through the tissues of the body. Tachyzoites are also known as "tachyzoic merozoites", a descriptive term that conveys more precisely the parasitological nature of this stage.<ref>{{cite journal|last1=Markus|first1=MB|title=Terms for coccidian merozoites|journal=Annals of Tropical Medicine and Parasitology|date=1987|volume=81|issue=4|pages=463|doi=10.1080/00034983.1987.11812147|pmid=3446034}}</ref> After proliferating, tachyzoites convert into [[bradyzoites]], which are inside latent intracellular tissue [[cyst]]s that form mainly in the muscles and brain. The formation of cysts is in part triggered by the pressure of the host immune system.<ref name=Miller2009/> The bradyzoites (also called "bradyzoic merozoites") are not responsive to antibiotics. Bradyzoites, once formed, can remain in the tissues for the lifespan of the host. In a healthy host, if some bradyzoites convert back into active tachyzoites, the immune system will quickly destroy them. However, in immunocompromised individuals, or in fetuses, which lack a developed immune system, the tachyzoites can run rampant and cause significant neurological damage.<ref name="Robert-GangneuxDarde2012"/>

The parasite's survival is dependent on a balance between host survival and parasite proliferation.<ref name=Miller2009>{{cite journal|author1=Miller CM|author2=Boulter NR|author3=Ikin RJ|author4=Smith NC|title=The immunobiology of the innate response to ''Toxoplasma gondii''|journal=International Journal for Parasitology|date=January 2009|volume=39|issue=1|pages=23–39|doi=10.1016/j.ijpara.2008.08.002|pmid=18775432}}</ref> ''T.&nbsp;gondii'' achieves this balance by manipulating the host's immune response, reducing the host's immune response, and enhancing the parasite's reproductive advantage.<ref name=Miller2009 /> Once it infects a normal host cell, it resists damage caused by the host's immune system, and changes the host's immune processes.<ref>{{cite journal |last1=Brasil |first1=Thaís Rigueti |last2=Freire-de-Lima |first2=Celio Geraldo |last3=Morrot |first3=Alexandre |last4=Vetö Arnholdt |first4=Andrea Cristina |title=Host-Toxoplasma gondii Coadaptation Leads to Fine Tuning of the Immune Response |journal=Frontiers in Immunology |date=2017 |volume=8 |page=1080 |doi=10.3389/fimmu.2017.01080 |pmid=28955329 |pmc=5601305 |doi-access=free }}</ref>
As it forces its way into the host cell, the parasite forms a [[parasitophorous vacuole]] (PV) membrane from the membrane of the host cell.<ref name=Hunter2012>{{cite journal|last1=Hunter|first1=CA|last2=Sibley|first2=LD|title=Modulation of innate immunity by ''Toxoplasma gondii'' virulence effectors|journal=Nature Reviews Microbiology|date=November 2012|volume=10|issue=11|pages=766–78|doi=10.1038/nrmicro2858|pmid=23070557|pmc=3689224}}</ref><ref name=Martens2005>{{cite journal|author1=Martens S|author2=Parvanova I|author3=Zerrahn J|author4=Griffiths G|author5=Schell G|author6=Reichmann G|author7=Howard JC|title=Disruption of ''Toxoplasma gondii'' parasitophorous vacuoles by the mouse p47-resistance GTPases |journal=PLOS Pathogens |date=November 2005 |volume=1 |issue=3 |pages=e24 |doi=10.1371/journal.ppat.0010024 |pmid=16304607|pmc=1287907 |doi-access=free }}</ref> The PV encapsulates the parasite, and is both resistant to the activity of the endolysosomal system, and can take control of the host's [[mitochondria]] and [[endoplasmic reticulum]].<ref name=Hunter2012 /><ref name=Martens2005 />

When first invading the cell, the parasite releases ROP proteins from the bulb of the [[rhoptry]] organelle.<ref name=Hunter2012 /> These proteins translocate to the nucleus and the surface of the PV membrane where they can activate [[STAT protein|STAT]] pathways to modulate the expression of [[cytokine]]s at the transcriptional level, bind and inactivate PV membrane destroying [[IRGs|IRG]] proteins, among other possible effects.<ref name=Hunter2012 /><ref name=Martens2005 /><ref name=Denkers2012>{{cite journal |last1=Denkers |first1=Eric Y. |last2=Schneider |first2=Anne G. |last3=Cohen |first3=Sara B. |last4=Butcher |first4=Barbara A. |title=Phagocyte Responses to Protozoan Infection and How Toxoplasma gondii Meets the Challenge |journal=PLOS Pathogens |date=2 August 2012 |volume=8 |issue=8 |pages=e1002794 |doi=10.1371/journal.ppat.1002794 |pmid=22876173 |pmc=3410898 |doi-access=free }}</ref> Additionally, certain strains of ''T.&nbsp;gondii'' can secrete a protein known as GRA15, activating the [[NF-κB]] pathway, which upregulates the pro-inflammatory [[cytokine]] [[Interleukin 12|IL-12]] in the early immune response, possibly leading to the parasite's latent phase.<ref name=Hunter2012 /> The parasite's ability to secrete these proteins depends on its genotype and affects its virulence.<ref name=Hunter2012 /><ref name=Denkers2012 />

The parasite also influences an anti-apoptotic mechanism, allowing the infected host cells to persist and replicate. One method of [[apoptosis]] resistance is by disrupting pro-apoptosis effector proteins, such as [[Bcl-2-associated X protein|BAX]] and [[Bcl-2 homologous antagonist killer|BAK]].<ref name="Hippe_2009">{{cite journal |vauthors=Hippe D, Weber A, Zhou L, Chang DC, Häcker G, Lüder CG | title = ''Toxoplasma gondii'' infection confers resistance against Bim<sub>S</sub>-induced apoptosis by preventing the activation and mitochondrial targeting of pro-apoptotic Bax | journal = Journal of Cell Science | volume = 122 | issue = Pt 19 | pages = 3511–21 | year = 2009 | pmid = 19737817 | doi = 10.1242/jcs.050963 | doi-access = free }}</ref> To disrupt these proteins, ''T.&nbsp;gondii'' causes conformational changes to the proteins, which prevent the proteins from being transported to various cellular compartments where they initiate apoptosis events. ''T.&nbsp;gondii'' does not, however, cause downregulation of the pro-apoptosis effector proteins.<ref name="Hippe_2009" />

''T. gondii'' also has the ability to initiate [[autophagy]] of the host's cells.<ref name="Wang">{{cite journal |vauthors=Wang Y, Weiss LM, Orlofsky A | title = Host cell autophagy is induced by ''Toxoplasma gondii'' and contributes to parasite growth | journal = The Journal of Biological Chemistry | volume = 284 | issue = 3 | pages = 1694–701 | year = 2009 | pmid = 19028680 | pmc = 2615531 | doi = 10.1074/jbc.M807890200 | doi-access = free }}</ref> This leads to a decrease in healthy, uninfected cells, and consequently fewer host cells to attack the infected cells. Research by Wang ''et al'' finds that infected cells lead to higher levels of autophagosomes in normal and infected cells.<ref name="Wang" /> Their research reveals that ''T.&nbsp;gondii'' causes host cell autophagy using a calcium-dependent pathway.<ref name="Wang" /> Another study suggests that the parasite can directly affect calcium being released from calcium stores, which are important for the signalling processes of cells.<ref name="Hippe_2009" />

The mechanisms above allow ''T.&nbsp;gondii'' to persist in a host. Some limiting factors for the toxoplasma is that its influence on the host cells is stronger in a weak immune system and is quantity-dependent, so a large number of ''T.&nbsp;gondii'' per host cell cause a more severe effect.<ref name="Laliberte_2008">{{cite journal |vauthors=Laliberté J, Carruthers VB | title = Host cell manipulation by the human pathogen ''Toxoplasma gondii'' | journal = Cellular and Molecular Life Sciences | volume = 65 | issue = 12 | pages = 1900–15 | year = 2008 | pmid = 18327664 | pmc = 2662853 | doi = 10.1007/s00018-008-7556-x }}</ref> The effect on the host also depends on the strength of the host immune system. Immunocompetent individuals do not normally show severe symptoms or any at all, while fatality or severe complications can result in immunocompromised individuals.<ref name="Laliberte_2008" />

''T. gondii'' has been shown to produce a protein called GRA28, released by the MYR1 secretory pathway, which interferes with gene expression in infected cells and results in cells that behave like dendritic cells, becoming highly mobile in the body.<ref>{{cite journal |last1=ten Hoeve |first1=Arne L. |last2=Braun |first2=Laurence |last3=Rodriguez |first3=Matias E. |last4=Olivera |first4=Gabriela C. |last5=Bougdour |first5=Alexandre |last6=Belmudes |first6=Lucid |last7=Couté |first7=Yohann |last8=Saeij |first8=Jeroen P.J. |last9=Hakimi |first9=Mohamed-Ali |last10=Barragan |first10=Antonio |title=The Toxoplasma effector GRA28 promotes parasite dissemination by inducing dendritic cell-like migratory properties in infected macrophages |journal=Cell Host & Microbe |date=November 2022 |volume=30 |issue=11 |pages=1570–1588.e7 |doi=10.1016/j.chom.2022.10.001 |pmc=9710525 |pmid=36309013 }}</ref>

Since the parasite can change the host's immune response, it may also have an effect, positive or negative, on the immune response to other pathogenic threats.<ref name=Miller2009 /> This includes, but is not limited to, the responses to infections by ''[[Helicobacter felis]]'', ''[[Leishmania major]]'', or other parasites, such as ''[[Nippostrongylus brasiliensis]]''.<ref name=Miller2009 />

=== Transmission ===
Toxoplasmosis is generally transmitted through the mouth when ''Toxoplasma gondii'' [[oocyst]]s or tissue cysts are accidentally eaten.<ref name=Weiss_Dubey_2009/> Congenital transmittance from mother to fetus can also occur.{{sfn|Weiss|Kim|2007|p={{pn|date=August 2024}}}} Transmission may also occur during the solid organ transplant process<ref name=Der2008/> or hematogenous stem cell transplants.<ref name=Kh2016/>

Oral transmission may occur through:
* Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing ''Toxoplasma'' cysts: Infection prevalence in countries where undercooked meat is traditionally eaten has been related to this transmission method. Tissue cysts may also be ingested during hand-to-mouth contact after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by raw meat.<ref name=CDC>{{cite web |url = http://www.dpd.cdc.gov/DPDx/HTML/Toxoplasmosis.htm |title = Toxoplasmosis |publisher   = Centers of Disease Control and Prevention |date = 2004-11-22 |url-status = live |archive-url  = https://web.archive.org/web/20061006065005/http://www.dpd.cdc.gov/dpdx/HTML/Toxoplasmosis.htm |archive-date = 2006-10-06 }}</ref>
* Ingestion of unwashed fruit or vegetables that have been in contact with contaminated soil containing infected cat feces.<ref name=Jones2012Foodborne/>
* Ingestion of cat [[feces]] containing oocysts: This can occur through hand-to-mouth contact following gardening, cleaning a cat's [[litter box]], contact with children's sandpits; the parasite can survive in the environment for months.<ref>{{cite web |url=http://www.ncagr.gov/vet/FactSheets/Toxoplasmosis.htm |title=Swine Toxoplasmosis |website=Veterinary Division – Animal Health Programs |author=Dubey, J.P. |url-status=live |archive-url=https://web.archive.org/web/20170322202229/http://www.ncagr.gov/vet/FactSheets/Toxoplasmosis.htm |archive-date=2017-03-22 }}</ref>
* Ingestion of untreated, unfiltered water through direct consumption or utilization of water for food preparation.<ref>{{cite book|last1=Signori Pereira|first1=Karen|last2=Franco|first2=Regina|last3=Leal|first3=Diego|chapter=Transmission of Toxoplasmosis (Toxoplasma gondii) by Foods|title=Advances in Food Nutrition and Research|date=2010|volume=60|pages=1–19|doi=10.1016/S1043-4526(10)60001-0|pmid=20691951|isbn=9780123809445|series=<!---->}}</ref>
* Ingestion of unpasteurized milk and milk products, particularly goat's milk.<ref>{{cite journal |last1=Boughattas |first1=Sonia |title=''Toxoplasma'' infection and milk consumption: Meta-analysis of assumptions and evidences |journal=Critical Reviews in Food Science and Nutrition |date=14 October 2015 |volume=57 |issue=13 |pages=2924–2933 |doi=10.1080/10408398.2015.1084993 |pmid=26467987 }}</ref>
* Ingestion of raw seafood.<ref>{{cite journal |last1=Jones |first1=Jeffrey |last2=Dargelas |first2=Valerie |last3=Roberts |first3=Jacquelin |last4=Press |first4=Cindy |last5=Remington |first5=Jack |last6=Montoya |first6=Jose |title=Risk Factors for Toxoplasma gondii Infection in the United States |journal=Clinical Infectious Diseases |date=15 September 2009 |volume=49 |issue=6 |pages=878–884 |doi=10.1086/605433|pmid=19663709 |s2cid=12816757 |doi-access=free }}</ref>
Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by eating an infected intermediate host that could include mammals (like rodents) or birds. Oocyst shedding usually starts from the third day after ingestion of infected intermediate hosts, and may continue for weeks. The oocysts are not infective when excreted.  After about a day, the oocyst undergoes a process called sporulation and becomes potentially pathogenic.<ref name=CDC2>{{cite web |url         = https://www.cdc.gov/parasites/toxoplasmosis/biology.html |title       = Parasites – Toxoplasmosis (Toxoplasma infection) |publisher   = Centers of Disease Control and Prevention |date        = 2011-04-05 |url-status     = live |archive-url  = https://web.archive.org/web/20150828061023/http://www.cdc.gov/parasites/toxoplasmosis/biology.html |archive-date = 2015-08-28 }}</ref> In addition to cats, birds and mammals including human beings are also intermediate hosts of the parasite and are involved in the transmission process. However the pathogenicity varies with the age and species involved in infection and the mode of transmission of ''T.&nbsp;gondii''.<ref>{{cite journal|last1=Assadi-Rad|first1=A.M.|last2=New|first2=John C.|last3=Patton|first3=Sharon|title=Risk factors associated with transmission of ''Toxoplasma gondii'' to sows kept in different management systems in Tennessee |journal=Veterinary Parasitology |date=April 1995 |volume=57 |issue=4 |pages=289–297 |doi=10.1016/0304-4017(94)00677-5|pmid=7660566}}</ref>

Toxoplasmosis may also be transmitted through solid organ transplants. Toxoplasma-seronegative recipients who receive organs from recently infected Toxoplasma-seropositive donors are at risk. Organ recipients who have latent toxoplasmosis are at risk of the disease reactivating in their system due to the immunosuppression occurring during solid organ transplant.<ref name=Der2008/> Recipients of hematogenous stem cell transplants may experience higher risk of infection due to longer periods of immunosuppression.<ref name=Kh2016>{{cite journal|last1=Khurana|first1=Sumeeta|last2=Batra|first2=Nitya|title=Toxoplasmosis in organ transplant recipients: Evaluation, implication, and prevention|journal=Tropical Parasitology|date=2016|volume=6|issue=2|pages=123–128|doi=10.4103/2229-5070.190814|pmid=27722100|pmc=5048698 |doi-access=free }}</ref>

Heart and lung transplants provide the highest risk for toxoplasmosis infection due to the striated muscle making up the heart,<ref name=Der2008>{{cite journal|last1=Derouin|first1=F|last2=Pelloux|first2=H|last3=ESCMID Study Group on Clinical|first3=Parasitology.|title=Prevention of toxoplasmosis in transplant patients|journal=Clinical Microbiology and Infection|date=December 2008|volume=14|issue=12|pages=1089–101|doi=10.1111/j.1469-0691.2008.02091.x|pmid=19018809|doi-access=free}}</ref> which can contain cysts, and risks for other organs and tissues vary widely.<ref name=Cos2013>{{cite journal|last1=Coster|first1=LO|title=Parasitic infections in solid organ transplant recipients|journal=Infectious Disease Clinics of North America|date=June 2013|volume=27|issue=2|pages=395–427|doi=10.1016/j.idc.2013.02.008|pmid=23714347}}</ref> Risk of transmission can be reduced by screening donors and recipients prior to the transplant procedure and providing treatment.<ref name=Cos2013/>

=== Pregnancy precautions ===
[[Congenital]] toxoplasmosis is a specific form of toxoplasmosis in which an unborn fetus is infected via the [[placenta]].<ref name="Sterkers_2011">{{cite journal |vauthors=Sterkers Y, Ribot J, Albaba S, Issert E, Bastien P, Pratlong F | title = Diagnosis of congenital toxoplasmosis by polymerase chain reaction on neonatal peripheral blood | journal = Diagnostic Microbiology and Infectious Disease | volume = 71 | issue = 2 | pages = 174–6 | year = 2011 | pmid = 21856107 | doi = 10.1016/j.diagmicrobio.2011.06.006 }}</ref> Congenital toxoplasmosis is associated with fetal death and miscarriage, and in infants, it is associated with hydrocephalus, cerebral calcifications and [[chorioretinitis]], leading to encephalopathy and possibly blindness.<ref name="TorgersonMastroiacovo2013"/> If a woman receives her first exposure to ''T.&nbsp;gondii'' while pregnant, the fetus is at particular risk.<ref name="TorgersonMastroiacovo2013" /> A simple blood draw at the first prenatal doctor visit can determine whether or not a woman has had previous exposure and therefore whether or not she is at risk. A positive antibody [[titer]] indicates previous exposure and immunity, and largely ensures the unborn fetus' safety.

