Toxoplasmosis is an infection caused by Toxoplasma gondii, a microscopic parasite found around the world. An estimated 30% to 50% of people have been exposed to it, though rates differ depending on local food habits and environmental conditions. The infection is mainly spread by eating undercooked meat, especially pork, lamb, or venison, coming into contact with cat feces, or from an infected pregnant mother to her fetus. People can also become infected by eating or drinking food or water contaminated with cat feces, particularly when hands are not washed properly. Cats are the main animals in which the parasite completes its life cycle, and humans commonly become infected while cleaning litter boxes or touching soil that contains the parasite’s eggs.
Most healthy people do not notice any symptoms, or they may develop mild, flu-like signs such as swollen lymph nodes, fever, headache, body aches, and tiredness. The infection can be much more serious in people with weakened immune systems, such as those with advanced HIV infection or those taking medications that suppress the immune system. In these cases, it can cause toxoplasmic encephalitis, a dangerous inflammation of the brain. When infection occurs during pregnancy, about 20% to 40% of fetuses may become infected, which can lead to miscarriage, stillbirth, smaller-than-normal head size, enlarged liver, or long-term problems with the brain and eyes.
Prevention focuses on reducing exposure to the parasite. Recommended measures include thoroughly cooking meat, washing hands and kitchen tools after handling raw meat, washing fruits and vegetables, and avoiding unpasteurized goat’s milk. Pregnant individuals and people with weakened immune systems should avoid cleaning cat litter when possible, or take precautions such as wearing gloves and washing hands afterward. Other preventive steps include wearing gloves while gardening and covering sandboxes to keep cats from contaminating them.
Causative Agent
Toxoplasma gondii is the organism responsible for causing toxoplasmosis. It is a single-celled protozoan parasite belonging to the phylum Apicomplexa, a group that includes other medically important parasites such as Plasmodium (which causes malaria). T. gondii is highly adaptable and has a broad host range, infecting nearly all warm-blooded animals, including humans, livestock, birds, and rodents. Despite this wide host spectrum, cats and other felines are the only definitive hosts, meaning they are the only animals in which the parasite undergoes sexual reproduction and produces environmentally resistant oocysts.
The life cycle of T. gondii is complex and consists of several developmental stages:
- Tachyzoites: These are the rapidly dividing forms responsible for acute infection. They spread throughout the host’s body via the bloodstream and are the stage most directly associated with early symptoms.
- Bradyzoites (Tissue Cysts): After the initial infection, tachyzoites convert to the slower-growing bradyzoite form, encasing themselves within tissue cysts. These cysts commonly persist in the brain, muscles, and eyes and can remain dormant for the lifetime of the host. Reactivation can occur if immunity weakens.
- Sporozoites (Inside Oocysts): Cats shed oocysts, a hardy, environmentally resistant stage, through their feces. Once in the environment, these oocysts mature and produce sporozoites capable of infecting new hosts. Mature oocysts can survive in soil and water for months to over a year, contributing to widespread environmental contamination.
Genetically, T. gondii is highly diverse. In many regions, particularly North America and Europe, three main clonal lineages (Types I, II, and III) dominate. However, in South America, strains are far more genetically varied and often more virulent, contributing to more severe disease presentations in those regions. This genetic diversity influences the parasite’s ability to cause disease, its likelihood of reactivation, and its severity in both immunocompetent and immunocompromised individuals.
Transmission Pathways
Toxoplasma gondii spreads through several well-characterized routes, reflecting the parasite’s flexible life cycle and ability to survive in various environments.
Foodborne Transmission
One of the most common pathways is the ingestion of undercooked or raw meat containing tissue cysts. Meats such as pork, lamb, goat, and venison are particularly associated with transmission. Improper food handling, cross-contamination in kitchens, and tasting meat before it is fully cooked can increase risk. Surveys in many countries show that meatborne transmission is a major source of human infection, especially in regions where consumption of raw or lightly cooked meat is common.
Environmental Exposure
Cats infected with T. gondii can shed millions of oocysts in a single day, and these oocysts become infectious after 1–5 days in the environment. They can persist in soil, sand, and freshwater for long periods. Humans may accidentally ingest oocysts by touching contaminated soil, such as through gardening, farming, playing in outdoor sandboxes, or cleaning areas where cats defecate, and then touching their mouth. Fresh produce grown in contaminated soil or irrigated with contaminated water can also carry oocysts if not washed thoroughly.
