Toxoplasmosis – Guideline (R.I.V.M.)
Toxoplasmosis is an infection caused by the parasite Toxoplasma gondii. Toxoplasmosis is spread worldwide exclusively through cats. It is one of the most common zoonoses worldwide. A zoonosis is a disease that spreads to humans from animals. Stray cats spread this parasite through their feces. Toxoplasmosis can cause serious symptoms in humans. Miscarriages and congenital (brain) abnormalities in babies are the most well-known serious complications.Blindness, personality disorders and a greater risk of developing schizophrenia have also been described. There is a lot of unknowns. As also described in the guideline, doctors rarely consider the possibility of a Toxoplasma infection, which means that the diagnosis is made far too rarely.
It is known that Toxoplasmosis, spread through cats, is also a major problem in wildlife worldwide. Toxoplasmosis is a known cause of death in squirrels in the Netherlands, but also in the Californian sea otter and many bird species. Infection can occur orally (through the mouth) or through vertical transmission (from the mother to the unborn child). After an incubation period of 10-23 days, the infection usually progresses without or with mild atypical symptoms. It is an important responsibility of cat owners to prevent the spread of Toxoplasmosis.
Below is a guideline that explains the problem.
Summary
- Causative agent: Parasite Toxoplasma gondii
- Route of infection: Oral, vertical, organ transplantation
- Incubation period: 10-23 days
- Contagious period: Not applicable Measures: Prophylaxis when indicated
- Symptoms: Congenital toxoplasmosis: symptoms depend on the trimester in which a woman became infected. Acquired toxoplasmosis: most none or only mild, atypical. Most common: lymphadenopathy.
Please note: the validity period of this guideline has expired. The information may be outdated. The directive will be revised.
Illness & Contagiousness
- Diagnostics
- Risk groups
- Epidemiology
- Prevention
- Measures
- Prophylaxis & Treatment
- History
Version control
Adopted LOI July 2009.
February 2019: this guideline is currently under review.
Changes:
- April 2018: health and safety paragraphs added.
- April 2014: veterinary information added
Illness & Contagiousness
Cause
Toxoplasma gondii is an obligate intracellular single-celled parasite. The name refers to the arcuate shape of the parasite (toxon = arc). The development cycle of the parasite consists of two parts: sexual and asexual.
The sexual cycle takes place exclusively in the cat or feline (= final host). The cat becomes infected by ingestion of infectious oöcysts or tissue cysts from prey animals. In the epithelial cells of the small intestine, the gametocytes develop into oöcysts, which end up in the environment via the cat feces. The cat is the definitive host and produces oöcysts for a maximum of 2 weeks. The oöcysts are only infectious after a maturation phase (sporulation); This lasts about 2 to 3 days in a temperate climate such as in the Netherlands. The oöcysts are very resistant and can remain infectious for more than a year under warm and humid conditions. (Dub70).
The asexual cycle can take place in any type of cell 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 tachyzoet. After ingestion, it is released from the oöcyst or from the tissue cyst, penetrates the host cell and divides intracellularly. The division process continues until the host cell bursts. The released tachyzoans immediately enter new cells and start dividing again. Due to a mechanism that is not yet fully understood, this process reverses after some time and tissue cysts develop. These contain bradyzoans, i.e. a much slower stage of the parasite with a very low metabolic rate and only little division. The tissue cysts vary in size (up to 200 μm) and contain varying numbers of parasites, ranging from a few to 3000 bradyzoans.
Pathogenesis
In humans, only the asexual cycle takes place. One to 2 weeks after infection, the formation of tissue cysts (containing bradyzoans) occurs. 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 nearly round and do not cause an inflammatory response in the 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 in the first 3 months of pregnancy. Then an adequate immune response will not occur and the infection will not be contained.
It was long assumed that Toxoplasma had little mutual variation, despite the fact that the parasite was found in many animal species. However, through the application of molecular techniques, several strains of the parasite appear to exist, which are morphologically identical but differ in virulence in mice. (Sae05) In Europe and North America there are mainly three separate clonal lineages (type I, II and III), with type II strains predominating. (Ajz06, Leh06, Dar08) In Brazil; all types occur, but also many atypical strains. (Val05, Kha06) Type I strains and atypical Toxoplasma strains are associated with more severe ocular toxoplasmosis, compared to type II strains. This may explain the much more serious course of toxoplasmosis in Brazil.
