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drs. Jan Hooimeijer

04-12-2025 16:00

Toxoplasmosis – Guideline

Toxoplasmosis is an infection caused by the parasite Toxoplasma gondii. Infection can occur orally or through vertical transmission. After an incubation period of 10–23 days, the infection usually progresses without or with mild, atypical symptoms.

Toxoplasmosis – Guideline
Toxoplasmosis is an infection caused by the parasite Toxoplasma gondii. Infection can occur orally or through vertical transmission. After an incubation period of 10–23 days, the infection usually progresses without or with mild, atypical symptoms, with lymph node swelling being the most common. This guideline supports bird advisory practice in recognition, risk assessment, and prevention.

Below is a guideline explaining the issue.

Summary

  • Causative agent: Parasite Toxoplasma gondii
  • Route of infection: Oral, vertical, organ transplantation
  • Incubation period: 10-23 days
  • Infectious period: Not applicable. Measures: Prophylaxis as indicated
  • Symptoms: Congenital toxoplasmosis: symptoms depend on the trimester in which the woman was infected. Acquired toxoplasmosis: mostly none or only mild, atypical. Most common: lymphadenopathy.

Note: This guideline has expired. The information may be outdated. The guideline will be revised.

Disease & Contagiousness

  • Diagnosis
  • Risk Groups
  • Epidemiology
  • Prevention
  • Measures
  • Prophylaxis & Treatment
  • History

Version Control

Approved by the LOI in July 2009.
February 2019: This guideline is currently being revised.

Changes:

  • April 2018: Occupational Health and Safety sections added.
  • April 2014: Veterinary information added.

Disease & Contagiousness

Pathogen

Toxoplasma gondii is an obligate intracellular, protozoan parasite. The name refers to the arched shape of the parasite (toxon = arch). The parasite's developmental cycle consists of two parts: sexual and asexual.

The sexual cycle occurs exclusively in the cat or feline (the definitive host). The cat becomes infected by ingesting infectious oocytes or tissue cysts from prey animals. In the epithelial cells of the small intestine, the gametocytes develop into oocytes, which are then excreted into the environment via cat feces. The cat is the definitive host and produces oocytes for a maximum of two weeks. The oocytes only become infectious after a maturation phase (sporulation), which lasts about two to three days in a temperate climate such as the Netherlands. The oocytes are very resistant and can remain infectious for more than a year under warm and humid conditions. (Dub70)

The asexual cycle can occur in any cell type of the intermediate host (humans, but also a wide variety of animals), except in red blood cells. The active stage of the parasite is the tachyzoite. After ingestion, this tachyzoite is released from the oocyte or tissue cyst, invades the host cell, and divides intracellularly. The division process continues until the host cell ruptures. The released tachyzoites immediately invade new cells and begin dividing again. Through a mechanism not yet fully understood, this process is reversed after some time, and tissue cysts are formed. These contain bradyzoites, a much slower stage of the parasite with a very low metabolic rate and only a few divisions. The tissue cysts vary in size (up to 200 μm) and contain varying numbers of parasites, ranging from a few to 3,000 bradyzoites.

Pathogenesis
In humans, only the asexual cycle occurs. One to two weeks after infection, tissue cysts (containing bradyzoites) form. The cysts can be located and persist in any tissue, but the organs most commonly affected are the brain, retina, muscle tissue, and heart muscle. These tissue cysts are almost spherical and do not cause an inflammatory response in surrounding tissues. The number and location of the tissue cysts can vary, as can the damage they can cause.

A congenital infection occurs when a fetus is infected intrauterinely. This can lead to serious consequences, especially if the infection occurs during the first three months of pregnancy. In that case, an adequate immune response does not occur, and the infection is not controlled.

Toxoplasma was long believed to have little interspecific variation, despite the fact that the parasite was found in many animal species. However, molecular techniques have revealed the existence of multiple strains of the parasite, which are morphologically identical but differ in virulence in mice. (Sae05) In Europe and North America, three distinct clonal lineages (type I, II, and III) predominate, with type II strains predominating. (Ajz06, Leh06, Dar08) In Brazil, all types occur, but also many atypical strains. (Val05, Kha06) Type I and atypical Toxoplasma strains are associated with more severe ocular toxoplasmosis compared to type II strains. This may explain the much more severe course of toxoplasmosis in Brazil.

Incubation PeriodThe incubation period is 10 to 23 days.