Waterborne Transmission
Waterborne outbreaks have been documented, including major incidents involving municipal water supplies. Oocysts washed into reservoirs or groundwater can remain infectious despite common water treatment processes. This route is particularly significant in areas with poor sanitation or heavy rainfall that increases runoff from contaminated soil.
Cat Feces and Domestic Exposure
Handling cat litter is a known risk factor, especially when litter boxes are not cleaned daily. Because oocysts require time to become infectious, daily cleaning reduces but does not eliminate risk. Stray and outdoor cats, who may hunt infected prey, contribute significantly to environmental contamination, even though domestic indoor cats fed commercial diets are less likely to shed oocysts.
Congenital Transmission
Congenital toxoplasmosis occurs when a pregnant individual acquires a new infection during pregnancy. The parasite can cross the placenta and infect the fetus. The risk of transmission increases as pregnancy progresses, but early-pregnancy infections often lead to more severe outcomes. Globally, congenital toxoplasmosis affects an estimated 190,000 infants per year, with risks ranging from miscarriage and stillbirth to lifelong impairments such as vision loss and neurological disabilities.
Less Common Routes
- Organ transplantation: Infection can be transmitted through organs containing tissue cysts, particularly in heart, liver, or kidney transplants. Immunosuppressed patients are at higher risk of severe disease following transmission.
- Blood transfusion: Transmission through blood is rare but possible, as tachyzoites can survive briefly in stored blood.
- Laboratory accidents: Laboratory personnel working with parasite cultures or infected animal tissues face occupational exposure risks.
Epidemiology of Toxoplasmosis
Toxoplasmosis shows substantial global variation in its distribution, with seroprevalence influenced by environmental conditions, cultural practices, and levels of sanitation. In many northern European and North American countries, fewer than 10% of the population shows evidence of prior infection. In contrast, prevalence exceeds 60% in parts of Latin America, West and Central Africa, and regions of continental Europe, where warmer climates, higher humidity, and greater environmental contamination support the long-term survival of Toxoplasma gondii oocysts. Food-related practices also play a major role; populations that commonly consume undercooked meat, particularly pork, lamb, or game, tend to have higher rates of infection. Soil and water contamination with oocysts is an additional contributor, especially in areas with large stray cat populations or inadequate waste management systems.
Risk factors for acquiring toxoplasmosis often overlap with local living conditions and occupations. Poor sanitation, limited access to clean water, and food-handling practices that allow cross-contamination significantly increase the likelihood of exposure. People who regularly work with animals or soil—such as farmers, gardeners, butchers, and veterinarians, experience higher exposure due to frequent contact with either infected animals or contaminated environments. Although most infections in healthy individuals remain asymptomatic, the widespread nature of the parasite makes toxoplasmosis a common lifelong infection, with potential health impacts if immunity later declines.
Pregnant individuals represent a particularly important high-risk group because new infection during pregnancy can lead to congenital toxoplasmosis. Globally, an estimated 190,000 infants are affected each year, with outcomes ranging from mild symptoms to severe complications such as neurological impairment or vision loss. For this reason, several countries, especially in Europe and parts of the Middle East, have implemented routine screening during pregnancy to identify acute infections early and reduce fetal risk. The effectiveness of such programs varies based on adherence, available treatment options, and public health infrastructure.
Individuals with weakened immune systems face a distinct set of risks, particularly those with advanced HIV infection, those receiving chemotherapy, or those taking immunosuppressive drugs following organ transplantation. In these populations, latent tissue cysts acquired earlier in life can reactivate, causing severe or life-threatening disease, including toxoplasmic encephalitis. This form of the illness accounts for a significant proportion of neurological complications among untreated HIV-positive individuals in regions where T. gondii exposure is common. Children in highly endemic areas may also exhibit higher infection rates due to frequent contact with contaminated soil, untreated water, or inadequately cooked foods, reflecting the intersection between environmental exposure and early-life vulnerability.