Not much evidence exists around the effect of education before pregnancy to prevent congenital toxoplasmosis.<ref name=Di2015>{{cite journal |last1=Di Mario |first1=Simona |last2=Basevi |first2=Vittorio |last3=Gagliotti |first3=Carlo |last4=Spettoli |first4=Daniela |last5=Gori |first5=Gianfranco |last6=D'Amico |first6=Roberto |last7=Magrini |first7=Nicola |title=Prenatal education for congenital toxoplasmosis |journal=Cochrane Database of Systematic Reviews |date=23 October 2015 |volume=2015 |issue=10 |pages=CD006171 |doi=10.1002/14651858.CD006171.pub4 |pmid=26493047 |pmc=9272404 }}</ref> However educating parents before the baby is born has been suggested to be effective because it may improve food, personal and pet hygiene.<ref name=Di2015/> More research is needed to find whether antenatal education can reduce congenital toxoplasmosis.<ref name=Di2015/>

For pregnant women with negative antibody titers, indicating no previous exposure to ''T.&nbsp;gondii'', serology testing as frequent as monthly is advisable as treatment during pregnancy for those women exposed to ''T.&nbsp;gondii'' for the first time dramatically decreases the risk of passing the parasite to the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with antiprotozoans, an infection can be very serious in the young.{{citation needed|date=January 2021}}

Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries, for reasons of cost-effectiveness and the high number of [[false positives]] generated; [[Portugal]],<ref name=Circular_DGS>{{cite web|url=http://www.srsdocs.com/parcerias/normas/circulares/dgs/2006/cuidados_pre_concepcionais.pdf |title=Circular Normativa sobre Cuidados Pré-Concepcionais – Direcção-Geral de Saúde |url-status=dead |archive-url=https://web.archive.org/web/20110716124341/http://www.srsdocs.com/parcerias/normas/circulares/dgs/2006/cuidados_pre_concepcionais.pdf |archive-date=2011-07-16 }}</ref> [[France]],<ref name=Sukthana_2006>{{cite journal | author = Sukthana Y | title = Toxoplasmosis: beyond animals to humans | journal = Trends in Parasitology | volume = 22 | issue = 3 | pages = 137–42 | date = March 2006 | pmid = 16446116 | doi = 10.1016/j.pt.2006.01.007 }}</ref> [[Austria]],<ref name=Sukthana_2006 /> [[Uruguay]],<ref name="elpais">[http://participacion.elpais.com.uy/lasalud/2008/05/20/los-gatos-domesticos-transmiten-toxoplasmosis/] {{webarchive|url=https://web.archive.org/web/20110824023934/http://participacion.elpais.com.uy/lasalud/2008/05/20/los-gatos-domesticos-transmiten-toxoplasmosis/|date=August 24, 2011}}</ref> and [[Italy]]<ref name="Paschale_2008">{{cite journal |vauthors=De Paschale M, Agrappi C, Clerici P, Mirri P, Manco MT, Cavallari S, Viganò EF | title = Seroprevalence and incidence of ''Toxoplasma gondii'' infection in the Legnano area of Italy | journal = Clinical Microbiology and Infection | volume = 14 | issue = 2 | pages = 186–9 | year = 2008 | pmid = 18034857 | doi = 10.1111/j.1469-0691.2007.01883.x | doi-access = free }}</ref> are notable exceptions, and some regional screening programmes operate in [[Germany]], [[Switzerland]] and [[Belgium]].<ref name=Paschale_2008/> As invasive [[prenatal]] testing incurs some risk to the [[fetus]] (18.5 pregnancy losses per toxoplasmosis case prevented),<ref name=Sukthana_2006/> [[postnatal]] or [[neonatal]] screening is preferred. The exceptions are cases where [[fetal]] abnormalities are noted, and thus screening can be targeted.<ref name=Sukthana_2006/>

Pregnant women should avoid handling [[raw meat]], drinking [[raw milk]] (especially goat milk) and be advised to not eat raw or undercooked meat regardless of type.<ref name="Kapperud_1996">{{cite journal |first1 = Georg|last1 = Kapperud|first2 = Pal A.|last2 = Jenum|first3 = Babill|last3 = Stray-Pedersen|first4 = Kjetil K.|last4 = Melby|first5 = Anne|last5 = Eskild|first6 = Jan|last6 = Eng | title = Risk factors for ''Toxoplasma gondii'' infection in pregnancy. Results of a prospective case-control study in Norway | journal = American Journal of Epidemiology | volume = 144 | issue = 4 | pages = 405–412 | year = 1996 | pmid = 8712198 | doi = 10.1093/oxfordjournals.aje.a008942 |doi-access = free}}</ref> Because of the obvious relationship between ''Toxoplasma'' and cats it is also often advised to avoid exposure to cat feces, and refrain from gardening (cat feces are common in garden soil) or at least wear gloves when so engaged.<ref name="Kapperud_1996"/> Most cats are not actively shedding [[oocyst]]s, since they get infected in the first six months of their life, when they shed oocysts for a short period of time (1–2 weeks).<ref name="Hill_2002">{{cite journal |vauthors=Hill D, Dubey JP | title = ''Toxoplasma gondii'': transmission, diagnosis and prevention | journal = Clinical Microbiology and Infection | volume = 8 | issue = 10 | pages = 634–40 | year = 2002 | pmid = 12390281 | doi = 10.1046/j.1469-0691.2002.00485.x | doi-access = free }}</ref> However, these oocysts get buried in the soil, sporulate and remain infectious for periods ranging from several months to more than a year.<ref name="Kapperud_1996"/> Numerous studies have shown living in a household with a cat is not a significant risk factor for ''T.&nbsp;gondii'' infection,<ref name="Kapperud_1996"/><ref name=Cook_2000>{{cite journal |vauthors=Cook AJ, Gilbert RE, Buffolano W, Zufferey J, Petersen E, Jenum PA, Foulon W, Semprini AE, Dunn DT | title = Sources of toxoplasma infection in pregnant women: European multicentre case-control study. European Research Network on Congenital Toxoplasmosis | journal = BMJ | volume = 321 | issue = 7254 | pages = 142–7 | date = Jul 15, 2000 | pmid = 10894691 | pmc = 27431 | doi = 10.1136/bmj.321.7254.142 }}</ref><ref name=Bobic1998>{{cite journal |vauthors=Bobić B, Jevremović I, Marinković J, Sibalić D, Djurković-Djaković O | title = Risk factors for ''Toxoplasma'' infection in a reproductive age female population in the area of Belgrade, Yugoslavia | journal = European Journal of Epidemiology | volume = 14 | issue = 6 | pages = 605–10 | date = September 1998 | pmid = 9794128 | doi = 10.1023/A:1007461225944 | s2cid = 9423818 }}</ref> though living with several kittens has some significance.<ref>{{cite journal |vauthors=Jones JL, Dargelas V, Roberts J, Press C, Remington JS, Montoya JG | title = Risk Factors forToxoplasma gondiiInfection in the United States | journal = Clinical Infectious Diseases | volume = 49 | issue = 6 | pages = 878–884 | year = 2009 | pmid = 19663709 | doi = 10.1086/605433 | doi-access = free }}</ref>

In 2006, a Czech research team<ref name="pmid17028886">{{cite journal |vauthors=Kanková S, Sulc J, Nouzová K, Fajfrlík K, Frynta D, Flegr J | title = Women infected with parasite ''Toxoplasma'' have more sons | journal = Die Naturwissenschaften | volume = 94 | issue = 2 | pages = 122–7 | year = 2007 | pmid = 17028886 | doi = 10.1007/s00114-006-0166-2 | bibcode = 2007NW.....94..122K | s2cid = 9610443 }}</ref> discovered women with high levels of toxoplasmosis antibodies were significantly more likely to give birth to baby boys than baby girls. In most populations, the birth rate is around 51% boys, but people infected with ''T.&nbsp;gondii'' had up to a 72% chance of a boy.<ref>{{cite news |last1=Sample |first1=Ian |title=Pregnant women infected by cat parasite more likely to give birth to boys, say researchers |url=https://www.theguardian.com/science/2006/oct/12/uk.health |work=The Guardian |date=12 October 2006 }}</ref>

==Diagnosis==

[[File:BrainToxoplasmosis MRI 2 09.png|thumb|MRI: Cerebral toxoplasmosis with primary involvement in the right occipital lobe (at left and below of the image). 48-year-old woman with [[AIDS]]]]
<!-- uncited, explain RhD Quite contrary to a low percentages of humans who manifest excesses in extracellular dopamine levels and are thus vulnerable to ''T. gondii'' that elevates dopamine levels in the brain, others, with some common genetic mutations can benefit from ''T. gondii''. This excludes RhD negative blood typed humans who do not have the genotypes that will be discussed in the following paragraphs.-->
Toxoplasmosis in humans is diagnosed through biological, serological, histological, or molecular methods, or by some combination of the above.<ref name="Hill_2002"/> Toxoplasmosis can be difficult to distinguish from [[primary central nervous system lymphoma]]. Its symptoms mimic several other infectious diseases, so clinical signs are non-specific and are not sufficiently characteristic for a definite diagnosis. A failed trial of antimicrobial therapy ([[pyrimethamine]], [[sulfadiazine]], and [[folinic acid]] ([[United States Adopted Name|USAN]]: leucovorin)), makes an alternative diagnosis more likely.{{cn|date=January 2023}}

''T. gondii'' may also be detected in [[blood]], [[amniotic fluid]], or [[cerebrospinal fluid]] by using [[polymerase chain reaction]].<ref name="SwitajEtc2005">{{cite journal |vauthors=Switaj K, Master A, Skrzypczak M, Zaborowski P |title=Recent trends in molecular diagnostics for ''Toxoplasma gondii'' infections |journal=Clinical Microbiology and Infection |volume=11 |issue=3 |pages=170–6 |year=2005 |pmid=15715713 |doi=10.1111/j.1469-0691.2004.01073.x |doi-access=free }}</ref> ''T.&nbsp;gondii'' may exist in a host as an inactive cyst that would likely evade detection.{{citation needed|date=January 2021}}

[[Serology|Serological]] testing can detect ''T.&nbsp;gondii'' antibodies in blood serum, using methods including the [[Sabin–Feldman dye test]] (DT), the indirect [[hemagglutination assay]], the [[Indirect fluorescent antibody|indirect fluorescent antibody assay (IFA)]], the [[direct agglutination test]], the [[latex agglutination test]] (LAT), the [[ELISA|enzyme-linked immunosorbent assay (ELISA)]], and the immunosorbent agglutination assay test (IAAT).<ref name="Hill_2002"/>

<!--sections of "IgG antibody" are taken directly from the 2002 Montoya paper-->
The most commonly used tests to measure [[IgG]] antibody are the DT, the ELISA, the IFA, and the modified direct agglutination test.<ref name="Montoya_2002">{{cite journal | author = Montoya JG | title = Laboratory diagnosis of ''Toxoplasma gondii'' infection and toxoplasmosis | journal = The Journal of Infectious Diseases | volume = 185 | issue = Suppl 1 | pages = S73–82 | year = 2002 | pmid = 11865443 | doi = 10.1086/338827 | doi-access = free }}</ref> IgG antibodies usually appear within a week or two of infection, peak within one to two months, then decline at various rates.<ref name="Montoya_2002"/> ''Toxoplasma'' IgG antibodies generally persist for life, and therefore may be present in the bloodstream as a result of either current or previous infection.<ref name="JonesPariseFiore2014">{{cite journal | vauthors = Jones JL, Parise ME, Fiore AE | title = Neglected parasitic infections in the United States: toxoplasmosis | journal = American Journal of Tropical Medicine and Hygiene | volume = 90 | issue = 5 | pages = 794–9 | year = 2014 | pmid = 24808246 | pmc = 4015566 | doi = 10.4269/ajtmh.13-0722 }}</ref>

To some extent, acute toxoplasmosis infections can be differentiated from chronic infections using an IgG [[avidity]] test, which is a variation on the ELISA. In the first response to infection, toxoplasma-specific IgG has a low affinity for the toxoplasma antigen; in the following weeks and month, IgG affinity for the antigen increases. Based on the IgG avidity test, if the IgG in the infected individual has a high affinity, it means that the infection began three to five months before testing. This is particularly useful in congenital infection, where pregnancy status and gestational age at time of infection determines treatment.<ref name="RemingtonThulliez2004">{{cite journal |last1=Remington |first1=Jack S. |last2=Thulliez |first2=Philippe |last3=Montoya |first3=Jose G. |title=Recent Developments for Diagnosis of Toxoplasmosis |journal=Journal of Clinical Microbiology |date=March 2004 |volume=42 |issue=3 |pages=941–945 |doi=10.1128/JCM.42.3.941-945.2004 |pmid=15004036 |pmc=356902 }}</ref>

<!--sections of "IgM antibody" are taken directly from the 2002 Montoya paper-->
In contrast to IgG, IgM antibodies can be used to detect acute infection but generally not chronic infection.<ref name="JonesPariseFiore2014"/> The IgM antibodies appear sooner after infection than the IgG antibodies and disappear faster than IgG antibodies after recovery.<ref name="Hill_2002"/> In most cases, ''T.&nbsp;gondii''-specific IgM antibodies can first be detected approximately a week after acquiring primary infection and decrease within one to six months; 25% of those infected are negative for ''T.&nbsp;gondii''-specific IgM within seven months.<ref name="JonesPariseFiore2014"/> However, IgM may be detectable months or years after infection, during the chronic phase, and false positives for acute infection are possible.<ref name="Montoya_2002"/>  The most commonly used tests for the measurement of IgM antibody are [[ELISA#Sandwich ELISA|double-sandwich IgM-ELISA]], the [[Indirect fluorescent antibody technique|IFA test]], and the immunosorbent agglutination assay (IgM-ISAGA). Commercial test kits often have low specificity, and the reported results are frequently misinterpreted.<ref name="Montoya_2002"/>