Pregnancy

Congenital toxoplasmosis
Only if a woman comes into contact with Toxoplasma for the first time during pregnancy and becomes infected (primary infection) is there a risk of congenital toxoplasmosis. The risk of transmission increases with gestation, from approximately 6% at 10 weeks to over 80% at 38 weeks. (Dun99) The clinical symptoms of congenital infection depend strongly on the trimester in which the mother became infected. If the child is infected in the first trimester, the damage is greatest, with a high risk of serious pathology. This can include hydrocephalus, cerebral calcifications, intellectual disability, microcephaly, eye abnormalities, and deafness.

Some of these pregnancies will end prematurely due to intrauterine fetal death (spontaneous abortion). Infection in the second and third trimesters of pregnancy reduces the risk of harm to the fetus. If infection occurs in the last three months of pregnancy, the child may be born with clinical symptoms of toxoplasmosis: fever, rash, thrombocytopenia, anemia, liver and spleen enlargement, or eye infection. Most children (>60%) are born without symptoms of toxoplasmosis (Dun99, Gra05). How many of them will eventually develop symptoms and to what extent this can be prevented with therapy remains unclear. Damage to the eyes from choreoretinitis occurs primarily after 15-20 years of age (Kop92). There appears to be a significant difference in the occurrence of ocular abnormalities in Brazil compared to Europe. In Brazil, Children have more lesions, these are larger, more often multiple and they more often cause visual disturbances. (Gil08)

Available data from the Netherlands indicate that a large proportion (80%) of congenitally infected untreated children develop eye problems with visual impairment and blindness after 18 years of age (Loe85, Kop92). In a large European study (European Multicenter Study of Congenital Toxoplasmosis EMSCOT), in which most children were treated, one or more ocular lesions were found in 17% of children after a median follow-up time of 4.8 years. Of the children with choreoretinitis, 9% had severely impaired bilateral vision. (Hoo07)

Symptoms of the disease

Acquired toxoplasmosis
The majority of acquired infections are benign. There are no or only mild, atypical symptoms that are often poorly recognized. The most common symptom is lymphadenopathy, particularly of the lymph nodes in the neck. Other symptoms may include fever, general malaise, eye infection, liver and spleen enlargement, and skin rash. Sometimes symptoms occur as a result of encephalitis, pneumonia, or myositis. Only a small percentage of patients with a primary infection will develop a serious manifestation of the disease. (McCa87) Once acquired, an infection persists for the rest of a person's life. Tissue cysts remain, providing continued antigenic stimulation that maintains antibody production. These cysts can persist in many tissues. Normally, in an immunocompetent person, a latent infection will not flare up or cause symptoms. With ocular toxoplasmosis, however, this is often the case, namely in 2.7-29% of cases, depending on the time elapsed since the infection. (Holl 08)

With immunosuppression, a latent infection can resurface and cause serious pathologies such as encephalitis with behavioral changes and headaches, but also myocarditis, pneumonia, hepatitis, and eye infections. This is the case, for example, in patients with HIV or AIDS, cancer, and transplant recipients after long-term immunosuppressive therapy. Without prophylaxis, toxoplasmosis would be a significant cause of death in immunocompromised patients.

Acquired ocular toxoplasmosis is more common than previously thought and is certainly not limited to immunocompromised individuals. (Gil99, Sta06) During primary acquired infection, ocular toxoplasmosis often remains subclinical, resulting in individuals often not seeking medical attention or reporting only vague clinical symptoms (e.g., fatigue); eye problems usually develop later. Despite therapy, 25% of people with ocular toxoplasmosis develop blindness or low vision. (Bos02)

In recent years, evidence has emerged that Toxoplasma infection is associated with changes in personality traits (Fle96), decreased IQ (Fle03), and reduced psychomotor performance. (Hav01)

In French Guiana and Suriname, a severe form of toxoplasmosis has been observed for several years now, with a completely different clinical picture than elsewhere in the world, namely fever and lung problems (acute respiratory distress syndrome, ARDS). There appears to be a link to eating undercooked meat from rainforest animals. (Dem07)

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Symptoms related to work
The majority of acquired infections are benign, with no or only mild symptoms (which are often not properly recognized). Only a small percentage will develop into a serious illness with temporarily reduced work capacity..