Symptoms and Clinical Manifestations
Toxoplasmosis presents with distinct symptoms depending on the stage and mode of infection. Manifestations vary significantly between acute, congenital, and chronic forms, each requiring specific recognition and management.
Acute Infection Signs
During acute infection, most immunocompetent individuals remain asymptomatic or exhibit mild flu-like symptoms. Common signs include fever, fatigue, headache, and muscle aches lasting from days to several weeks.
Lymphadenopathy, especially in the neck, is a hallmark feature. Some patients develop mild hepatitis or respiratory symptoms. In rare cases, severe presentations such as encephalitis or myocarditis can occur, especially in immunocompromised individuals.
Laboratory tests typically show elevated inflammatory markers and sometimes abnormal liver function tests. Early identification relies on clinical suspicion combined with serological testing.
Congenital Toxoplasmosis
Congenital toxoplasmosis results from transplacental transmission during maternal infection, often asymptomatic at birth. However, it may cause severe complications such as chorioretinitis, hydrocephalus, and intracranial calcifications.
Infants may present with jaundice, hepatosplenomegaly, seizures, or developmental delays. Ocular damage can lead to vision loss later in life, even if initially unnoticed.
Screening during pregnancy and prompt treatment significantly reduce the risk and severity. Diagnosis involves prenatal ultrasound and serologic assays in both mother and newborn.
Chronic Toxoplasmosis
In chronic toxoplasmosis, the parasite forms tissue cysts primarily in muscles and the brain, remaining dormant but potentially reactivating.
Most chronically infected immunocompetent individuals are asymptomatic. However, subtle neurological symptoms such as headaches or mood changes can occasionally appear.
In immunosuppressed patients, reactivation leads to toxoplasmic encephalitis, characterized by fever, confusion, seizures, and focal neurological deficits requiring immediate treatment.
Serological tests confirm past exposure but do not indicate active disease without clinical correlation.
Diagnosis of Toxoplasmosis
Serological testing allows clinicians to determine both the timing and likelihood of infection. Blood tests that detect Toxoplasma gondii-specific IgG and IgM antibodies are the most widely used. The presence of IgM antibodies typically signals a recent or acute infection, although these antibodies can occasionally persist for months, which may complicate interpretation. IgG antibodies, in contrast, indicate past exposure and can remain detectable for life, serving as evidence of chronic or latent infection. In some high-risk situations, such as pregnancy, specialized IgG avidity testing may be performed to help distinguish between recent infection and one that occurred months earlier, a crucial distinction because new infections during pregnancy pose a significant risk to fetal health.
Molecular testing has become increasingly important, particularly in complex or high-stakes cases. Polymerase chain reaction (PCR) can directly detect T. gondii DNA in blood, cerebrospinal fluid, or amniotic fluid, offering a method of confirming active infection even when antibody responses are unclear or absent. PCR is especially valuable in suspected congenital toxoplasmosis, where early identification can help prevent severe outcomes, and in immunocompromised individuals, whose weakened immune systems may fail to produce detectable antibodies. Although highly sensitive, PCR availability varies across regions, and test accuracy may depend on sample type and parasite load.
Several classic diagnostic tools exist but are used less frequently today. The Sabin–Feldman dye test, once considered the gold standard for detecting T. gondii antibodies, remains highly accurate but requires living parasites and specialized laboratory conditions, limiting its use to reference centers. Other serological assays, including indirect fluorescent antibody tests and enzyme-linked immunosorbent assays (ELISA), provide more practical alternatives and are widely available in clinical laboratories worldwide.
Imaging plays an essential role in diagnosing cases involving the brain or eyes, particularly among individuals with advanced immunosuppression. In suspected toxoplasmic encephalitis, magnetic resonance imaging (MRI) and computed tomography (CT) scans typically reveal multiple ring-enhancing lesions. These lesions often appear in deep brain regions such as the basal ganglia, thalamus, or at the junction between the cortex and underlying white matter. Although these findings strongly suggest toxoplasmosis in patients with compromised immune systems, such as those with untreated HIV/AIDS or post-transplant immunosuppression, they are not unique to the disease. Similar lesions can occur with primary brain tumors, metastases, bacterial abscesses, tuberculosis, or central nervous system lymphoma, making laboratory confirmation essential for accurate diagnosis.