<!--This section is adapted from the 2021 systematic review paper-->
In 2021, twenty commercial anti-''Toxoplasma'' IgG assays were evaluated in a [[systematic review]], in comparison with an accepted reference method.<ref name="Robert-GangneuxGuegan2021"/> Most of them were enzyme-immunoassays, followed by agglutination tests, immunochromatographic tests, and a [[Western-Blot]] assay. The mean sensitivity of IgG assays ranged from 89.7% to 100% for standard titers and from 13.4% to 99.2% for low IgG titers. A few studies pointed out the ability of some methods, especially WB to detect IgG early after primary infection. The specificity of IgG assays was generally high, ranging from 91.3% to 100%; and higher than 99% for most EIA assays. The [[positive and negative predictive values|positive predictive value]] (PPV) was not a discriminant indicator among methods, whereas significant disparities (87.5–100%) were reported among negative predictive values (NPV), a key-parameter assessing the ability to definitively rule out a ''Toxoplasma'' infection in patients at-risk for opportunistic infections.<ref name="Robert-GangneuxGuegan2021">{{cite journal|last1=Robert-Gangneux|first1=Florence|last2=Guegan|first2=Hélène|title=Anti-''Toxoplasma'' IgG assays: What performances for what purpose? A systematic review|journal=Parasite|volume=28|year=2021|pages=39|doi=10.1051/parasite/2021035|pmid=33904818|pmc=8078101|doi-access=free}} {{openaccess}}</ref>

===Congenital===
[[File:Toxoplasmosis, Congenital.jpg|thumb|Child with congenital toxoplasmosis]]
Recommendations for the diagnosis of congenital toxoplasmosis include: prenatal diagnosis based on [[Amniocentesis|testing]] of [[amniotic fluid]] and [[ultrasound]] examinations; neonatal diagnosis based on molecular testing of placenta and [[cord blood]] and comparative mother-child serologic tests and a clinical examination at birth; and early childhood diagnosis based on [[neurologic]] and [[ophthalmologic]] examinations and a serologic survey during the first year of life.<ref name="Sterkers_2011"/> During pregnancy, serological testing is recommended at three week intervals.<ref name="Sensini2006">{{cite journal |last1=Sensini |first1=A. |title=Toxoplasma gondii infection in pregnancy: opportunities and pitfalls of serological diagnosis |journal=Clinical Microbiology and Infection |date=June 2006 |volume=12 |issue=6 |pages=504–512 |doi=10.1111/j.1469-0691.2006.01444.x |pmid=16700697 |doi-access=free }}</ref>

Even though diagnosis of toxoplasmosis heavily relies on serological detection of specific anti-''Toxoplasma'' immunoglobulin, serological testing has limitations. For example, it may fail to detect the active phase of ''T.&nbsp;gondii'' infection because the specific anti-''Toxoplasma'' [[Immunoglobulin G|IgG]] or [[Immunoglobulin M|IgM]] may not be produced until after several weeks of infection. As a result, a pregnant woman might test negative during the active phase of ''T.&nbsp;gondii'' infection leading to undetected and therefore untreated congenital toxoplasmosis.<ref name="Lin_2000">{{cite journal |vauthors=Lin MH, Chen TC, Kuo TT, Tseng CC, Tseng CP | title = Real-time PCR for quantitative detection of ''Toxoplasma gondii'' | journal = Journal of Clinical Microbiology | volume = 38 | issue = 11 | pages = 4121–5 | year = 2000 | pmid = 11060078 | pmc = 87551 | doi = 10.1128/JCM.38.11.4121-4125.2000}}</ref> Also, the test may not detect ''T.&nbsp;gondii'' infections in immunocompromised patients because the titers of specific anti-''Toxoplasma'' IgG or IgM may not rise in this type of patient.{{citation needed|date=January 2021}}

Many PCR-based techniques have been developed to diagnose toxoplasmosis using clinical specimens that include amniotic fluid, [[blood]], [[cerebrospinal fluid]], and [[tissue biopsy]]. The most sensitive PCR-based technique is [[nested PCR]], followed by hybridization of PCR products.<ref name="Lin_2000"/> The major downside to these techniques is that they are time-consuming and do not provide quantitative data.<ref name="Lin_2000"/>

Real-time PCR is useful in pathogen detection, gene expression and regulation, and allelic discrimination. This PCR technique utilizes the 5' nuclease activity of ''Taq'' DNA polymerase to cleave a nonextendible, fluorescence-labeled hybridization probe during the extension phase of PCR.<ref name="Lin_2000"/> A second fluorescent dye, e.g., 6-carboxy-tetramethyl-rhodamine, quenches the fluorescence of the intact probe.<ref name="Lin_2000"/> The nuclease cleavage of the hybridization probe during the PCR releases the effect of quenching resulting in an increase of fluorescence proportional to the amount of PCR product, which can be monitored by a sequence detector.<ref name="Lin_2000"/>

Lymph nodes affected by ''Toxoplasma'' have characteristic changes, including poorly demarcated reactive [[germinal centers]], clusters of monocytoid B cells, and scattered epithelioid [[histiocyte]]s.{{cn|date=January 2023}}

The classic triad of congenital toxoplasmosis includes: [[chorioretinitis]], [[hydrocephalus]], and [[intracranial arteriosclerosis]].<ref>{{cite journal|last1=Jones|first1=J|last2=Lopez|first2=A|last3=Wilson|first3=M|title=Congenital toxoplasmosis|journal=American Family Physician|date=15 May 2003|volume=67|issue=10|pages=2131–8|pmid=12776962}}</ref> Other consequences include sensorineural deafness, seizures, and intellectual disability.<ref>{{MedlinePlusEncyclopedia|001360|Congenital toxoplasmosis}}</ref>

Congenital toxoplasmosis may also impact a child's hearing. Up to 30% of newborns have some degree of sensorineural hearing loss.<ref>{{cite journal |last1=Corrêa |first1=Camila |last2=Maximino |first2=Luciana |last3=Weber |first3=Silke |title=Hearing Disorders in Congenital Toxoplasmosis: A Literature Review |journal=International Archives of Otorhinolaryngology |date=7 August 2017 |volume=22 |issue=3 |pages=330–333 |doi=10.1055/s-0037-1605377 |pmc=6033603 |pmid=29983776 }}</ref> The child's communication skills may also be affected. A study published in 2010 looked at 106 patients, all of whom received toxoplasmosis treatment prior to 2.5 months. Of this group, 26.4% presented with language disorders.<ref>{{cite journal |last1=De Resende |first1=Luciana Macedo |last2=Andrade |first2=Gláucia Queiroz Manzan de |last3=Azevedo |first3=Marisa Frasson de |last4=Perissinoto |first4=Jacy |last5=Vieira |first5=Andrêza Batista Cheloni |title=Congenital toxoplasmosis: Auditory and language outcomes in early diagnosed and treated children |journal=Scientia Medica |date=16 April 2010 |volume=20 |issue=1 |pages=13 |doi=10.15448/1980-6108.2010.1.5927 |doi-broken-date=1 November 2024 |url=https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5927 }}</ref>

== Treatment ==
Treatment is recommended for people with serious health problems, such as people with [[HIV]] whose [[CD4]] counts are under 200 cells/mm<sup>3</sup>. [[Trimethoprim/sulfamethoxazole]] is the drug of choice to prevent toxoplasmosis, but not for treating active disease.
A 2012 study shows a promising new way to treat the active and latent form of this disease using two [[ELQ-300|endochin-like quinolones]].<ref name="Doggett_2012">{{cite journal |vauthors=Doggett JS, Nilsen A, Forquer I, Wegmann KW, Jones-Brando L, Yolken RH, Bordón C, Charman SA, Katneni K, Schultz T, Burrows JN, Hinrichs DJ, Meunier B, Carruthers VB, Riscoe MK | title = Endochin-like quinolones are highly efficacious against acute and latent experimental toxoplasmosis | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 39 | pages = 15936–41 | year = 2012 | pmid = 23019377 | pmc = 3465437 | doi = 10.1073/pnas.1208069109 | bibcode = 2012PNAS..10915936D | doi-access = free }}</ref>

===Acute===
The medications prescribed for acute toxoplasmosis are the following:{{cn|date=January 2023}}
* [[Pyrimethamine]] – an [[antimalarial medication]]
* [[Sulfadiazine]] – an [[antibiotic]] used in combination with pyrimethamine to treat toxoplasmosis
** Combination therapy is usually given with folic acid supplements to reduce incidence of [[thrombocytopaenia]].
** Combination therapy is most useful in the setting of HIV.
* [[Clindamycin]]<ref>{{cite journal |vauthors=Rolston KV, Hoy J |title = Role of clindamycin in the treatment of central nervous system toxoplasmosis | journal = American Journal of Medicine | volume = 83 |issue = 3 | pages = 551–554 | year = 1987 | pmid = 3661590 | doi=10.1016/0002-9343(87)90769-8}}</ref>
* [[Spiramycin]] – an antibiotic used most often for pregnant women to prevent the infection of their children.

(other antibiotics, such as [[minocycline]], have seen some use as a [[salvage therapy]]).

If infected during pregnancy, spiramycin is recommended in the first and early second trimesters while pyrimethamine/sulfadiazine and [[leucovorin]] is recommended in the late second and third trimesters.<ref>{{cite web|title=CDC – Toxoplasmosis – Resources for Health Professionals|url=https://www.cdc.gov/parasites/toxoplasmosis/health_professionals/index.html#tx|website=www.cdc.gov|access-date=5 December 2016|url-status=live|archive-url=https://web.archive.org/web/20161126092819/http://www.cdc.gov/parasites/toxoplasmosis/health_professionals/index.html#tx|archive-date=26 November 2016}}</ref>

===Latent===
In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not reach the [[bradyzoite]]s in sufficient concentration.

The medications prescribed for latent toxoplasmosis are:
* [[Atovaquone]] – an antibiotic that has been used to kill ''Toxoplasma'' cysts inside [[AIDS]] patients<ref>{{cite web|title=Toxoplasmosis – treatment key research |url=http://www.aidsmap.com/cms1032641.asp |archive-url=https://archive.today/20071022085155/http://www.aidsmap.com/cms1032641.asp |url-status=dead |archive-date=2007-10-22 |date=2005-11-02 |publisher=NAM & aidsmap }}</ref>
* [[Clindamycin]] – an antibiotic that, in combination with [[atovaquone]], seemed to optimally kill cysts in mice<ref>{{cite journal | vauthors = Djurković-Djaković O, Milenković V, Nikolić A, Bobić B, Grujić J | title = Efficacy of atovaquone combined with clindamycin against murine infection with a cystogenic (Me<sub>49</sub>) strain of ''Toxoplasma gondii'' | journal = Journal of Antimicrobial Chemotherapy | volume = 50 | issue = 6 | pages = 981–7 | year = 2002 | pmid = 12461021 | doi = 10.1093/jac/dkf251 | doi-access = free }}</ref>

===Congenital===
When a pregnant woman is diagnosed with acute toxoplasmosis, amniocentesis can be used to determine whether the fetus has been infected or not. When a pregnant woman develops acute toxoplasmosis, the [[tachyzoites]] have approximately a 30% chance of entering the placental tissue, and from there entering and infecting the fetus. As gestational age at the time of infection increases, the chance of fetal infection also increases.<ref name="Robert-GangneuxDarde2012">{{cite journal |last1=Robert-Gangneux |first1=Florence |last2=Dardé |first2=Marie-Laure |title=Epidemiology of and Diagnostic Strategies for Toxoplasmosis |journal=Clinical Microbiology Reviews |date=April 2012 |volume=25 |issue=2 |pages=264–296 |doi=10.1128/CMR.05013-11 |pmid=22491772 |pmc=3346298 }}</ref>

If the parasite has not yet reached the fetus, [[spiramycin]] can help to prevent placental transmission. If the fetus has been infected, the pregnant woman can be treated with [[pyrimethamine]] and [[sulfadiazine]], with [[folinic acid]], after the first trimester. They are treated after the first trimester because pyrimethamine has an antifolate effect, and lack of folic acid can interfere with [[Neural tube defect|fetal brain formation]] and cause [[thrombocytopaenia]].<ref name="JonesLopez2003">{{cite journal |vauthors=Jones J, Lopez A, Wilson M |title=Congenital toxoplasmosis |journal=American Family Physician |volume=67 |issue=10 |pages=2131–8 |year=2003 |pmid=12776962 }}</ref> Infection in earlier gestational stages correlates with poorer fetal and neonatal outcomes, particularly when the infection is untreated.<ref name=McLeod2009>{{cite journal |vauthors=McLeod R, Kieffer F, Sautter M, Hosten T, Pelloux H |title=Why prevent, diagnose and treat congenital toxoplasmosis? |journal=Memórias do Instituto Oswaldo Cruz |volume=104 |issue=2 |pages=320–44 |year=2009 |pmid=19430661 |pmc=2735102 |doi= 10.1590/s0074-02762009000200029}}</ref>

Newborns who undergo 12 months of postnatal anti-toxoplasmosis treatment have a low chance of sensorineural hearing loss.<ref>{{Cite journal|vauthors=McLeod R, Boyer K, Karrison T, Kasza K, Swisher C, Roizen N, Jalbrzikowski J, Remington J, Heydemann P, Noble AG, Mets M, Holfels E, Withers S, Latkany P, Meier P|collaboration=Toxoplasmosis Study Group|date=15 May 2006|title=Outcome of Treatment for Congenital Toxoplasmosis, 1981–2004: The National Collaborative Chicago-Based, Congenital Toxoplasmosis Study|journal=Clinical Infectious Diseases|volume=42|issue=10|pages=1383–1394|doi=10.1086/501360|pmid=16619149|doi-access=free}}</ref> Information regarding treatment milestones for children with congenital toxoplasmosis have been created for this group.<ref>{{cite web |title=Congenital Toxoplasmosis |website=Baby's First Test |url=https://www.babysfirsttest.org/newborn-screening/conditions/congenital-toxoplasmosis |access-date=2 April 2020}}</ref>

== Epidemiology ==
''T. gondii'' infections occur throughout the world, although infection rates differ significantly by country.<ref name="Pappas_2009">{{cite journal |vauthors=Pappas G, Roussos N, Falagas ME | title = Toxoplasmosis snapshots: global status of ''Toxoplasma gondii'' seroprevalence and implications for pregnancy and congenital toxoplasmosis | journal = International Journal for Parasitology | volume = 39 | issue = 12 | pages = 1385–94 | date = October 2009 | pmid = 19433092 | doi = 10.1016/j.ijpara.2009.04.003 }}</ref> For women of childbearing age, a survey of 99 studies within 44 countries found the areas of highest prevalence are within [[Latin America]] (about 50–80%), parts of [[Eastern Europe|Eastern]] and [[Central Europe]] (about 20–60%), the [[Middle East]] (about 30–50%), parts of [[Southeast Asia]] (about 20–60%), and parts of [[Africa]] (about 20–55%).<ref name="Pappas_2009" />