Veterinary

Signs of Disease in Animals
In cats, primary infection with T. gondii is asymptomatic. Young animals or cats infected with FeLV or FIV cannot always control the spread of tachyzoites. Symptoms such as fever, anorexia, and lethargy may be observed. When tachyzoites affect the central nervous system, eyes, or lungs, symptoms such as ataxia, blindness, or pneumonia may occur. In sheep and goats (intermediate hosts), infection can lead to abortion in the last month of pregnancy, the birth of weak or dead lambs, encephalitis, and eye abnormalities (Tenter, 2000).

Natural Immunity
After a primary infection, lifelong immunity develops based on pre-immunity, that is, as long as a latent infection persists. In immunocompromised individuals, a latent infection can resurface and cause severe symptoms.

Veterinary

Natural immunity in animals
Although cats generally shed oocytes once after an initial infection, in rare cases a second infection can lead to further oocyte shedding (Dubey 1995). When the immune system is suppressed, such as after infection with feline immunodeficiency virus (FVD) or FeLV (feline leukemia virus), cats can shed oocytes again even without reinfection (Lappin 1994).

Reservoir
 Cats and felids (including lions, cougars, etc.) are the definitive hosts and produce oocytes. All warm-blooded animals that come into contact with oocyte-containing feces can develop tissue cysts and serve as reservoirs (so-called intermediate hosts).

Route of infection

Transmission to humans can occur by:

  • Ingestion of tissue cysts present in undercooked meat or uncooked processed meats (cured ham, salami);
  • Ingestion of oocytes excreted in feces by infected cats: from the litter box, from the fecal-contaminated environment, either directly, for example, through hands during gardening, or with vegetables or water;
  • In utero transmission from the primarily infected pregnant woman (vertical transmission);
  • Transplantation of organs containing tissue cysts (very rarely via blood products).

Cats defecate in the environment in a variety of places and generally hide their feces. This can also occur in sandboxes, planters, and gardens. Even a well-covered outdoor sandbox can contain cat feces. (Jan93) It is unknown whether sandboxes containing infectious oocytes play a role in the transmission of Toxoplasma.

In animals that serve as food sources for humans, tissue cysts are primarily found in pigs, sheep, and goats. They are less common in chickens, rabbits, horses, pigeons, and hares. Although tissue cysts are believed to develop less frequently in cattle, recent research indicates that beef can be an important source for humans (Opsteegh et al., 2011). Contaminated shellfish and crustaceans can serve as a source of infection for both marine mammals and humans (Conrad et al., 2005, Jones et al., 2009)..

Contagious period

Not applicable.

Relevant transmission routes in animals
Cats become infected by ingesting tissue cysts in prey or meat (offal). Cats can also become infected with tachyzoates congenitally (via milk or transplacentally). Although cats are less susceptible, they can become infected by ingesting infectious oocytes. Intermediate hosts such as cows or sheep can become infected when grazing on oocyte-infested pasture where cats defecate. Intermediate hosts do not infect each other.

However, a cat is not required to maintain the asexual cycle: pigs can become infected by eating dead rodents with tissue cysts, and vertical transmission (transplacental or via milk) can occur in sheep, goats, and rodents (Duncansona, 2001). In sheep, T. gondii can also be sexually transmitted from rams to ewe (sheep) (Lopes, 2013).

BContagiousness
Humans are not directly infectious to their environment. The infection can be transmitted from person to person through the transplantation of organs containing tissue cysts..

Freshly shed oocytes are not immediately infectious. They sporulate after 1 to 24 days. They survive for extended periods (>1 year) in the environment, and thrive best in moist conditions and moderate temperatures.

Veterinary

Infectious period in animals
The cat sheds large quantities of oocytes intermittently for 3 to 10 days after infection and continues for 1 to 3 weeks. Primary infection usually occurs in young cats when they are just starting to go outdoors and hunt. Initially, it was thought that cats would no longer shed oocytes after reinfection. Laboratory studies show that cats experimentally infected at a young age can still shed oocytes if they are re-exposed to the parasite years later (Dub95), or when their immune system is compromised (old age, Feline Immunodeficiency Virus, Feline Leukemia Virus). Such cats may show signs of illness, but they do not shed oocytes at that time (incubation period 21 days, oocytes are shed as early as 3 to 10 days after ingestion of tissue cysts).

In species other than felines, tissue cysts develop one week after ingestion of oocytes. These are immediately infectious and can persist for life in heart, muscle, and brain tissue. In the event of abortion or birth in an infected sheep or goat, tachyzoites can be released in birth products and vaginal discharge (up to 3 weeks postpartum).

Diagnostics

In cooperation with the NVMM.
See also the Diagnostic Vademecum Toxoplasma gondii.