Ocular toxoplasmosis is assessed primarily by fundoscopy, which can reveal active retinal inflammation or scars from prior infection. In severe or ambiguous cases, optical coherence tomography or fluorescein angiography may support diagnosis by providing detailed images of the retina and adjacent structures. As with central nervous system disease, ocular findings must be interpreted carefully, as conditions such as cytomegalovirus retinitis or syphilitic chorioretinitis may appear similar but require different treatments.
Treatment Options
Pharmacological Therapy
Pharmacological therapy typically centers on a combination of pyrimethamine and sulfadiazine, which work synergistically to inhibit the parasite’s folic acid metabolism. Because pyrimethamine can suppress bone marrow function, leucovorin (a folinic acid supplement) is routinely administered to protect against hematologic toxicity. Standard treatment courses last approximately four to six weeks, though longer durations may be required in cases with slow clinical response or in infections involving the central nervous system or the eyes. Patients are often monitored with blood tests during therapy to assess for bone marrow suppression, kidney function abnormalities, or allergic reactions. In severe disseminated disease, especially toxoplasmic encephalitis, initial therapy may need to be delivered intravenously to ensure adequate drug absorption and rapid parasite suppression. Repeat imaging, usually MRI, may be performed in severe cases to confirm radiologic improvement.
Alternative medications are available for individuals who cannot tolerate sulfonamides. Clindamycin is a common substitute for sulfadiazine, often paired with pyrimethamine and leucovorin. Atovaquone and azithromycin represent additional alternatives, although they are generally less effective than standard regimens and are used in cases of intolerance or limited drug availability. In certain situations, such as ocular toxoplasmosis, local therapies, including intravitreal injections of clindamycin or steroids, may be used alongside systemic treatment to achieve faster control of retinal inflammation. Treatment of ocular disease often requires long-term follow-up because recurrence is common, especially in the first year after an acute episode.
Treatment in Special Populations
Management in special populations requires tailored approaches due to the risks posed by both the infection and the medications used to treat it. For pregnant individuals, careful balance is needed to avoid fetal harm while minimizing the chance of congenital transmission. Spiramycin is the drug of choice during early pregnancy because it concentrates in the placenta and reduces the risk of the parasite crossing to the fetus; it is widely used in Europe as part of routine antenatal programs where screening for toxoplasmosis is implemented. If fetal infection is confirmed through amniocentesis or PCR testing, treatment is typically switched to pyrimethamine, sulfadiazine, and leucovorin after the first trimester, when the risk of teratogenic effects is lower. These cases require close collaboration between infectious disease specialists and obstetric teams to coordinate monitoring of maternal health, fetal growth, and treatment response.
Immunocompromised individuals, particularly people with advanced HIV infection, organ-transplant recipients, or those receiving chemotherapy, face a high risk of severe disease, prolonged illness, and relapse. In HIV-positive individuals, toxoplasmic encephalitis remains one of the most common opportunistic infections in regions where T. gondii exposure is prevalent. Standard therapy is similar to that used in immunocompetent hosts but is often extended for six weeks or longer, depending on clinical response and imaging findings. Following acute treatment, patients generally require lifelong suppressive therapy (secondary prophylaxis) with pyrimethamine, leucovorin, and either sulfadiazine or clindamycin until their immune system recovers, usually defined by a sustained increase in CD4 count above 200 cells/µL for at least three months. Organ-transplant recipients may require modified regimens depending on their graft function and drug interactions, and prophylaxis with medications such as trimethoprim–sulfamethoxazole is frequently used to prevent toxoplasmosis reactivation.
Supportive Care
Patients with neurological involvement may require anticonvulsant medications if seizures occur, and corticosteroids may be used when significant swelling or mass effect is present, although they must be administered cautiously to avoid diminishing immune control of the infection. Adequate hydration, correction of electrolyte imbalances, and nutritional support contribute to recovery, particularly in individuals with systemic disease or coexisting conditions that impair immune function. Visual disturbances or ocular pain in cases of retinal involvement may improve with anti-inflammatory therapy, but ophthalmologic monitoring is essential due to the risk of long-term vision impairment or recurrent lesions.
Prevention and Control
Proper practices reduce infection risk by limiting exposure to the parasite’s sources.
