[13][14] However, symptoms may manifest and are often influenza-like: swollen lymph nodes, headaches, fever, and fatigue,[15] or muscle aches and pains that last for a month or more.

[15] Young children and immunocompromised people, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis.

[7][25][26] This latent state of infection has recently been associated with numerous disease burdens,[7] neural alterations,[23][25] and subtle sex-dependent behavioral changes in immunocompetent humans,[27][28] as well as an increased risk of motor vehicle collisions.

However, in immunocompromised individuals, or in fetuses, which lack a developed immune system, the tachyzoites can run rampant and cause significant neurological damage.

[2][36][37] Additionally, certain strains of T. gondii can secrete a protein known as GRA15, activating the NF-κB pathway, which upregulates the pro-inflammatory cytokine IL-12 in the early immune response, possibly leading to the parasite's latent phase.

[45] Oral transmission may occur through: 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.

[52] In addition to cats, birds and mammals including human beings are also intermediate hosts of the parasite and are involved in the transmission process.

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.

[60] As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented),[58] postnatal or neonatal screening is preferred.

A failed trial of antimicrobial therapy (pyrimethamine, sulfadiazine, and folinic acid (USAN: leucovorin)), makes an alternative diagnosis more likely.

As a result, a pregnant woman might test negative during the active phase of T. gondii infection leading to undetected and therefore untreated congenital toxoplasmosis.

[74] Lymph nodes affected by Toxoplasma have characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B cells, and scattered epithelioid histiocytes.

They are treated after the first trimester because pyrimethamine has an antifolate effect, and lack of folic acid can interfere with fetal brain formation and cause thrombocytopaenia.

[91] Because the parasite poses a particular threat to fetuses when it is contracted during pregnancy,[92] much of the global epidemiological data regarding T. gondii comes from seropositivity tests in women of childbearing age.

[11] Wolf, Cowen and Page reviewed additional cases and concluded that T. gondii produced recognizable symptoms and could be transmitted from mother to child.

[11] 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.

"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.

[115] Wallabies, koalas, wombats, pademelons and small dasyurids can be killed by it, with eastern barred bandicoots typically dying within about 3 weeks of infection.

[127] A single live attenuated vaccine, Toxovax, is currently available to mitigate the negative impacts of congenital toxoplasmosis on the sheep industry.

[146][143] Infection with T. gondii has been shown to alter the behavior of mice and rats in ways thought to increase the rodents' chances of being preyed upon by cats.

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.

[161] Infected rodents have also been shown to have lower anxiety, using traditional models such as elevated plus mazes, open field arenas, and social interaction tests.

[175][176][177] A 2011 study of 161 Pacific Northwest marine mammals ranging from a sperm whale to harbor porpoises that had either become stranded or died found that 42 percent tested positive for both T. gondii and S.

[178] 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.

[190] Latent T. gondii infection in humans has been associated with a higher risk of automobile accidents,[191] potentially due to impaired psychomotor performance or enhanced risk-taking personality profiles.

[192] Shifts in bird, rodent, and insect populations and migration patterns can impact the distribution of T. gondii due to their role as reservoir and vector.

[192] "G9a appears to be a critical control point for epigenetic regulation in NAc, as we know it functions in two negative feedback loops.

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).

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.