In the United States, data from the [[National Health and Nutrition Examination Survey]] (NHANES) from 1999 to 2004 found 9.0% of US-born persons 12–49 years of age were [[seropositive]] for [[IgG]] [[antibodies]] against ''T.&nbsp;gondii'', down from 14.1% as measured in the NHANES 1988–1994.<ref name="Jones_2007">{{cite journal |vauthors=Jones JL, Kruszon-Moran D, Sanders-Lewis K, Wilson M | title = ''Toxoplasma gondii'' infection in the United States, 1999 2004, decline from the prior decade | journal = American Journal of Tropical Medicine and Hygiene | volume = 77 | issue = 3 | pages = 405–10 | date = September 2007 | pmid = 17827351 | doi = 10.4269/ajtmh.2007.77.405 | doi-access = free }}</ref> In the 1999–2004 survey, 7.7% of US-born and 28.1% of foreign-born women 15–44 years of age were ''T.&nbsp;gondii'' seropositive.<ref name="Jones_2007" /> A trend of decreasing [[seroprevalence]] has been observed by numerous studies in the United States and many European countries.<ref name="Pappas_2009" /> ''Toxoplasma gondii'' is considered the second leading cause of [[Foodborne illness|foodborne]]-related deaths and the fourth leading cause of foodborne-related hospitalizations in the United States.<ref name="Scallan">{{cite journal|last1=Scallan|first1=Elaine|last2=Hoekstra|first2=Robert|last3=Angulo|first3=Frederick|last4=Tauxe|first4=Robert|last5=Widdowson|first5=Marc-Alain|last6=Roy|first6=Sharon|last7=Jones|first7=Jeffery|last8=Griffin|first8=Patricia|title=Foodborne Illness Acquired in the United States - Major Pathogens|journal=Emerging Infectious Diseases|date=January 2011|volume=17|issue=1|pages=7–15|doi=10.3201/eid1701.P11101|pmid=21192848|pmc=3375761}}</ref>

The protist responsible for toxoplasmosis is ''T.&nbsp;gondii''. Three major types of ''T.&nbsp;gondii'' are responsible for the patterns of toxoplasmosis throughout the world, named types I, II, and III. These three types of ''T.&nbsp;gondii'' have differing effects on certain hosts, mainly mice and humans due to their variation in genotypes.<ref name="Dalimi">{{cite journal |last1=Dalimi |first1=A. |last2=Abdoli |first2=A. |title=Latent toxoplasmosis and human |journal=Iranian Journal of Parasitology |date=2012 |volume=7 |issue=1 |pages=1–17 |pmid=23133466 |pmc=3488815 }}</ref>
* Type I: virulent in mice and humans, seen in [[people with AIDS]].
* Type II: non-virulent in mice, virulent in humans (mostly Europe and North America), seen in people with AIDS.
* Type III: non-virulent in mice, virulent mainly in animals but seen to a lesser degree in humans as well.

Current [[serotyping]] techniques can only separate type I or III from type II parasites.<ref name=Sibley2009>{{cite journal|author1=Sibley LD|author2=Khan A|author3=Ajioka JW|author4=Rosenthal BM|title=Genetic diversity of ''Toxoplasma gondii'' in animals and humans|journal=Philosophical Transactions of the Royal Society B: Biological Sciences|date=2009|volume=364|issue=1530|pages=2749–2761|doi=10.1098/rstb.2009.0087|pmid=19687043|pmc=2865090}}</ref>

Because the parasite poses a particular threat to fetuses when it is contracted during pregnancy,<ref name=CDCPregnant>{{cite web|title=CDC: Parasites – Toxoplasmosis (Toxoplasma infection) – Pregnant Women|url=https://www.cdc.gov/parasites/toxoplasmosis/gen_info/pregnant.html|access-date=13 March 2013|url-status=live|archive-url=https://web.archive.org/web/20130307191447/http://www.cdc.gov/parasites/toxoplasmosis/gen_info/pregnant.html|archive-date=7 March 2013}}</ref> much of the global [[epidemiological]] data regarding ''T.&nbsp;gondii'' comes from seropositivity tests in women of childbearing age. Seropositivity tests look for the presence of antibodies against ''T.&nbsp;gondii'' in blood, so while seropositivity guarantees one has been exposed to the parasite, it does not necessarily guarantee one is chronically infected.<ref name=Dubey_1998_Rats>{{cite journal |vauthors=Dubey JP, Frenkel JK | title = Toxoplasmosis of rats: a review, with considerations of their value as an animal model and their possible role in epidemiology | journal = Veterinary Parasitology | volume = 77 | issue = 1 | pages = 1–32 | date = May 1998 | pmid = 9652380 | doi = 10.1016/S0304-4017(97)00227-6 | url = https://zenodo.org/record/1260015 }}</ref>

== History ==
''[[Toxoplasma gondii]]'' was first described in 1908 by Nicolle and Manceaux in Tunisia, and independently by Splendore in Brazil.<ref name=Ferguson_2009/> Splendore reported the [[protozoan]] in a rabbit, while Nicolle and Manceaux identified it in a North African rodent, the gundi ([[Ctenodactylus gundi]]).<ref name=Weiss_Dubey_2009 /> In 1909 Nicolle and Manceaux differentiated the protozoan from ''[[Leishmania]]''.<ref name=Ferguson_2009 /> Nicolle and Manceaux then named it ''Toxoplasma gondii'' after the curved shape of its infectious stage (Greek root {{lang|grc-Latn|toxon}} = bow).<ref name=Ferguson_2009 />

The first recorded case of congenital toxoplasmosis was in 1923, but it was not identified as caused by ''T.&nbsp;gondii''.<ref name=Weiss_Dubey_2009>{{cite journal|vauthors=Weiss LM, Dubey JP|title=Toxoplasmosis: A history of clinical observations|journal=International Journal for Parasitology|volume=39|issue=8|pages=895–901|year=2009|pmid=19217908|pmc=2704023|doi= 10.1016/j.ijpara.2009.02.004}}</ref> Janků (1923) described in detail the autopsy results of an 11-month-old boy who had presented to hospital with [[hydrocephalus]]. The boy had classic marks of toxoplasmosis including [[chorioretinitis]] (inflammation of the choroid and retina of the eye).<ref name=Weiss_Dubey_2009 /> Histology revealed a number of "sporocytes", though Janků did not identify these as ''T.&nbsp;gondii''.<ref name=Weiss_Dubey_2009 />

It was not until 1937 that the first detailed scientific analysis of ''T.&nbsp;gondii'' took place using techniques previously developed for analyzing viruses.<ref name=Ferguson_2009 /> In 1937 Sabin and Olitsky analyzed ''T.&nbsp;gondii'' in laboratory monkeys and mice. Sabin and Olitsky showed that ''T.&nbsp;gondii'' was an obligate intracellular parasite and that mice fed ''T.&nbsp;gondii''-contaminated tissue also contracted the infection.<ref name=Ferguson_2009 /> Thus Sabin and Olitsky demonstrated ''T.&nbsp;gondii'' as a [[pathogen]] transmissible between animals.{{cn|date=January 2023}}

''T. gondii'' was first described as a human pathogen in 1939 at [[Babies Hospital]] in [[New York City]].<ref name=Ferguson_2009 /><ref>{{cite book|title=The Lion In the Living Room: How House Cats Tamed Us And Took Over the World|first=Abigail |last=Tucker |date=2016|isbn=978-1-4767-3823-9|publisher=Simon & Schuster|page=108}}</ref> Wolf, Cowen and Paige identified ''T.&nbsp;gondii'' infection in an infant girl delivered full-term by [[Caesarean]] section.<ref name=Weiss_Dubey_2009 /> The infant developed seizures and had chorioretinitis in both eyes at three days. The infant then developed encephalomyelitis and died at one month of age. Wolf, Cowen and Paige isolated ''T.&nbsp;gondii'' from brain tissue lesions. Intracranial injection of brain and spinal cord samples into mice, rabbits and rats produced encephalitis in the animals.<ref name=Ferguson_2009 /> Wolf, Cowen and Page reviewed additional cases and concluded that ''T.&nbsp;gondii'' produced recognizable symptoms and could be transmitted from mother to child.<ref name=Weiss_Dubey_2009 />

The first adult case of toxoplasmosis was reported in 1940 with no neurological signs. Pinkerton and Weinman reported the presence of ''Toxoplasma'' in a 22-year-old man from Peru who died from a subsequent bacterial infection and fever.<ref name=Weiss_Dubey_2009 />

In 1948, a serological dye test was created by Sabin and Feldman based on the ability of the patient's antibodies to alter staining of ''Toxoplasma''.<ref name=Ferguson_2009 /><ref>{{cite web|url=http://www.pamf.org/serology/clinicianguide.html#toxosero|title=Laboratory Tests For The Diagnosis Of Toxoplasmosis|publisher=Toxoplasma Serology Laboratory|url-status=live|archive-url=https://web.archive.org/web/20071223225426/http://www.pamf.org/serology/clinicianguide.html#toxosero|archive-date=2007-12-23}}</ref> The Sabin Feldman Dye Test is now the gold standard for identifying ''Toxoplasma'' infection.<ref name=Ferguson_2009 />

Transmission of ''Toxoplasma'' by eating raw or undercooked meat was demonstrated by Desmonts et al. in 1965 Paris.<ref name=Ferguson_2009 /> Desmonts observed that the therapeutic consumption of raw beef or horse meat in a [[tuberculosis]] hospital was associated with a 50% per year increase in ''Toxoplasma'' antibodies.<ref name=Ferguson_2009 /> This means that more ''T.&nbsp;gondii'' was being transmitted through the raw meat.

In 1974, Desmonts and Couvreur showed that infection during the first two trimesters produces most harm to the fetus, that transmission depended on when mothers were infected during pregnancy, that mothers with antibodies before pregnancy did not transmit the infection to the fetus, and that [[spiramycin]] lowered the transmission to the fetus.<ref name=Weiss_Dubey_2009 />

''Toxoplasma'' gained more attention in the 1970s with the rise of immune-suppressant treatment given after organ or bone marrow transplants and the [[AIDS]] epidemic of the 1980s.<ref name=Ferguson_2009 /> Patients with lowered immune system function are much more susceptible to disease.

==Society and culture==

=== "Crazy cat-lady" ===
"Crazy cat-lady syndrome" is a term coined by news organizations to describe scientific findings that link the parasite ''[[Toxoplasma gondii]]'' to several [[mental disorders]] and behavioral problems.<ref name=KMcAuliff_Atlantic>{{cite magazine |url=https://www.theatlantic.com/magazine/archive/2012/03/how-your-cat-is-making-you-crazy/308873/ |title=How Your Cat Is Making You Crazy – Kathleen McAuliffe |magazine=The Atlantic |date=2012-02-06 |access-date=2013-06-03 |url-status=live |archive-url=https://web.archive.org/web/20130603010600/http://www.theatlantic.com/magazine/archive/2012/03/how-your-cat-is-making-you-crazy/308873/ |archive-date=2013-06-03 }}</ref><ref name=RSkloot_NYT>{{cite news|url=https://www.nytimes.com/2007/12/09/magazine/09_10_catcoat.html|title='Cat Lady' Conundrum – Rebecca Skloot|newspaper=The New York Times|date=2007-12-09|url-status=live|archive-url=https://web.archive.org/web/20170118000720/http://www.nytimes.com/2007/12/09/magazine/09_10_catcoat.html|archive-date=2017-01-18}}</ref> The suspected correlation between cat ownership in childhood and later development of [[schizophrenia]] suggested that further studies were needed to determine a risk factor for children;<ref>{{Cite journal|title = Is childhood cat ownership a risk factor for schizophrenia later in life?|last1 = Torrey|first1 = E.|date = June 2015|journal = Schizophrenia Research| volume = 165| issue = 1|doi = 10.1016/j.schres.2015.03.036|pmid = 25892720|last2 = Simmons|first2 = Wendy|last3 = Yolken|first3 = Robert|pages=1–2|s2cid = 205073283}}</ref> however, a later study found that childhood cat ownership was not predictive of psychotic experiences at ages 13 or 18.<ref>{{Cite journal |title=Curiosity killed the cat: no evidence of an association between cat ownership and psychotic symptoms at ages 13 and 18 years in a UK general population cohort|first1=F.|last1=Solmi|first2=J. F.|last2=Hayes|first3=G.|last3=Lewis|first4=J. B.|last4=Kirkbride|date=July 31, 2017|journal=Psychological Medicine|volume=47|issue=9|pages=1659–1667|doi=10.1017/S0033291717000125|pmid=28222824|pmc=5939988}}</ref> Researchers also found that cat ownership does not strongly increase the risk of a ''T.&nbsp;gondii'' infection in pregnant women.<ref name="Kapperud_1996"/><ref>{{cite journal |last1=Cook |first1=A J C |title=Sources of toxoplasma infection in pregnant women: European multicentre case-control study Commentary: Congenital toxoplasmosis---further thought for food |journal=BMJ |date=15 July 2000 |volume=321 |issue=7254 |pages=142–147 |doi=10.1136/bmj.321.7254.142 |pmid=10894691 |pmc=27431 }}</ref>

The term ''crazy cat-lady syndrome'' draws on both stereotype and popular cultural reference. It was originated as instances of the aforementioned afflictions were noted amongst the populace. A [[cat lady]] is a cultural stereotype of a woman who compulsively [[Hoarding|hoards]] and dotes upon cats. The biologist [[Jaroslav Flegr]] is a proponent of the theory that toxoplasmosis affects human behaviour.<ref name=howyourcat>{{cite magazine |title=How Your Cat is Making You Crazy |author=Kathleen McAuliffe |magazine=The Atlantic |date=March 2012 |url=https://www.theatlantic.com/magazine/archive/2012/03/how-your-cat-is-making-you-crazy/8873/ |url-status=live |archive-url=https://web.archive.org/web/20120816212719/http://www.theatlantic.com/magazine/archive/2012/03/how-your-cat-is-making-you-crazy/8873/ |archive-date=2012-08-16 }}</ref><ref>{{cite journal |last1=Flegr |first1=J. |title=Effects of Toxoplasma on Human Behavior |journal=Schizophrenia Bulletin |date=19 March 2007 |volume=33 |issue=3 |pages=757–760 |doi=10.1093/schbul/sbl074 |pmid=17218612 |pmc=2526142 }}</ref>