Food Safety Measures
Thorough food safety practices are among the most effective ways to prevent toxoplasmosis. Cooking meat to an internal temperature of at least 67°C (153°F) reliably destroys T. gondii tissue cysts, which may be present in pork, lamb, venison, and other meats. Using a food thermometer ensures accurate temperature readings, as visual cues such as color can be misleading. Freezing meat at −12°C (10°F) for several days further reduces infectivity, although this method may not eliminate all cysts in every type of tissue, so it should be paired with proper cooking.
Washing fruits and vegetables under running water removes soil, pesticide residue, and oocysts that may cling to the surface after contact with contaminated environments. Scrubbing firm produce such as potatoes, apples, or carrots provides additional protection. Preventing cross-contamination is equally essential: raw meat should be prepared on designated cutting boards, and knives or utensils used for raw products must be washed thoroughly before touching ready-to-eat foods. Kitchen surfaces should be disinfected regularly to avoid accidental spread.
Consuming only pasteurized dairy products prevents exposure to the parasite through unpasteurized milk, which may harbor infectious organisms. Pregnant women and immunocompromised individuals should exercise particular caution by strictly following food safety guidelines. Avoid high-risk foods altogether, such as raw meat dishes, unwashed produce, and unpasteurized dairy, to minimize the likelihood of infection.
Pet and Environmental Hygiene
Because cats are the definitive hosts for Toxoplasma gondii, understanding and managing cat-related risks is essential. Infected cats can shed millions of oocysts in their feces, and these oocysts become infectious after 1–5 days, meaning daily cleaning of litter boxes significantly reduces risk. Using gloves while handling litter and washing hands afterward helps prevent accidental ingestion. Pregnant individuals should ideally delegate litter box duties to someone else.
Gardening, farming, or any activity involving soil contact may expose individuals to oocysts deposited by outdoor cats. Wearing gloves during yard work and washing hands thoroughly afterward reduce environmental exposure. Avoiding direct contact with sandboxes or outdoor play areas frequented by animals is also important for young children.
Responsible cat ownership further reduces risk. Keeping cats indoors minimizes their chances of hunting infected rodents or birds, the primary source of infection for felines. Indoor cats fed commercial cat food or thoroughly cooked meat are far less likely to become infected, reducing household risk. Feeding cats raw or undercooked meat should be avoided, as it can introduce the parasite into the home environment.
Complications and Prognosis
Toxoplasmosis can lead to a range of complications depending on the patient’s immune status and stage of infection. Some individuals experience lasting effects that impact quality of life, while others recover fully.
Potential Long-Term Effects
In immunocompetent individuals, toxoplasmosis typically resolves without leaving permanent damage. Most people clear the acute infection with supportive care or no treatment at all, although the parasite remains latent within tissue cysts throughout life. In rare cases, however, neurological complications may persist. These include chronic headaches, reduced concentration, or subtle cognitive deficits. In a small number of patients, the infection can trigger seizures or contribute to long-standing neuroinflammatory changes.
Congenital toxoplasmosis, transmitted from mother to fetus when the mother becomes infected during pregnancy, is associated with the most serious long-term consequences. Infants may be asymptomatic at birth but develop complications months or years later as tissue cysts cause ongoing inflammation. Classic manifestations include hydrocephalus, chorioretinitis, intracranial calcifications, and global developmental delays. Chorioretinitis, the most common long-term issue, leads to recurring inflammation of the retina and choroid, often causing progressive visual impairment. Some children experience episodes of reactivation throughout childhood and adulthood, which can eventually result in partial or total vision loss if not properly managed.
In immunocompromised patients, particularly those with HIV/AIDS, organ transplant recipients, or individuals receiving long-term corticosteroid or chemotherapy treatment, toxoplasmosis poses a significant threat. Latent infections may reactivate due to weakened cellular immunity, leading to toxoplasmic encephalitis (TE)—a serious and sometimes fatal condition. TE causes brain lesions, seizures, hemiparesis, speech disturbances, and changes in mental status. Even with treatment, some patients experience chronic neurological dysfunction. Beyond the central nervous system, disseminated toxoplasmosis may affect the lungs, heart, and liver, causing pneumonitis, myocarditis, or hepatitis
Prognosis by Patient Group
The prognosis for immunocompetent adults is overwhelmingly positive. Most individuals recover fully, and long-term complications are rare. While antiparasitic therapy may be recommended for severe or prolonged symptoms, many mild cases resolve without medication. Once the acute infection is over, the parasite typically remains dormant and does not cause future clinical illness unless the person becomes immunocompromised later in life.