Microbiological diagnostics
The diagnosis of toxoplasmosis is divided into two parts: demonstrating the infection in mostly symptomatic patients and screening patients (immunocompromised individuals and pregnant women).

Serologie
 If toxoplasmosis is suspected, serological testing—that is, the detection of IgG, IgM, and IgA antibodies—is usually sufficient. Many serological methods are available, such as the classic Sabin-Feldman test, immunofluorescence, ELISA, and immunoblot.

The appearance of antibodies in a previously seronegative individual (seroconversion) indicates that the infection occurred in the intervening period. The presence of specific IgM or IgA antibodies can support the diagnosis of a recent infection. It should be emphasized that IgM determinations are not suitable for diagnosing recent infections because IgM remains detectable for a long time, in a significant proportion even up to two years after seroconversion. (Gra04) In practice, when there is a genuine suspicion, a second serum sample should be analyzed to confirm seroconversion or a significant increase in titer.

If it is important to understand the duration of the infection, IgG avidity can be determined. At the beginning of an infection, avidity is low and increases over the course of the infection. (Sen06) With high avidity, the infection has persisted for at least four months. The advantage is that a single serum can be used to determine the likelihood of an older infection. This quickly clarifies the situation for most patients. However, this method has several limitations. For example, some patients do not develop high-avid antibodies: these patients are therefore wrongly suspected of having a recent infection. Furthermore, the method is not useful for low IgG titers (<10 U). It is also important to note that pregnancy and treatment with spiramycin influence the development of avidity. (Lef06, Lef07)

M Molecular techniques
Besides serology, it is also possible to detect parasite DNA. (Con91, Coz98, Wal99, Rom01, Tha05) PCR (polymerase chain reaction) can detect Toxoplasma DNA in amniotic fluid, placenta, tissue biopsies, cerebrospinal fluid, ocular fluid, and blood. This allows detection of a resurgence of a latent infection in immunocompromised individuals and the presence of an intrauterine infection in pregnant women.

Cultivation
The parasite can be cultured using mouse inoculation or tissue culture. The use of these methods has decreased dramatically due to the use of the PCR method.

Diagnosis of congenital infection in the mother
If there is a clinical suspicion of toxoplasmosis during pregnancy, for example, due to abnormalities in the child, serodiagnosis is performed first. IgG and IgM antibodies directed against Toxoplasma are determined, possibly supplemented with an IgG avidity test. If there is a high level of suspicion (seroconversion or a significant titer increase (>4-fold) or low avidity), amniocentesis using molecular methods is the next step. Amniotic fluid must be collected before starting therapy because medication can negatively affect the sensitivity of the PCR..

Diagnosis of congenital infection in the child
Blood samples are taken from both mother and child at birth. If there is a strong suspicion, serology should be repeated in the child after 10 days and then every 3 months until the child becomes completely negative. In a neonate, infection can be detected by examining the various immunoglobulin subclasses and differences in IgG patterns between mother and child (Western immunoblotting). If IgM and/or IgA antibodies directed against T. gondii are detectable in a newborn, this indicates a congenital infection, as these immunoglobulins cannot cross the placenta. (Wal99) However, production may be very low or delayed, so a negative result does not rule out infection. (Gil07) IgG antibodies are transmitted from mother to child. If the child (in the absence of therapy) becomes seronegative during the first year of life, a congenital infection is ruled out.

Serodiagnosis of ocular toxoplasmosis
Serology and aqueous fluid analysis (PCR and antibody determinations on paired blood and ocular fluid samples) are important for confirming ocular toxoplasmosis. (Gro06) In reactivation of ocular toxoplasmosis, serology is of little value. Serology is also not very informative for diagnosing eye infection in HIV/AIDS patients and severely immunosuppressed transplant recipients.

Screening
For a screening question (has the patient ever had contact with T. gondii before), determining IgG antibodies is usually sufficient. An IgM test is not suitable for screening during pregnancy due to the possible persistence of IgM antibodies. There is no consensus on how to handle a pregnant woman who has had contact with cats or other exposures and has no symptoms. The chance of infection occurring during a single contact or risky behavior is very small. In these situations, counseling on how to avoid risky behavior and reassure the patient is often preferable to serodiagnosis..