=== Notable cases ===
* Tennis player [[Arthur Ashe]] developed neurological problems from toxoplasmosis (and was later found to be [[HIV]]-positive).<ref>[http://www.aegis.com/news/ads/1993/ad930239.html Arthur Ashe, Tennis Star, is Dead at 49] {{webarchive |url=https://web.archive.org/web/20081210083031/http://www.aegis.com/news/ads/1993/ad930239.html |date=December 10, 2008 }} ''New York Times'' (02/08/93)</ref>
* Actor [[Merritt Butrick]] was HIV-positive and died from toxoplasmosis as a result of his already-weakened immune system.<ref>[https://www.angelfire.com/celeb2/merrittbutrick/Biography.html Merritt Butrick, A Biography]  ''Angelfire.com'', accessdate Mar 18, 2011</ref>
* [[Pedro Zamora]], reality television personality and HIV/AIDS activist, was diagnosed with toxoplasmosis as a result of his immune system being weakened by HIV.<ref>{{cite web|url=http://www.broward.org/HumanServices/CommunityPartnerships/RyanWhiteProgram/Pages/TheFaceThatDefinedAIDS.aspx|title=The Face That Defined AIDS|url-status=live|archive-url=https://web.archive.org/web/20160402003625/http://www.broward.org/HumanServices/CommunityPartnerships/RyanWhiteProgram/Pages/TheFaceThatDefinedAIDS.aspx|archive-date=2016-04-02}}</ref>
* [[Prince François, Count of Clermont]], [[pretender]] to the [[throne of France]], had congenital toxoplasmosis; his disability caused him to be overlooked in the line of succession.
* Actress [[Leslie Ash]] contracted toxoplasmosis in the second month of pregnancy.<ref>{{cite news | url=http://news.bbc.co.uk/1/hi/health/1109818.stm | work=BBC News | title=Pregnancy superfoods revealed | date=January 10, 2001 | access-date=May 25, 2010 | url-status=live | archive-url=https://web.archive.org/web/20070105125031/http://news.bbc.co.uk/1/hi/health/1109818.stm | archive-date=January 5, 2007 }}</ref>
* British middle-distance runner [[Sebastian Coe]] contracted toxoplasmosis in 1983, which was probably transmitted by a cat while he trained in Italy.<ref>{{cite news | url=http://www.timesonline.co.uk/tol/sport/article537461.ece | work=The Times | location=London | title=Olympics bid Coes finest race | date=June 26, 2005 | access-date=May 25, 2010 | url-status=dead | archive-url=https://web.archive.org/web/20110510204637/http://www.timesonline.co.uk/tol/sport/article537461.ece | archive-date=May 10, 2011 |url-access=subscription}}</ref><ref>{{cite news|url=https://www.nytimes.com/1983/09/03/sports/sports-people-coe-s-disorder-rare.html|title=SPORTS PEOPLE; Coe's Disorder Rare|newspaper=The New York Times|date=3 September 1983|access-date=3 May 2018}}</ref>
* Tennis player [[Martina Navratilova]] experienced toxoplasmosis during the [[1982 US Open – Women's Singles|1982 US Open]].<ref>{{cite news|title=PERSONAL HEALTH|url=https://www.nytimes.com/1982/10/27/garden/personal-health-247906.html|newspaper=New York Times|date=27 October 1982|first=Jane E.|last=Brody|url-status=live|archive-url=https://web.archive.org/web/20170827215239/http://www.nytimes.com/1982/10/27/garden/personal-health-247906.html|archive-date=27 August 2017}}</ref>

== Other animals ==
[[File:Parasite140105-fig3 Toxoplasmosis in a bar-shouldered dove - TEM of 2 tachyzoites.tif|thumb|''Toxoplasma gondii'' infects virtually all warm-blooded animals; these [[tachyzoite]]s were found in a bird<ref name="RigouletHennache2014">{{cite journal |last1=Rigoulet |first1=Jacques |last2=Hennache |first2=Alain |last3=Lagourette |first3=Pierre |last4=George |first4=Catherine |last5=Longeart |first5=Loïc |last6=Le Net |first6=Jean-Loïc |last7=Dubey |first7=Jitender P. |title=Toxoplasmosis in a bar-shouldered dove (''Geopelia humeralis'') from the Zoo of Clères, France |journal=Parasite |date=2014 |volume=21 |pages=62 |doi=10.1051/parasite/2014062 |pmid=25407506 |pmc=4236686 }}</ref>]]
[[File:Parasite150075-fig1 Toxoplasma gondii in Giant panda.tif|thumb|''Toxoplasma gondii'' in the lung of a [[giant panda]].<ref name="MaWang2015"/> Arrow: [[macrophage]]s containing [[tachyzoite]]s.]]

Although ''T. gondii'' has the capability of infecting virtually all warm-blooded animals, susceptibility and rates of infection vary widely between different [[genera]] and [[species]].{{sfnp|Dubey|2016|p=needed}}<ref name="RouatbiAmairia2019">{{cite journal |last1=Rouatbi |first1=Mariem |last2=Amairia |first2=Safa |last3=Amdouni |first3=Yosra |last4=Boussaadoun |first4=Mohamed Anis |last5=Ayadi |first5=Ouarda |last6=Al-Hosary |first6=Amira Adel Taha |last7=Rekik |first7=Mourad |last8=Ben Abdallah |first8=Rym |last9=Aoun |first9=Karim |last10=Darghouth |first10=Mohamed Aziz |last11=Wieland |first11=Barbara |last12=Gharbi |first12=Mohamed |title=''Toxoplasma gondii'' infection and toxoplasmosis in North Africa: a review |journal=Parasite |date=2019 |volume=26 |pages=6 |doi=10.1051/parasite/2019006 |pmid=30767889 |pmc=6376878 }}</ref> Rates of infection in populations of the same species can also vary widely due to differences in location, diet, and other factors.{{cn|date=January 2023}}

Although infection with ''T.&nbsp;gondii'' has been noted in several species of Asian primates, seroprevalence of ''T.&nbsp;gondii'' antibodies were found for the first time in toque macaques (''[[Macaca sinica]]'') that are endemic to the island of Sri Lanka.<ref>{{cite journal|last1=Ekanayake|first1=D. K.|last2=Rajapakse|first2=R. P V. J.|last3=Dubey|first3=J. P.|last4=Dittus|first4=W. P J.|title=Seroprevalence of ''Toxoplasma gondii'' in wild toque macaques (''Macaca sinica'') at Polonnaruwa, Sri Lanka |journal=Journal of Parasitology |date=2004 |volume=90 |issue=4 |pages=870–871 |pmid=15357087 |doi=10.1645/GE-291R|s2cid=23829241}}</ref>

Australian [[marsupials]] are particularly susceptible to toxoplasmosis.<ref>{{cite journal |last1=Hollings |first1=Tracey |last2=Jones |first2=Menna |last3=Mooney |first3=Nick |last4=McCallum |first4=Hamish |title=Wildlife disease ecology in changing landscapes: Mesopredator release and toxoplasmosis |journal=International Journal for Parasitology: Parasites and Wildlife |date=2013 |volume=2 |pages=110–118 |doi=10.1016/j.ijppaw.2013.02.002|pmid=24533323 |pmc=3862529 |bibcode=2013IJPPW...2..110H }}</ref> [[wallaby|Wallabies]], [[koalas]], [[wombats]], [[pademelon]]s and small [[Dasyuromorphia|dasyurids]] can be killed by it, with [[eastern barred bandicoot]]s typically dying within about 3 weeks of infection.<ref>{{cite news|last1=Fancourt|first1=Bronwyn|title=Toxoplasmosis: how feral cats kill wildlife without lifting a paw|url=https://theconversation.com/toxoplasmosis-how-feral-cats-kill-wildlife-without-lifting-a-paw-32228|access-date=23 December 2016|work=The Conversation|date=5 October 2014|url-status=live|archive-url=https://web.archive.org/web/20161223133635/https://theconversation.com/toxoplasmosis-how-feral-cats-kill-wildlife-without-lifting-a-paw-32228|archive-date=23 December 2016}}</ref>

It is estimated that 23% of wild swine worldwide are seropositive for ''T.&nbsp;gondii''.<ref name="Riahi">{{cite journal|last1=Riahi|first1=Mohammad|last2=Fakhri|first2=Yadollah|last3=Hanifehpour|first3=Hooman|last4=Valizadeh|first4=Soghra|last5=Gholizadeh|first5=Majid|last6=Hosseini-Pouya|first6=Rokhsane|last7=Gamble|first7=H.Ray|title=The global seroprevalence of Toxoplasma gondii among wild boars: A systematic review and meta-analysis|journal=Veterinary Parasitology|date=September 2017|volume=244|pages=12–20|doi=10.1016/j.vetpar.2017.07.013|pmid=28917302}}</ref>  Seroprevalence varies across the globe with the highest seroprevalence in North America (32%) and Europe (26%) and the lowest in Asia (13%) and South America (5%).<ref name="Riahi" /> Geographical regions located at higher latitudes and regions that experience warmer, humid climates are associated with increased seroprevalence of ''T.&nbsp;gondii'' among wild boar.<ref name="Riahi" />  Wild boar infected with ''T.&nbsp;gondii'' pose a potential health risk for humans who consume their meat.<ref name="Riahi" />

=== Livestock ===
Among [[livestock]], pigs,<ref name="Dubey-2009">{{cite journal |last1=Dubey |first1=J.P. |title=Toxoplasmosis in pigs—The last 20 years |journal=Veterinary Parasitology |date=October 2009 |volume=164 |issue=2–4 |pages=89–103 |doi=10.1016/j.vetpar.2009.05.018 |pmid=19559531 }}</ref>{{sfnp|Dubey|2016|p=145}}<ref name="Nissapatorn-et-al-2013">{{cite book |doi=10.1007/978-3-7091-1553-4_8 |date=2013 |isbn=978-3-7091-1552-7 |last1=Nissapatorn |first1=Veeranoot |last2=Lau |first2=Yee-Ling |last3=Fong |first3=Mun-Yik |title=Parasites and their vectors |chapter=Toxoplasma gondii: The Parasite in Trend |publisher=Springer |location=Vienna }}</ref> sheep<ref name="pmid24534616">{{cite journal |vauthors=Chessa G, Chisu V, Porcu R, Masala G | title = Molecular characterization of ''Toxoplasma gondii'' Type II in sheep abortion in Sardinia, Italy | journal = Parasite | volume = 21 | page = 6 | year = 2014 | pmid = 24534616 | pmc = 3927306 | doi = 10.1051/parasite/2014007 }} {{open access}}</ref> and goats have the highest rates of chronic ''T.&nbsp;gondii'' infection.<ref name=Tenter2000>{{cite journal |vauthors=Tenter AM, Heckeroth AR, Weiss LM | title = ''Toxoplasma gondii'': from animals to humans | journal = International Journal for Parasitology | volume = 30 | issue = 12–13 | pages = 1217–58 | date = November 2000 | pmid = 11113252 | pmc = 3109627 | doi = 10.1016/S0020-7519(00)00124-7 }}</ref> The prevalence of ''T.&nbsp;gondii'' in meat-producing animals varies widely both within and among countries,<ref name=Tenter2000 /> and rates of infection have been shown to be dramatically influenced by varying farming and management practices.<ref name=Dubey2008>{{cite journal |vauthors=Dubey JP, Jones JL | title = ''Toxoplasma gondii'' infection in humans and animals in the United States | journal = International Journal for Parasitology | volume = 38 | issue = 11 | pages = 1257–78 | date = September 2008 | pmid = 18508057 | doi = 10.1016/j.ijpara.2008.03.007 }}</ref> For instance, animals kept outdoors or in [[Free range|free-ranging]] environments are more at risk of infection than animals raised indoors or in commercial [[Factory farming|confinement operations]].<ref name=Dubey2008 /><ref name=Jones2012Foodborne>{{cite journal |vauthors=Jones JL, Dubey JP | title = Foodborne toxoplasmosis | journal = Clinical Infectious Diseases | volume = 55 | issue = 6 | pages = 845–51 | date = September 2012 | pmid = 22618566 | doi = 10.1093/cid/cis508 | doi-access = free }}</ref>

====Pigs====
Worldwide, the percentage of pigs harboring viable parasites has been measured to be 3–71.43%<ref name="Nissapatorn-et-al-2013" /> and in the United States (via [[bioassay]] in mice or cats) to be as high as 92.7% and as low as 0%, depending on the farm or herd.<ref name=Jones2012Foodborne /> Surveys of seroprevalence (''T.&nbsp;gondii'' antibodies in blood) are more common, and such measurements are indicative of the high relative seroprevalence in pigs across the world.{{sfnp|Dubey|2016|pp=145–151}} Neonatal [[piglet (animal)|piglet]]s have been found to experience the entire range of severity, including progression to [[stillbirth]].{{sfnp|Dubey|2016|p=153}}<ref name="Dubey-2009" />{{rp|95}} This was especially demonstrated in the foundational Thiptara et al. 2006, reporting a litter birth of three stillborns and six live in Thailand. This observation has been relevant not only to that country but to toxoplasmosis control in [[porciculture]] around the world.{{sfnp|Dubey|2016|p=154}}<ref name="Dubey-2009" />{{rp|95}}<ref name="Nissapatorn-et-al-2013" />

====Sheep====
Along with pigs, sheep and goats are among the most commonly infected livestock of epidemiological significance for human infection.<ref name=Tenter2000 /> Prevalence of viable ''T.&nbsp;gondii'' in sheep tissue has been measured (via bioassay) to be as high as 78% in the United States,<ref>{{cite journal |vauthors=Dubey JP, Sundar N, Hill D, Velmurugan GV, Bandini LA, Kwok OC, Majumdar D, Su C | title = High prevalence and abundant atypical genotypes of ''Toxoplasma gondii'' isolated from lambs destined for human consumption in the USA | journal = [[International Journal for Parasitology]] | volume = 38 | issue = 8–9 | pages = 999–1006 | date = July 2008 | pmid = 18191859 | doi = 10.1016/j.ijpara.2007.11.012 }}</ref> and a 2011 survey of goats intended for consumption in the United States found a seroprevalence of 53.4%.<ref>{{cite journal |vauthors=Dubey JP, Rajendran C, Ferreira LR, Martins J, Kwok OC, Hill DE, Villena I, Zhou H, Su C, Jones JL | title = High prevalence and genotypes of ''Toxoplasma gondii'' isolated from goats, from a retail meat store, destined for human consumption in the USA | journal = [[International Journal for Parasitology]] | volume = 41 | issue = 8 | pages = 827–833 | date = July 2011 | pmid = 21515278 | doi = 10.1016/j.ijpara.2011.03.006 }}</ref> A single live attenuated vaccine, Toxovax, is currently available to mitigate the negative impacts of congenital toxoplasmosis on the sheep industry.<ref name="pmid36090161">{{cite journal |vauthors=Hasan T, Nishikawa Y |title=Advances in vaccine development and the immune response against toxoplasmosis in sheep and goats |journal=Frontiers in Veterinary Science |volume=9 |issue= |pages=951584 |date=2022 |pmid=36090161 |pmc=9453163 |doi=10.3389/fvets.2022.951584|doi-access=free }}</ref><ref name="pmid36310233">{{cite journal |vauthors=Zhang Y, Li D, Lu S, Zheng B |title=Toxoplasmosis vaccines: what we have and where to go? |journal=npj Vaccines |volume=7 |issue=1 |pages=131 |date=October 2022 |pmid=36310233 |pmc=9618413 |doi=10.1038/s41541-022-00563-0}}</ref>

====Chickens====
Due to a lack of exposure to the outdoors, chickens raised in large-scale indoor confinement operations are not commonly infected with ''T.&nbsp;gondii''.<ref name=Dubey2008 /> Free-ranging or backyard-raised chickens are much more commonly infected.<ref name=Dubey2008 /> A survey of free-ranging chickens in the United States found its prevalence to be 17–100%, depending on the farm.<ref>{{cite journal | author = Dubey JP | title = ''Toxoplasma gondii'' infections in chickens (''Gallus domesticus''): prevalence, clinical disease, diagnosis and public health significance | journal = Zoonoses and Public Health | volume = 57 | issue = 1 | pages = 60–73 | date = February 2010 | pmid = 19744305 | doi = 10.1111/j.1863-2378.2009.01274.x | s2cid = 9228587 }}</ref> Because chicken meat is generally cooked thoroughly before consumption, poultry is not generally considered to be a significant risk factor for human ''T.&nbsp;gondii'' infection.{{sfn|Weiss|Kim|2007|p=723}}