For pregnant women, the prognosis is more complex, as it depends on both maternal and fetal factors. Primary infection early in pregnancy carries the highest risk of severe fetal damage, even though the likelihood of transmission is lower during the first trimester. Infections acquired in later trimesters are more likely to be transmitted but usually result in milder fetal disease. Prenatal treatment with spiramycin or pyrimethamine-sulfadiazine (depending on gestational age) can reduce the severity of fetal infection, but some infants still develop neurological or visual impairments.
The prognosis for immunocompromised patients is generally poor without immediate treatment. Reactivation of latent toxoplasmosis in individuals with AIDS, for example, is a major cause of encephalitis and is associated with high morbidity and mortality. Combination therapy with pyrimethamine, sulfadiazine, and leucovorin is typically required, and treatment may need to be continued indefinitely to prevent relapse if immune reconstitution does not occur. Mortality rates increase significantly when toxoplasmosis becomes disseminated, affecting multiple organs or causing respiratory or cardiac failure.
Toxoplasmosis in Animals
Certain animals act as primary hosts, while others serve as reservoirs, influencing the pathogen’s spread across ecosystems.
Feline Hosts
Domestic cats and wild felids are the definitive hosts of Toxoplasma gondii, meaning they are the only animals in which the parasite undergoes sexual reproduction. After ingesting infected prey such as rodents or birds containing tissue cysts, cats develop intestinal infection that leads to the shedding of oocysts, the environmentally resistant stage of the parasite. These oocysts are extraordinarily durable, capable of surviving in soil, water, and vegetation for months to more than a year, particularly in moist or shaded environments. Once sporulated, they become highly infectious to other animals and humans.
Most adult cats do not exhibit noticeable symptoms, which contributes to the silent spread of the parasite. However, kittens and immunocompromised felines may develop severe clinical toxoplasmosis involving fever, pneumonia, hepatic inflammation, or neurological signs. This increased susceptibility stems from their underdeveloped or compromised immune systems. Following primary infection, cats typically shed oocysts for only 1–3 weeks, and although reinfection is possible, subsequent shedding episodes tend to be shorter and less intense. This limited shedding window makes early infection control, such as preventing cats from hunting, particularly effective.
Environmental contamination occurs primarily where domestic or feral cat populations are dense. Urban areas, farms, and wildlife-rich regions often have higher oocyst prevalence. Because a single infected cat can shed millions of oocysts, even short shedding periods can heavily contaminate ecosystems, posing risks to livestock, wildlife, and humans who come into contact with soil or water.
Other Animal Reservoirs
A vast range of warm-blooded intermediate hosts sustain the parasite’s presence in nature. Once animals such as sheep, pigs, goats, chickens, rodents, and even marine mammals ingest oocysts from the environment, the parasite transforms into tissue cysts that embed in muscles, the central nervous system, and various organs. These cysts remain viable for the animal’s lifetime and can be transmitted when predators, or humans, consume undercooked or raw tissue containing the parasite.
Livestock species play a particularly important role in foodborne transmission.
- Sheep and goats often acquire infection from grazing on contaminated pastures, which can result in fetal loss, weak newborns, or reduced productivity.
- Pigs, especially those raised outdoors or in free-range systems, are susceptible to infection through contact with soil or rodent-contaminated feed.
- Cattle appear more resistant to chronic infection, but occasional cases do occur.
- Poultry, including free-range chickens, frequently ingest oocysts while foraging and can harbor cysts in their muscle tissues.
Wildlife, including deer, koalas, sea otters, and various bird species, also contribute to the parasite’s ecological cycle. Oocysts washed into marine environments can infect sea mammals, and ingestion of contaminated vegetation exposes herbivores in natural habitats. These wildlife infections demonstrate how T. gondii can affect entire ecosystems, not merely domestic settings.