Non-microbiological diagnostics

Diagnosis of ocular toxoplasmosis
Ocular toxoplasmosis presents with chorioretinal lesions, and the diagnosis can be suspected based on clinical eye symptoms. In (newborn) children, the diagnosis is often delayed because they cannot verbalize their eye symptoms, and parents only raise the alarm when visual impairment or blindness occurs. A definitive diagnosis cannot be made based on clinical symptoms. (Sta02)

Veterinary

Diagnostics in animals
In cats, fecal testing to detect Toxoplasma eggs is not straightforward. Cats only shed oocytes intermittently for 1 to 3 weeks, and these ova are visually indistinguishable from coccidia such as Hammondia, Isospora, and Besnoitia. A positive serology result in a cat proves that the cat has had contact with the parasite at some point in its life, but a negative result does not guarantee that it is Toxoplasma-free. Determining IgG or IgM in cats is not useful for assessing individual risk, as most cats only seroconvert after oocyte shedding has stopped.

The RIVM can detect Toxoplasma in animals using PCR techniques. This is not done for routine diagnostics..

Risk groups

Increased risk of infection
Owning a cat or working in a slaughterhouse or veterinary practice (with cats) does not pose an increased risk (Kortbeek, 2004) (Shuhaiber, 2003). Meat processing is, however, indicated as a risk factor (Jones, 2009).

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Work-related risk groups
High-risk occupations

High-risk occupations include:

  • Laboratory workers when working specifically with the toxoplasma parasite and when using it on laboratory animals (e.g., needlestick injuries) (1,2);
  • Green or ground workers and employees who professionally clean cat litter boxes (e.g., animal shelters, home care);
  • Veterinarians and other persons working with small ruminants (especially pregnancy products);
  • Veterinarians and other persons working with cats when in contact with older cat feces (2,3,7);
  • Employees in slaughterhouses, meat processors (6), and butchers in butcher shops have a very low risk of transmission if they receive proper training, apply basic hygiene measures, and use personal protective equipment correctly (4,5,7); this also applies to employees in green waste processing.

Medically vulnerable employees
This group consists of pregnant women* (the risk of a serious course is high in the case of intrauterine infection early in pregnancy) and immunocompromised people (transplant patients, HIV or AIDS patients or those receiving immunosuppressive therapy)..

The Working Conditions Decree (Article 4.109) states that 'pregnant employees are prohibited from performing work in which they may be exposed to the toxoplasma parasite unless it has been proven that they are immune to it'..

Increased risk of a serious course
In immunocompromised individuals such as transplant patients and HIV or AIDS patients, the risk of a serious course is also high..

Pregnancy

Intrauterine infections
Intrauterine infections that occur early in pregnancy have a high chance of a serious course.

Epidemiology

Distribution in the world
Toxoplasmosis occurs everywhere in the world where cats or felines are present.

Seroprevalence in the Netherlands
The seroprevalence of the Dutch population increases with age, from 17.5% in people under 20 years of age to over 70% in people over 65 years of age. The average seroprevalence for the Dutch population was 40.5% in 1996, but this appears to have declined in recent decades. (Kortbeek 2004)

Arbo

Reports of occupational infections
The Netherlands Centre for Occupational Diseases (NCvB) received two reports (in 2003 and 2007) of occupational toxoplasmosis infections. This tells us little about occupationally acquired cases; the NCvB is experiencing underreporting, and the infection is often not properly recognized..

Veterinary

Seroprevalence in animals in the Netherlands
In the Netherlands, a seroprevalence of 20% was found in cats in 2007. Hunting and feeding raw meat are risk factors (Opsteegh et al. 2011)..

Prevention

Immunization
There is no vaccine for human use.

Veterinary

Immunization in animals
There is no vaccine for cats. There is a vaccine (Toxovax®) for sheep to prevent abortion, but it may not prevent the development of tissue cysts caused by field variants. This vaccine is rarely used in the Netherlands, despite its effectiveness against abortion. Due to the presence of live parasites, the vaccine may pose a risk of infection to humans.

General preventive measures

Preventing ingestion of oocytes by:

  • Wear gloves when gardening and working with soil;
  • Wash fruits and vegetables thoroughly before eating;
  • Clean the cat litter box daily (to prevent sporulation of oocytes). For pregnant women: wear gloves or have someone else do it.
  • Cook meat thoroughly and do not eat raw meat such as steak tartare or beef sausage. The tissue cysts in meat are not destroyed at normal refrigeration temperatures. At a temperature of 56°C for 10-15 minutes, the cysts lose their viability. Freezing (20°C) of edible meat is effective in inactivating the product, provided it is long enough to reach a sufficiently low temperature throughout the product; (kijl08)
  • Wash hands after handling raw meat;
  • Clean surfaces and utensils that have come into contact with raw meat;
  • Freeze meat (for at least 1 week at – 20°C).
    • `

Preventing ingestion of vital tissue cysts by: Determining the immune status of the donor and recipient with regard to toxoplasmosis at the time of transplantation.