====Cattle====
Although cattle and buffalo can be infected with ''T.&nbsp;gondii'', the parasite is generally eliminated or reduced to undetectable levels within a few weeks following exposure.<ref name=Dubey2008 /> Tissue cysts are rarely present in buffalo meat or beef, and meat from these animals is considered to be low-risk for harboring viable parasites.<ref name=Jones2012Foodborne /><ref name=Tenter2000 /><ref name="Blaga2019">{{cite journal |last1=Blaga |first1=Radu |last2=Aubert |first2=Dominique |last3=Thébault |first3=Anne |last4=Perret |first4=Catherine |last5=Geers |first5=Régine |last6=Thomas |first6=Myriam |last7=Alliot |first7=Annie |last8=Djokic |first8=Vitomir |last9=Ortis |first9=Naïma |last10=Halos |first10=Lénaïg |last11=Durand |first11=Benoît |last12=Mercier |first12=Aurélien |last13=Villena |first13=Isabelle |last14=Boireau |first14=Pascal |title=''Toxoplasma gondii'' in beef consumed in France: regional variation in seroprevalence and parasite isolation |journal=Parasite |date=2019 |volume=26 |pages=77 |doi=10.1051/parasite/2019076 |pmid=31868577 |pmc=6927255 }}</ref>

====Horses====
Horses are considered resistant to chronic ''T.&nbsp;gondii'' infection.<ref name=Dubey2008 /> However, viable cells have been isolated from US horses slaughtered for export, and severe human toxoplasmosis in France has been epidemiologically linked to the consumption of [[horse meat]].<ref name=Jones2012Foodborne /><ref name="AroussiVignoles2015">{{cite journal |last1=Aroussi |first1=Abdelkrim |last2=Vignoles |first2=Philippe |last3=Dalmay |first3=François |last4=Wimel |first4=Laurence |last5=Dardé |first5=Marie-Laure |last6=Mercier |first6=Aurélien |last7=Ajzenberg |first7=Daniel |title=Detection of ''Toxoplasma gondii'' DNA in horse meat from supermarkets in France and performance evaluation of two serological tests |journal=Parasite |date=2015 |volume=22 |pages=14 |doi=10.1051/parasite/2015014 |pmid=25809058 |pmc=4374124 }}</ref>

=== Domestic cats ===
In 1942, the first case of feline toxoplasmosis was diagnosed and reported in a domestic cat in Middletown, New York.<ref>{{cite journal |last1=Dubey |first1=Jitender P. |title=The History of ''Toxoplasma gondii''—The First 100 Years |journal=Journal of Eukaryotic Microbiology |date=November 2008 |volume=55 |issue=6 |pages=467–475 |doi=10.1111/j.1550-7408.2008.00345.x |pmid=19120791 }}</ref> The investigators isolated oocysts from feline feces and found that the oocysts could be infectious for up to 12 months in the environment.<ref>{{Cite journal|title=Experimental transmission of Toxoplasma gondii|last=Hutchison|first=W. M.|journal=Nature|volume=206|issue=987|pages=961–2|date=1965-05-29|pmid=5839865|doi=10.1038/206961a0|bibcode=1965Natur.206..961H|s2cid=4207372}}</ref>

The seroprevalence of ''T.&nbsp;gondii'' in [[domestic cat]]s, worldwide has been estimated to be around 30–40%<ref name="Elmore_2010">{{cite journal |last1=Elmore |first1=Stacey A. |last2=Jones |first2=Jeffrey L. |last3=Conrad |first3=Patricia A. |last4=Patton |first4=Sharon |last5=Lindsay |first5=David S. |last6=Dubey |first6=J.P. |title=Toxoplasma gondii: epidemiology, feline clinical aspects, and prevention |journal=Trends in Parasitology |date=April 2010 |volume=26 |issue=4 |pages=190–196 |doi=10.1016/j.pt.2010.01.009 |pmid=20202907 }}</ref> and exhibits significant geographical variation. In the United States, no official national estimate has been made, but local surveys have shown levels varying between 16% and 80%.<ref name="Elmore_2010" /> A 2012 survey of 445 [[purebred]] pet cats and 45 shelter cats in [[Finland]] found an overall seroprevalence of 48.4%,<ref>{{cite journal |vauthors=Jokelainen P, Simola O, Rantanen E, Näreaho A, Lohi H, Sukura A | title = Feline toxoplasmosis in Finland: cross-sectional epidemiological study and case series study | journal = Journal of Veterinary Diagnostic Investigation | volume = 24 | issue = 6 | pages = 1115–1124 | date = November 2012 | pmid = 23012380 | doi = 10.1177/1040638712461787 | doi-access = free }}</ref> while a 2010 survey of feral cats from [[Giza, Egypt]] found a seroprevalence rate of 97.4%.<ref>{{cite journal |vauthors=Al-Kappany YM, Rajendran C, Ferreira LR, Kwok OC, Abu-Elwafa SA, Hilali M, Dubey JP | title = High prevalence of toxoplasmosis in cats from Egypt: isolation of viable ''Toxoplasma gondii'', tissue distribution, and isolate designation | journal = The Journal of Parasitology | volume = 96 | issue = 6 | pages = 1115–1118 | date = December 2010 | pmid = 21158619 | doi = 10.1645/GE-2554.1 | s2cid = 25574092 }}</ref> Another survey from Colombia recorded seroprevalence of 89.3%,{{sfnp|Dubey|2016|p=96}} whereas a Chinese ([[Guangdong]]) study found just a 2.1% prevalence.{{sfnp|Dubey|2016|p=98}}

''T. gondii'' infection rates in domestic cats vary widely depending on the cats' diets and lifestyles.{{sfnp|Dubey|2016|p=95}} [[Feral cat]]s that hunt for their food are more likely to be infected than domestic cats, and naturally also depends on the prevalence of ''T.&nbsp;gondii''-infected prey such as birds and small [[mammals]].{{sfnp|Dubey|2016|p=46}}

Most infected cats will shed oocysts in their feces only once in their lifetime, typically for 3-10 days after infection. This shedding can release millions of oocysts, each capable of spreading and surviving for months. After infection, most cats will develop antibodies to ''T. gondii'' and will no longer shed oocysts.<ref name="pmid23813830">{{cite journal |vauthors=Hartmann K, Addie D, Belák S, Boucraut-Baralon C, Egberink H, Frymus T, Gruffydd-Jones T, Hosie MJ, Lloret A, Lutz H, Marsilio F, Möstl K, Pennisi MG, Radford AD, Thiry E, Truyen U, Horzinek MC |title=Toxoplasma gondii infection in cats: ABCD guidelines on prevention and management |journal=Journal of Feline Medicine and Surgery |volume=15 |issue=7 |pages=631–7 |date=July 2013 |pmid=23813830 |doi=10.1177/1098612X13489228|pmc=11148961 }}</ref><ref name=Elmore_2010 /> An estimated 1% of cats at any given time are actively shedding oocysts.<ref name=Dubey2008 />

It is difficult to control the cat population with the infected oocysts due to the lack of an approved vaccine. This remains a challenge in most cases, and the programs that are readily available are questionable in efficacy.<ref name="pmid36310233">{{cite journal |vauthors=Zhang Y, Li D, Lu S, Zheng B |title=Toxoplasmosis vaccines: what we have and where to go? |journal=npj Vaccines |volume=7 |issue=1 |pages=131 |date=October 2022 |pmid=36310233 |pmc=9618413 |doi=10.1038/s41541-022-00563-0}}</ref><ref>{{cite journal |last1=Andersen |first1=Mark C. |last2=Martin |first2=Brent J. |last3=Roemer |first3=Gary W. |title=Use of matrix population models to estimate the efficacy of euthanasia versus trap-neuter-return for management of free-roaming cats |journal=Journal of the American Veterinary Medical Association |date=December 2004 |volume=225 |issue=12 |pages=1871–1876 |doi=10.2460/javma.2004.225.1871 |pmid=15643836 }}</ref><ref name="pmid31926434">{{cite journal |vauthors=Bonačić Marinović AA, Opsteegh M, Deng H, Suijkerbuijk AW, van Gils PF, van der Giessen J |title=Prospects of toxoplasmosis control by cat vaccination |journal=Epidemics |volume=30 |pages=100380 |date=December 2019 |pmid=31926434 |doi=10.1016/j.epidem.2019.100380|doi-access=free }}</ref> Research into feline vaccines for toxoplasmosis is ongoing, with several candidates showing positive results in clinical trials.<ref name="pmid36310233"/><ref name="pmid31926434"/>

Current methods of control of ''T. gondii'' in cats typically rely on preventing them from hunting (where they might acquire the parasite), not allowing the cat to consume raw meat, and maintaining good hygiene around litter boxes to minimize environmental oocyst contamination.<ref name="CDC 2018">{{cite web |title=Parasites - Toxoplasmosis (Toxoplasma infection) - Prevention & Control |website=Centers for Disease Control and Prevention |date=27 September 2018 |url=https://www.cdc.gov/parasites/toxoplasmosis/prevent.html | access-date=26 April 2024}}</ref><ref name="pmid23813830"/>

=== Rodents ===
Infection with ''T. gondii'' has been shown to [[Behavior-altering parasites and parasitoids|alter the behavior]] of mice and rats in ways thought to increase the rodents' chances of being preyed upon by cats.<ref name=Webster_2010/><ref name=Webster_2007>{{cite journal |last1=Webster |first1=J. P. |title=The Effect of Toxoplasma gondii on Animal Behavior: Playing Cat and Mouse |journal=Schizophrenia Bulletin |date=19 March 2007 |volume=33 |issue=3 |pages=752–756 |doi=10.1093/schbul/sbl073 |pmid=17218613 |pmc=2526137 }}</ref><ref name=Berdoy_2000>{{cite journal |last1=Berdoy |first1=M. |last2=Webster |first2=J. P. |last3=Macdonald |first3=D. W. | title = Fatal attraction in rats infected with ''Toxoplasma gondii'' | journal = Proceedings of the Royal Society B: Biological Sciences | volume = 267 | issue = 1452 | pages = 1591–1594 | date = August 7, 2000 | pmid = 11007336 | pmc = 1690701 | doi = 10.1098/rspb.2000.1182 }}</ref> Infected rodents show a reduction in their innate aversion to cat odors; while uninfected mice and rats will generally avoid areas marked with cat [[urine]] or with cat body odor, this avoidance is reduced or eliminated in infected animals.<ref name=Webster_2010 /><ref name=Berdoy_2000 /><ref name=Vyas2007BehavioralChanges>{{cite journal |vauthors=Vyas A, Kim SK, Giacomini N, Boothroyd JC, Sapolsky RM | title = Behavioral changes induced by ''Toxoplasma'' infection of rodents are highly specific to aversion of cat odors | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 104 | issue = 15 | pages = 6442–6447 | date = April 10, 2007 | pmid = 17404235 | pmc = 1851063 | doi = 10.1073/pnas.0608310104 | bibcode = 2007PNAS..104.6442V | doi-access = free }}</ref> Moreover, some evidence suggests this loss of aversion may be specific to feline odors: when given a choice between two [[predator]] odors (cat or [[mink]]), infected rodents show a significantly stronger preference to cat odors than do uninfected [[control (experiment)|controls]].<ref name="Xiao_2012">{{cite journal |vauthors=Xiao J, Kannan G, Jones-Brando L, Brannock C, Krasnova IN, Cadet JL, Pletnikov M, Yolken RH | title = Sex-specific changes in gene expression and behavior induced by chronic ''Toxoplasma'' infection in mice | journal = Neuroscience | volume = 206 | pages = 39–48 | date = March 29, 2012 | pmid = 22240252 | doi = 10.1016/j.neuroscience.2011.12.051 | s2cid = 24725619 }}</ref><ref name=Lamberton2008>{{cite journal |vauthors=Lamberton PH, Donnelly CA, Webster JP | title = Specificity of the''Toxoplasma gondii''-altered behaviour to definitive versus non-definitive host predation risk | journal = Parasitology | volume = 135 | issue = 10 | pages = 1143–1150 | date = September 2008 | pmid = 18620624 | doi = 10.1017/S0031182008004666 | s2cid = 21601830 }}</ref>

In rodents, ''T.&nbsp;gondii''–induced behavioral changes occur through [[chromatin remodeling|epigenetic remodeling]] in neurons associated with observed behaviors;<ref name="TG Masterpiece review" /><ref name="Masterpiece of epigenetic engineering" /> for example, it modifies [[epigenetic methylation]] to induce hypomethylation of [[arginine vasopressin]]-related genes in the medial amygdala to greatly decrease predator aversion.<ref name="TG Masterpiece review">{{cite journal | vauthors = Hari Dass SA, Vyas A | title = ''Toxoplasma gondii'' infection reduces predator aversion in rats through epigenetic modulation in the host medial amygdala | journal = Molecular Ecology | volume = 23 | issue = 24 | pages = 6114–6122 | date  = December 2014 | pmid = 25142402 | doi = 10.1111/mec.12888 | bibcode = 2014MolEc..23.6114H | s2cid = 45290208 }}</ref><ref name="Masterpiece of epigenetic engineering">{{cite journal | vauthors = Flegr J, Markoš A | title = Masterpiece of epigenetic engineering – how ''Toxoplasma gondii'' reprogrammes host brains to change fear to sexual attraction | journal = Molecular Ecology | volume = 23 | issue = 24 | pages = 5934–5936 | date  = December 2014 | pmid = 25532868 | doi = 10.1111/mec.13006 | bibcode = 2014MolEc..23.5934F | s2cid = 17253786 | doi-access = free }}</ref> Similar epigenetically induced behavioral changes have also been observed in mouse models of addiction, where changes in the expression of [[histone-modifying enzyme]]s via [[gene knockout]] or [[enzyme inhibition]] in specific neurons produced alterations in drug-related behaviors.<ref name="Amphetamine epigenetics">{{cite journal | vauthors =  McCowan TJ, Dhasarathy A, Carvelli L | title = The Epigenetic Mechanisms of Amphetamine | journal = Journal of Addiction and Prevention | date = February 2015 | issue = S1 | pages = 1–7 | pmc = 4955852 | quote = Epigenetic modifications caused by addictive drugs play an important role in neuronal plasticity and in drug-induced behavioral responses. Although few studies have investigated the effects of AMPH on gene regulation (Table 1), current data suggest that AMPH acts at multiple levels to alter histone/DNA interaction and to recruit transcription factors which ultimately cause repression of some genes and activation of other genes. Importantly, some studies have also correlated the epigenetic regulation induced by AMPH with the behavioral outcomes caused by this drug, suggesting therefore that epigenetics remodeling underlies the behavioral changes induced by AMPH. If this proves to be true, the use of specific drugs that inhibit histone acetylation, methylation or DNA methylation might be an important therapeutic alternative to prevent and/or reverse AMPH addiction and mitigate the side effects generate by AMPH when used to treat ADHD. | pmid=27453897 | volume=2015}}</ref><ref name="pmid25486626">{{cite journal | vauthors = Walker DM, Cates HM, Heller EA, Nestler EJ | title = Regulation of chromatin states by drugs of abuse | journal = Current Opinion in Neurobiology | volume = 30 | pages = 112–121 | date = February 2015 | pmid = 25486626 | doi = 10.1016/j.conb.2014.11.002 | pmc=4293340}}</ref><ref name="pmid23643695">{{cite journal|vauthors=Nestler EJ|title=Epigenetic mechanisms of drug addiction|journal=Neuropharmacology|volume=76|issue=Pt B|pages=259–268|date=January 2014|pmid=23643695|pmc=3766384|doi=10.1016/j.neuropharm.2013.04.004|quote=Short-term increases in histone acetylation generally promote behavioral responses to the drugs, while sustained increases oppose cocaine's effects, based on the actions of systemic or intra-NAc administration of HDAC inhibitors.&nbsp;...  Genetic or pharmacological blockade of G9a in the NAc potentiates behavioral responses to cocaine and opiates, whereas increasing G9a function exerts the opposite effect (Maze et al., 2010; Sun et al., 2012a). Such drug-induced downregulation of G9a and H3K9me2 also sensitizes animals to the deleterious effects of subsequent chronic stress (Covington et al., 2011). Downregulation of G9a increases the dendritic arborization of NAc neurons, and is associated with increased expression of numerous proteins implicated in synaptic function, which directly connects altered G9a/H3K9me2 in the synaptic plasticity associated with addiction (Maze et al., 2010).<p><!-- continuing quotation across paragraph break-->"G9a appears to be a critical control point for epigenetic regulation in NAc, as we know it functions in two negative feedback loops. It opposes the induction of ΔFosB, a long-lasting transcription factor important for drug addiction (Robison and Nestler, 2011), while ΔFosB in turn suppresses G9a expression (Maze et al., 2010; Sun et al., 2012a).&nbsp;... Also, G9a is induced in NAc upon prolonged HDAC inhibition, which explains the paradoxical attenuation of cocaine's behavioral effects seen under these conditions, as noted above (Kennedy et al., 2013). GABAA receptor subunit genes are among those that are controlled by this feedback loop. Thus, chronic cocaine, or prolonged HDAC inhibition, induces several GABAA receptor subunits in NAc, which is associated with increased frequency of inhibitory postsynaptic currents (IPSCs). In striking contrast, combined exposure to cocaine and HDAC inhibition, which triggers the induction of G9a and increased global levels of H3K9me2, leads to blockade of GABAA receptor and IPSC regulation.</p>}}</ref> Widespread [[histone acetylation and deacetylation|histone–lysine acetylation]] in cortical [[astrocytes]] appears to be another epigenetic mechanism employed by ''T.&nbsp;gondii''.<ref name="T. Gondii has a HAT">{{cite journal |last1=Vanagas |first1=Laura |last2=Jeffers |first2=Victoria |last3=Bogado |first3=Silvina S |last4=Dalmasso |first4=Maria C |last5=Sullivan |first5=William J |last6=Angel |first6=Sergio O |title=''Toxoplasma'' histone acetylation remodelers as novel drug targets |journal=Expert Review of Anti-infective Therapy |date=October 2012 |volume=10 |issue=10 |pages=1189–1201 |doi=10.1586/eri.12.100 |pmid=23199404 |pmc=3581047 }}</ref><ref name="acetylation">{{cite journal | vauthors = Bouchut A, Chawla AR, Jeffers V, Hudmon A, Sullivan WJ | title = Proteome-wide lysine acetylation in cortical astrocytes and alterations that occur during infection with brain parasite ''Toxoplasma gondii'' | journal = PLOS ONE | volume = 10 | issue = 3 | pages = e0117966 | year = 2015 | pmid = 25786129 | pmc = 4364782 | doi = 10.1371/journal.pone.0117966 | bibcode = 2015PLoSO..1017966B | doi-access = free }}</ref>

''T. gondii''-infected rodents show a number of behavioral changes beyond altered responses to cat odors. Rats infected with the parasite show increased levels of activity and decreased [[neophobic]] behavior.<ref name=McConkey_2013>{{cite journal |vauthors=McConkey GA, Martin HL, Bristow GC, Webster JP | title = ''Toxoplasma gondii'' infection and behaviour – location, location, location? | journal = The Journal of Experimental Biology | volume = 216 | issue = Pt 1 | pages = 113–119 | date = January 1, 2013 | pmid = 23225873 | pmc = 3515035 | doi = 10.1242/jeb.074153 | bibcode = 2013JExpB.216..113M }}</ref> Similarly, infected mice show alterations in patterns of [[Animal locomotion|locomotion]] and exploratory behavior during experimental tests. These patterns include traveling greater distances, moving at higher speeds, accelerating for longer periods of time, and showing a decreased pause-time when placed in new arenas.<ref name=Afonso_2012>{{cite journal |vauthors=Afonso C, Paixão VB, Costa RM | title = Chronic ''Toxoplasma'' infection modifies the structure and the risk of host behavior | journal = PLOS ONE | volume = 7 | issue = 3 | pages = e32489 | year = 2012 | pmid = 22431975 | pmc = 3303785 | doi = 10.1371/journal.pone.0032489 | editor1-last = Hakimi | bibcode = 2012PLoSO...732489A | doi-access = free }}</ref> Infected rodents have also been shown to have lower [[anxiety (mood)|anxiety]], using traditional models such as [[elevated plus maze]]s, [[Open Field (animal test)|open field arenas]], and social interaction tests.<ref name=Afonso_2012 /><ref>{{cite journal |vauthors=Gonzalez LE, Rojnik B, Urrea F, Urdaneta H, Petrosino P, Colasante C, Pino S, Hernandez L | title = ''Toxoplasma gondii'' infection lower anxiety as measured in the plus-maze and social interaction tests in rats: A behavioral analysis | journal = Behavioural Brain Research | volume = 177 | issue = 1 | pages = 70–79 | date = February 12, 2007 | pmid = 17169442 | doi = 10.1016/j.bbr.2006.11.012 | s2cid = 33572709 }}</ref>

=== Marine mammals ===
A [[University of California, Davis]] study of dead [[sea otter]]s collected from 1998 to 2004 found toxoplasmosis was the cause of death for 13% of the animals.<ref name=Conrad_2005>{{cite journal |vauthors=Conrad PA, Miller MA, Kreuder C, James ER, Mazet J, Dabritz H, Jessup DA, Gulland F, Grigg ME | title = Transmission of ''Toxoplasma'': clues from the study of sea otters as sentinels of ''Toxoplasma gondii'' flow into the marine environment | journal = International Journal for Parasitology | volume = 35 | issue = 11–12 | pages = 1155–1168 | year = 2005 | pmid = 16157341 | doi = 10.1016/j.ijpara.2005.07.002 }}</ref> Proximity to freshwater outflows into the ocean was a major risk factor. Ingestion of [[oocysts]] from cat feces is considered to be the most likely ultimate source.<ref name="npr1">{{cite web | title=Treating Disease in the Developing World | website=Talk of the Nation Science Friday | date=December 16, 2005 | publisher=National Public Radio | url=https://www.npr.org/templates/story/story.php?storyId=5058325 | url-status=live | archive-url=https://web.archive.org/web/20060427075730/http://www.npr.org/templates/story/story.php?storyId=5058325 | archive-date=April 27, 2006 }}</ref> [[Surface runoff]] containing wild cat feces and litter from domestic cats flushed down toilets are possible sources of oocysts.<ref name=mag72>{{Cite news|url=http://www.magazine.noaa.gov/stories/mag72.htm|title=Parasite in cats killing sea otters|publisher=[[National Oceanic and Atmospheric Administration]]|date=21 January 2003|work=NOAA magazine|access-date=24 November 2007|url-status=dead|archive-url=https://web.archive.org/web/20071225205629/http://www.magazine.noaa.gov/stories/mag72.htm|archive-date=25 December 2007}}</ref><ref>{{cite web |url=https://www.nytimes.com/2019/08/28/science/california-sea-otters-cats.html| work=[[The New York Times]]| title=What's Killing California's Sea Otters? House Cats| date=September 3, 2019| last=Diep |first=Francie| access-date= 9 September 2019}}</ref> These same sources may have also introduced the toxoplasmosis infection to the endangered [[Hawaiian monk seal]].<ref name="scientificamerican.com">{{cite web|last1=Dawson|first1=Teresa|title=Cat Disease Threatens Endangered Monk Seals|url=https://www.scientificamerican.com/article/cat-disease-threatens-endangered-monk-seals/|website=Scientific American|access-date=11 October 2017}}</ref> Infection with the parasite has contributed to the death of at least four Hawaiian monk seals.<ref name="scientificamerican.com"/> A Hawaiian monk seal's infection with ''T.&nbsp;gondii'' was first noted in 2004.<ref>{{cite journal|last1=Honnold|first1=S. P.|last2=Braun|first2=R.|last3=Scott|first3=D. P.|last4=Sreekumar|first4=C.|last5=Dubey|first5=J. P.|title=Toxoplasmosis in a Hawaiian monk seal (''Monachus schauinslandi'')|journal=[[Journal of Parasitology]]|date=June 2005|volume=91|issue=3|pages=695–697|doi=10.1645/GE-469R|pmid=16108571|s2cid=13562317}}</ref> The parasite's spread threatens the recovery of this highly endangered pinniped. The parasites have been found in numerous cetacean species, such as the [[bottlenose dolphin]],<ref>{{cite journal |last1=Costa-Silva |first1=Samira |title=Toxoplasma gondii in cetaceans of Brazil: a histopathological and immunohistochemical survey |journal=Brazilian Journal of Veterinary Parasitology |date=2019 |volume=28 |issue=3 |pages=395–402|doi=10.1590/S1984-29612019051 |pmid=31411314 |doi-access=free }}</ref> [[spinner dolphin]],<ref>{{cite journal |last1=Landrau-Giovannetti |first1=Nelmarie |title=Prevalence and genotype of Toxoplasma gondii in stranded Hawaiian cetaceans |journal=Diseases of Aquatic Organisms |date=2022 |volume=152 |pages=27–36|doi=10.3354/dao03699 |pmid=36394138 |doi-access=free }}</ref> [[Risso's dolphin]],<ref>{{cite journal |last1=Resendes |first1=A. R |title=Disseminated toxoplasmosis in a Mediterranean pregnant Risso's dolphin (Grampus griseus) with transplacental fetal infection |journal=The Journal of Parasitology |date=2002 |volume=88 |issue=5 |pages=1029–1032|doi=10.1645/0022-3395(2002)088[1029:DTIAMP]2.0.CO;2 |pmid=12435153 }}</ref> [[Indo-Pacific humpback dolphin]],<ref>{{cite journal |last1=Bowater |first1=R. O |title=Toxoplasmosis in Indo-Pacific humpbacked dolphins (Sousa chinensis), from Queensland |journal=Australian Veterinary Journal |date=2003 |volume=81 |issue=10 |pages=627–632|doi=10.1111/j.1751-0813.2003.tb12509.x |pmid=15080475 |url=http://era.daf.qld.gov.au/id/eprint/470/ }}</ref> [[striped dolphin]],<ref>{{cite journal |last1=Di Guardo |first1=Giovanni |title=Toxoplasma gondii: Clues From Stranded Dolphins |journal=Veterinary Pathology |date=2013 |volume=50 |issue=5 |page=737|doi=10.1177/0300985813486816 |pmid=24014612 }}</ref> the [[beluga whale]],<ref>Sidhartha Banerjee (October 15, 2018). [https://www.cbc.ca/news/canada/montreal/parasite-spread-by-cats-threatens-quebec-s-endangered-belugas-study-shows-1.4864194 "Parasite spread by cats threatens Quebec's endangered belugas(whales)"]. ''CBC News''.</ref> and the critically endangered [[Māui dolphin]] and [[Hector's dolphin]].<ref>{{cite news |last1=Clark-Dow |first1=Emma |title=Dolphin found on Auckland beach died of disease often spread by cats |url=https://www.stuff.co.nz/environment/300856491/dolphin-found-on-auckland-beach-died-of-disease-often-spread-by-cats#:~:text=M%C4%81ui%20dolphins%20are%20one%20of,and%20oil%20exploration%20and%20toxoplasmosis.&text=The%20Government%20committed%20$4.88%20million,and%20reduce%20storm%20water%20runoff. |publisher=Stuff NZ |date=April 18, 2023}}</ref><ref name="Solomon_2013">{{cite news |last1=Solomon |first1=Christopher |title=How Kitty Is Killing the Dolphins |url=https://www.scientificamerican.com/article/pathogens-from-humans-cats-kill-seals-dolphins/ |publisher=Scientific American |date=May 1, 2013}}</ref><ref name="newscientist.com">{{cite web|url=https://www.newscientist.com/article/mg20427301.600-3-schizophrenia.html|title=3 Schizophrenia|url-status=live|archive-url=https://web.archive.org/web/20100102055421/http://www.newscientist.com/article/mg20427301.600-3-schizophrenia.html|archive-date=2010-01-02}}</ref> A 2011 study of 161 Pacific Northwest marine mammals ranging from a [[sperm whale]] to [[harbor porpoise]]s that had either become stranded or died found that 42 percent tested positive for both ''T. gondii'' and ''S. neurona''.<ref name="Solomon_2013" /> Researchers Black and Massie believe anchovies, which travel from estuaries into the open ocean, may be helping to spread the disease.<ref name="MassieWare2010">{{cite journal |last1=Massie |first1=Gloeta N. |last2=Ware |first2=Michael W. |last3=Villegas |first3=Eric N. |last4=Black |first4=Michael W. |title=Uptake and transmission of ''Toxoplasma gondii'' oocysts by migratory, filter-feeding fish |journal=Veterinary Parasitology |date=May 2010 |volume=169 |issue=3–4 |pages=296–303 |doi=10.1016/j.vetpar.2010.01.002 |pmid=20097009 }}</ref>

=== Giant panda ===
''Toxoplasma gondii'' has been reported as the cause of death of a [[giant panda]] kept in a zoo in China, who died in 2014 of acute [[gastroenteritis]] and [[respiratory disease]].<ref name="MaWang2015">{{cite journal |last1=Ma |first1=Hongyu |last2=Wang |first2=Zedong |last3=Wang |first3=Chengdong |last4=Li |first4=Caiwu |last5=Wei |first5=Feng |last6=Liu |first6=Quan |title=Fatal ''Toxoplasma gondii'' infection in the giant panda |journal=Parasite |date=2015 |volume=22 |pages=30 |doi=10.1051/parasite/2015030 |pmid=26514595 |pmc=4626621 }}</ref> Although seemingly [[anecdotal]], this report emphasizes that all warm-blooded species are likely to be infected by ''T.&nbsp;gondii'', including endangered species such as the giant panda.<ref name="MaWang2015" />

==Research==
[[Image:Toxoplasmosis lymphadenopathy - intermed mag.jpg|thumb|[[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]]]]
Chronic infection with ''T.&nbsp;gondii'' has traditionally been considered [[asymptomatic]] in people with normal immune function.<ref name=Fug2017>{{cite journal |last1=Fuglewicz |first1=AJ |last2=Piotrowski |first2=P |last3=Stodolak |first3=A |title=Relationship between toxoplasmosis and schizophrenia: A review |journal=Advances in Clinical and Experimental Medicine |date=September 2017 |volume=26 |issue=6 |pages=1031–1036 |pmid=29068607 |doi=10.17219/acem/61435|doi-access=free }}</ref> Some evidence suggests latent infection may subtly influence a range of human behaviors and tendencies, and infection may alter the susceptibility to or intensity of a number of [[Mental disorder|psychiatric]] or neurological disorders.<ref name=Webster_2013>{{cite journal |vauthors=Webster JP, Kaushik M, Bristow GC, McConkey GA | title = ''Toxoplasma gondii'' infection, from predation to schizophrenia: can animal behaviour help us understand human behaviour? | journal = The Journal of Experimental Biology | volume = 216 | issue = Pt 1 | pages = 99–112 | date = Jan 1, 2013 | pmid = 23225872 | pmc = 3515034 | doi = 10.1242/jeb.074716 | bibcode = 2013JExpB.216...99W }}</ref><ref name=Fug2017/>