Pregnancy

Prevention in pregnant women

  • See general preventive measures above.
  • See also the brochure "Pregnancy and Infections."
  • See also the page on toxoplasmosis and pregnancy with information for professionals.

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Preventive measures at work

  • Repeated information should be provided, starting upon employment, regarding the risk of exposure, the route of transmission, and the symptoms. The importance of general hygiene, environmental cleaning, and protective measures (particularly wearing gloves) should also be repeatedly emphasized. This is particularly important for medically vulnerable workers and should be supervised (1).
  • Employers in high-risk positions must have a broadly supported Pregnancy Policy. This policy must specify how information is provided, how employees of childbearing age/immunocompromised employees have access to the occupational health physician's office, and for whom and how testing for protection (previous toxoplasmosis) is organized. Adjust the work activities for seronegative pregnant women in high-risk occupations (8).

See also the general preventive measures mentioned above.

Disinfection
According to standard methods of cleaning, disinfection and sterilization.

Measures

Notification obligation
Geen.

Involving other agencies
Not necessary.

Source tracing
Not applicable.

Contact investigation
Not applicable.

Measures regarding patient and contacts
Not applicable.

Arbo

Reporting as an occupational disease
If the disease was (probably) contracted during the course of a professional career, this must be reported to the Dutch Centre for Occupational Diseases (www.beroepsziekten.nl).

Prevention from work, school or daycare
Rejection is not useful from a public health perspective.

Arbo

Work exclusion
Humans are not infectious to their environment, so work exclusion is pointless.

Prophylaxis & Treatment

Prophylaxis
For all seropositive patients with fewer than 100–200 CD4 cells/mm³ and IgG antibodies against toxoplasmosis, prophylaxis with co-trimoxazole is recommended. The healthcare provider determines the need for prophylaxis in a positive organ donor and a negative recipient.

Treatment
Treatment with pyrimethamine, sulfonamides, and spiramycin can kill the tachyzoites (which occur during the acute phase of infection), but the bradyzoites in the tissue cysts remain viable. Spiramycin has been withdrawn from the market in the Netherlands since 2005. No data from randomized, controlled trials of this therapy are available.

For treatment, see the guidelines of the Dutch Working Group on Antibiotic Policy (SWAB): http://www.swabid.nl/therapie.

For treatment, see the guidelines of the Dutch Working Group on Antibiotic Policy (SWAB): http://www.swabid.nl/theraongenitale toxoplasmose
The medication for congenital toxoplasmosis consists of pyrimethamine, sulfadiazine, folinic acid, and spiramycin. It is still unclear how many congenitally infected patients still develop symptoms after therapy. Therapeutic studies are still too short (<10 years) to provide clarity about the long-term effect on ocular lesions.pie.

A systematic review (SYROCOT: Systematic Review on Congenital Toxoplasmosis) found that prenatal treatment of T. gondii infection has little effect on transmission, regardless of the timing of treatment. However, early treatment does appear to have a clear effect on the onset of symptoms (Syr07).

Ocular Toxoplasmosis
There is no known therapy that cures an ocular Toxoplasma infection. (Sta03) Treatment is aimed at reducing damage to the eye and limiting visual impairment and blindness. It has been shown that treatment with antiparasitic agents for several weeks can limit damage to the eye. Treatment with anti-inflammatory agents can also prevent complications of the inflammatory process in the eye. (Rot93, Bos02) Instituting continuous therapy can reduce the number of recurrences. (Sil02)

Veterinary

Treatment in animals
Cats are not treated.

History

Toxoplasmosis is caused by the protozoan Toxoplasma (T.) gondii and is one of the most common parasitic zoonoses worldwide. The first T. gondii infection was described in a rodent in 1908, and the first human infection was described in 1923. It was not until 1937 that T. gondii was associated with a congenital infection in humans. (Wol39) Gradually it became clear that a large number of animal species could act as hosts. At the end of the 1960s, it was discovered that felines excrete oocytes and could be considered definitive hosts. (Fre70) Only then was the cycle fully described.

Toxoplasmosis consists of a wide range of clinical manifestations and can be divided into congenital toxoplasmosis and acquired toxoplasmosis.

Literature

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