In most of the current studies where positive correlations have been found between ''T.&nbsp;gondii'' antibody titers and certain behavioral traits or neurological disorders, ''T.&nbsp;gondii'' seropositivity tests are conducted after the onset of the examined disease or behavioral trait; that is, it is often unclear whether infection with the parasite increases the chances of having a certain trait or disorder, or if having a certain trait or disorder increases the chances of becoming infected with the parasite.<ref name="Flegr_2013">{{cite journal | author = Flegr J | title = Influence of latent ''Toxoplasma'' infection on human personality, physiology and morphology: pros and cons of the ''Toxoplasma''-human model in studying the manipulation hypothesis | journal = The Journal of Experimental Biology | volume = 216 | issue = Pt 1 | pages = 127–33 | date = Jan 1, 2013 | pmid = 23225875 | doi = 10.1242/jeb.073635 | doi-access = free | bibcode = 2013JExpB.216..127F }}</ref> Groups of individuals with certain behavioral traits or neurological disorders may share certain behavioral tendencies that increase the likelihood of exposure to and infection with ''T.&nbsp;gondii''; as a result, it is difficult to confirm causal relationships between ''T.&nbsp;gondii'' infections and associated neurological disorders or behavioral traits.<ref name="Flegr_2013" />

===Mental health===
Some evidence links ''T.&nbsp;gondii'' to [[schizophrenia]].<ref name=Fug2017/> Two 2012 meta-analyses found that the rates of [[antibodies]] to ''T.&nbsp;gondii'' in people with schizophrenia were 2.7 times higher than in controls.<ref name=Torrey2012>{{cite journal |last1=Torrey |first1=E. F. |last2=Bartko |first2=J. J. |last3=Yolken |first3=R. H. |title=Toxoplasma gondii and Other Risk Factors for Schizophrenia: An Update |journal=Schizophrenia Bulletin |date=23 March 2012 |volume=38 |issue=3 |pages=642–647 |doi=10.1093/schbul/sbs043 |pmid=22446566 |pmc=3329973 }}</ref><ref name=Ar2012>{{cite journal |last1=Arias |first1=Isabel |last2=Sorlozano |first2=Antonio |last3=Villegas |first3=Enrique |last4=Luna |first4=Juan de Dios |last5=McKenney |first5=Kathryn |last6=Cervilla |first6=Jorge |last7=Gutierrez |first7=Blanca |last8=Gutierrez |first8=Jose |title=Infectious agents associated with schizophrenia: A meta-analysis |journal=Schizophrenia Research |date=April 2012 |volume=136 |issue=1–3 |pages=128–136 |doi=10.1016/j.schres.2011.10.026 |pmid=22104141 |hdl=10481/90076 |hdl-access=free }}</ref> ''T.&nbsp;gondii'' antibody positivity was therefore considered an intermediate risk factor in relation to other known risk factors.<ref name=Torrey2012 /> Cautions noted include that the antibody tests do not detect toxoplasmosis directly, most people with schizophrenia do not have antibodies for toxoplasmosis, and [[publication bias]] might exist.<ref name=Ar2012/> While the majority of these studies tested people already diagnosed with schizophrenia for ''T.&nbsp;gondii'' antibodies, associations between ''T.&nbsp;gondii'' and schizophrenia have been found prior to the onset of schizophrenia symptoms.<ref name=Webster_2010 /><ref>{{Cite journal |last1=Burgdorf |first1=Kristoffer Sølvsten |last2=Trabjerg |first2=Betina B. |last3=Pedersen |first3=Marianne Giørtz |last4=Nissen |first4=Janna |last5=Banasik |first5=Karina |last6=Pedersen |first6=Ole Birger |last7=Sørensen |first7=Erik |last8=Nielsen |first8=Kaspar René |last9=Larsen |first9=Margit Hørup |last10=Erikstrup |first10=Christian |last11=Bruun-Rasmussen |first11=Peter |last12=Westergaard |first12=David |last13=Thørner |first13=Lise Wegner |last14=Hjalgrim |first14=Henrik |last15=Paarup |first15=Helene Martina |date=2019-07-01 |title=Large-scale study of Toxoplasma and Cytomegalovirus shows an association between infection and serious psychiatric disorders |url=https://www.sciencedirect.com/science/article/pii/S0889159118306998 |journal=Brain, Behavior, and Immunity |volume=79 |pages=152–158 |doi=10.1016/j.bbi.2019.01.026 |pmid=30685531 |issn=0889-1591}}</ref> Sex differences in the age of schizophrenia onset may be explained in part by a second peak of ''T.&nbsp;gondii'' infection incidence during ages 25–30 in females only.<ref name= Flegr2013>{{cite journal | author= Flegr J | title= How and why toxoplasma makes us crazy | journal= Trends in Parasitology | volume=29 | issue= 4 | pages= 156–163| date= 2013 | doi=10.1016/j.pt.2013.01.007 | pmid= 23433494 }}</ref> Although a mechanism supporting the association between schizophrenia and ''T.&nbsp;gondii'' infection is unclear, studies have investigated a molecular basis of this correlation.<ref name=Flegr2013 /> [[Antipsychotic|Antipsychotic drugs]] used in schizophrenia appear to inhibit the replication of ''T.&nbsp;gondii'' tachyzoites in cell culture.<ref name=Webster_2010>{{cite journal |vauthors=Webster JP, McConkey GA | title = ''Toxoplasma gondii''-altered host behaviour: clues as to mechanism of action | journal = Folia Parasitologica | volume = 57 | issue = 2 | pages = 95–104 | date = June 2010 | pmid = 20608471 | doi=10.14411/fp.2010.012| doi-access = free }}</ref> Supposing a causal link exists between ''T.&nbsp;gondii'' and schizophrenia, studies have yet to determine why only some individuals with latent toxoplasmosis develop schizophrenia; some plausible explanations include differing genetic susceptibility, parasite strain differences, and differences in the route of the acquired ''T.&nbsp;gondii'' infection.<ref name="Torrey_2007">{{cite journal |vauthors=Torrey EF, Yolken RH | title = Schizophrenia and toxoplasmosis | journal = Schizophrenia Bulletin | volume = 33 | issue = 3 | pages = 727–8 | date = May 2007 | pmid = 17426051 | pmc = 2526129 | doi = 10.1093/schbul/sbm026 }}</ref>

Correlations have also been found between antibody [[titer]]s to ''T.&nbsp;gondii'' and [[OCD]], as well as [[suicide]] among people with mood disorders including [[bipolar disorder]].<ref name=Webster_2013 /><ref>{{cite journal |last1=de Barros |first1=JLVM |last2=Barbosa |first2=IG |last3=Salem |first3=H |last4=Rocha |first4=NP |last5=Kummer |first5=A |last6=Okusaga |first6=OO |last7=Soares |first7=JC |last8=Teixeira |first8=AL |title=Is there any association between Toxoplasma gondii infection and bipolar disorder? A systematic review and meta-analysis |journal=Journal of Affective Disorders |date=February 2017 |volume=209 |pages=59–65 |doi=10.1016/j.jad.2016.11.016 |pmid=27889597}}</ref> Positive antibody titers to ''T.&nbsp;gondii'' appear to be uncorrelated with [[major depression]] or [[dysthymia]].<ref name=Pearce_2012>{{cite journal |vauthors=Pearce BD, Kruszon-Moran D, Jones JL | title = The relationship between ''Toxoplasma gondii'' infection and mood disorders in the third National Health and Nutrition Survey | journal = Biological Psychiatry | volume = 72 | issue = 4 | pages = 290–5 | date = Aug 15, 2012 | pmid = 22325983 | doi = 10.1016/j.biopsych.2012.01.003 | pmc=4750371}}</ref> Although there is a correlation between ''T.&nbsp;gondii'' and many psychological disorders, the underlying mechanism is unclear. A 2016 study of 236 persons with high levels of toxoplasmosis antibodies found that "there was little evidence that ''T.&nbsp;gondii'' was related to increased risk of psychiatric disorder, poor impulse control, personality aberrations or neurocognitive impairment".<ref>{{cite journal|last1=Sugden|first1=Karen|last2=Moffitt|first2=Terrie E.|last3=Pinto|first3=Lauriane|last4=Poulton|first4=Richie|last5=Williams|first5=Benjamin S.|last6=Caspi|first6=Avshalom|last7=Tanowitz|first7=Herbert B.|title=Is ''Toxoplasma Gondii'' Infection Related to Brain and Behavior Impairments in Humans? Evidence from a Population-Representative Birth Cohort|journal=PLOS ONE|date=17 February 2016|volume=11|issue=2|pages=e0148435|doi=10.1371/journal.pone.0148435|pmid=26886853|pmc=4757034|bibcode=2016PLoSO..1148435S|doi-access=free}}</ref>

===Neurological disorders===
Latent infection has been linked to [[Parkinson's disease]] and [[Alzheimer's disease]].<ref name=Webster_2013 />

Individuals with [[multiple sclerosis]] show infection rates around 15% lower than the general public.<ref name="Stascheit et. al_2015">{{cite journal |vauthors=Stascheit F, Paul F, Harms L, Rosche B | title = ''Toxoplasma gondii'' seropositivity is negatively associated with multiple sclerosis| journal = Journal of Neuroimmunology | volume = 285 | pages = 119–124 | year = 2015 | doi=10.1016/j.jneuroim.2015.05.011 | pmid = 26198927| s2cid = 33082008}}</ref>

=== Traffic accidents ===
Latent ''T. gondii'' infection in humans has been associated with a higher risk of [[automobile accidents]],<ref>{{cite journal |last1=Gohardehi |first1=Shaban |last2=Sharif |first2=Mehdi |last3=Sarvi |first3=Shahabeddin |last4=Moosazadeh |first4=Mahmood |last5=Alizadeh-Navaei |first5=Reza |last6=Hosseini |first6=Seyed Abdollah |last7=Amouei |first7=Afsaneh |last8=Pagheh |first8=Abdolsattar |last9=Sadeghi |first9=Mitra |last10=Daryani |first10=Ahmad |title=The potential risk of toxoplasmosis for traffic accidents: A systematic review and meta-analysis |journal=Experimental Parasitology |date=August 2018 |volume=191 |pages=19–24 |doi=10.1016/j.exppara.2018.06.003 |pmid=29906469 }}</ref> potentially due to impaired [[psychomotor learning|psychomotor]] performance or enhanced risk-taking personality profiles.<ref name=Webster_2013 />

===Climate change===
[[Climate change]] has been reported to affect the occurrence, survival, distribution and transmission of ''T.&nbsp;gondii''.<ref name="Yan">{{cite journal|last1=Yan|first1=Chao|last2=Liang|first2=Li-Jun|last3=Zheng|first3=Kui-Yang|last4=Zhu|first4=Xing-Quan|title=Impact of environmental factors on the emergence, transmission and distribution of Toxoplasma gondii|journal=Parasites & Vectors|date=2016|volume=9|issue=137|pages=137|doi=10.1186/s13071-016-1432-6|pmid=26965989|pmc=4785633 |doi-access=free }}</ref>  ''T.&nbsp;gondii'' has been identified in the Canadian arctic, a location that was once too cold for its survival.<ref name="Dolgin">{{cite journal|last1=Dolgin|first1=Elie|title=Climate change: As the ice melts|journal=Nature|date=March 30, 2017|volume=543|issue=7647|pages=S54–S55|doi=10.1038/543S54a|pmid=28355191|bibcode=2017Natur.543S..54D|s2cid=4448339}}</ref> Higher temperatures increase the survival time of ''T.&nbsp;gondii''.<ref name="Yan" />  More snowmelt and precipitation can increase the amount of ''T.&nbsp;gondii'' oocysts that are transported via river flow.<ref name="Yan" />  Shifts in bird, rodent, and insect populations and migration patterns can impact the distribution of ''T.&nbsp;gondii'' due to their role as reservoir and vector.<ref name="Yan" />  Urbanization and natural environmental degradation are also suggested to affect ''T.&nbsp;gondii'' transmission and increase risk of infection.<ref name="Yan" />

== See also ==
* [[TORCH complex|TORCH infection]]
* [[Toxoplasmic chorioretinitis]]

== References ==
{{Reflist}}
:* Parts of this article are taken from the public domain [https://www.cdc.gov/toxoplasmosis/ CDC factsheet: Toxoplasmosis]

==Bibliography==
* {{cite book |doi=10.1016/B978-0-12-369542-0.X5000-4 |date=2007 |isbn=978-0-12-369542-0 |title=Toxoplasma gondii: The Model Apicomplexan: Perspectives and Methods |publisher=Elsevier |editor1-first=Louis M. |editor1-last=Weiss |editor2-first=Kami |editor2-last=Kim }}
* {{cite book |first=J. P. |last=Dubey |title=Toxoplasmosis of Animals and Humans |edition=2nd |url=https://books.google.com/books?id=5Nm7t5p9APAC |date=2016 |publisher=[[CRC Press]] |isbn=978-1-4200-9237-0 | oclc=423572366 | pages=xvii+313 | publication-place=[[Boca Raton]]}} {{isbn|1-4200-9236-7}} {{isbn|9781420092363}}
* {{cite journal |vauthors=Dubey JP, Lindsay DS, Speer CA | title = Structures of ''Toxoplasma gondii'' tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts | journal = Clinical Microbiology Reviews | volume = 11 | issue = 2 | pages = 267–299 | date = April 1998 | pmid = 9564564 | pmc = 106833 | doi = 10.1128/CMR.11.2.267 }}
* {{cite book|author1=Jaroslav Flegr|title=Pozor, Toxo!|url=http://www.academia.cz/pozor-toxo.html|date=2011|publisher=Academia, Prague, Czech Republic|isbn=978-80-200-2022-2|access-date=2014-10-04|archive-date=2017-07-21|archive-url=https://web.archive.org/web/20170721113714/http://academia.cz/pozor-toxo.html|url-status=dead}}

== External links ==
* [https://web.archive.org/web/20130125121449/http://news.nationalgeographic.com/news/2013/01/220113-sneaky-cat-parasite-takes-over-human-brains-science/ How a cat-borne parasite infects humans] (National Geographic)
* {{MerckManual|14|186|h||Toxoplasmosis}}
* [https://www.gov.uk/guidance/toxoplasmosis Toxoplasmosis] at Health Protection Agency (HPA), United Kingdom
* [https://web.archive.org/web/20130113220407/http://rad.usuhs.edu/medpix/medpix.html?mode=image_finder&action=search&srchstr=toxoplasmosis#top Pictures of Toxoplasmosis] Medical Image Database
* [https://www.youtube.com/watch?v=m3x3TMdkGdQ Video-Interview] with Professor [[Robert Sapolsky]] on Toxoplasmosis and its effect on human behavior (24:27 min)
* {{cite web | url = https://medlineplus.gov/toxoplasmosis.html | publisher = U.S. National Library of Medicine | work = MedlinePlus | title = Toxoplasmosis }}

{{Medical condition classification and resources
|  DiseasesDB     = 13208
|  ICD10          = {{ICD10|B|58||b|50}}
|  ICD9           = {{ICD9|130}}
|  ICDO           =
|  OMIM           =
|  MedlinePlus    = 000637
|  eMedicineSubj  = med
|  eMedicineTopic = 2294
|  MeshID         = D014123
}}
{{Chromalveolate diseases}}{{Domestic cat}}
{{Authority control}}

[[Category:Biology of bipolar disorder]]
[[Category:Biology of obsessive–compulsive disorder]]
[[Category:Cat diseases]]
[[Category:Conoidasida]]
[[Category:Disorders causing seizures]]
[[Category:Health issues in pregnancy]]
[[Category:Medical triads]]
[[Category:Mind-altering parasites]]
[[Category:Parasitic infestations, stings, and bites of the skin]]
[[Category:Poultry diseases]]
[[Category:Protozoal diseases]]
[[Category:Wikipedia emergency medicine articles ready to translate]]
[[Category:Wikipedia medicine articles ready to translate]]
[[Category:Zoonoses]]