Incubation period
The 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 contracts an infection (primary infection), is there a risk of congenital toxoplasmosis. The risk of transmission increases with the duration of pregnancy from approximately 6% at 10 weeks to more than 80% at 38 weeks. (Dun99) The clinical symptoms of congenital infection are highly dependent on the trimester in which the mother became infected. When the child is infected in the first trimester, the damage is greatest, with a high risk of serious pathology. Hydrocephalus, cerebral calcification, mental retardation, microcephaly, eye abnormalities and deafness may occur.
Some of these pregnancies will end prematurely due to intrauterine death (spontaneous abortion). If an infection occurs in the second and third trimester of pregnancy, the risk of damage to the child is smaller. If an infection occurs in the last 3 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). It is still not clear how many of them will eventually develop symptoms and to what extent this can be prevented by therapy. The damage to the eyes due to choreoretinitis mainly occurs after 15-20 years. (Kop92) There appears to be a significant difference in the occurrence of ocular abnormalities in Brazil; compared to Europe. In Brazil; children have lesions more often, these are larger, more often multiple and they more often cause visual disturbances. (Gil08)
The available data from the Netherlands indicate that a large proportion (80%) of congenitally infected untreated children develop eye problems with vision loss and blindness after the age of 18. (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 not well recognized. The most common symptom is lymphadenopathy, especially of the lymph nodes in the neck. Other symptoms may include fever, general malaise, eye infection, liver and spleen enlargement and rash. Sometimes symptoms occur as a result of encephalitis, pneumonia or myositis. Only a small proportion of patients with a primary infection will develop a serious manifestation of the disease. (McCa87) An infection once acquired persists for the rest of life. Tissue cysts remain present with continuous antigenic stimulation that maintains antibody production. The cysts can persist in many tissues. Normally, in an immunocompetent person, a latent infection will not flare up or lead to symptoms. However, this is often the case with ocular toxoplasmosis, namely in 2.7-29% of cases, depending on the time that has passed since the infection. (Holl 08)
With immunosuppression, a latent infection can flare up and cause serious pathology such as encephalitis with symptoms such as behavioral changes and headache, but also myocarditis, pneumonia, hepatitis and eye infection. This is, for example, the case in patients with HIV or AIDS, cancer and transplant patients after long-term immunosuppressive therapy. Without prophylaxis therapy, toxoplasmosis would be a major cause of death in immunocompetent patients.
Acquired ocular toxoplasmosis is more common than initially thought and is certainly not limited to immunocompetent individuals. (Gil99, Sta06) During the primary infection, ocular toxoplasmosis often progresses subclinically, with the result that people often do not go to the doctor or only report vague clinical symptoms (e.g. fatigue); the eye problems usually come later. Despite therapy, 25% of people with ocular toxoplasmosis develop a blind or visually impaired eye. (Bos02)
In recent years, indications have been found that Toxoplasma infection is associated with a change in personality characteristics (Fle96), a reduced IQ (Fle03) and reduced psychomotor ability. (Hav01)
A serious form of toxoplasmosis has been seen in French Guiana and Suriname for a number of years, 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 relationship with eating undercooked meat from jungle 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 proportion will have a serious manifestation with temporarily reduced employability at work.
Veterinary
Symptoms in animals
In cats, a primary infection with T. gondii is without symptoms. Young animals or cats with FeLV or FIV infection cannot always prevent the spread of tachyzoans. Symptoms of illness such as fever, anorexia and lethargy can then be seen. When tachyzoans 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, birth of weak or dead lambs, encephalitis and eye abnormalities (Tenter, 2000).
Natural immunity
After a primary infection, lifelong immunity arises that is based on pre-immunity, that is, as long as there is a continuous latent infection. In immunocompetent individuals, a latent infection may flare up and cause severe symptoms.
Veterinary
Natural immunity in animals
Although cats generally excrete oöcysts once after a first infection, in special cases a second infection can lead to new excretion of oöcysts. (Dubey 1995). When the immune system is suppressed, such as after infection with the Feline Immunodeficiency Virus or the FeLV (Feline Leukemia Virus), cats can also excrete oöcysts again without reinfection (Lappin 1994).
Reservoir
Cats and felines (including lions, pumas, etc.) are definitive hosts and produce oöcysts. All warm-blooded animals that come into contact with cyst-containing cat feces can develop tissue cysts and serve as reservoirs (so-called intermediate hosts).
Contamination path
Transmission to humans can occur through:
- Ingestion of tissue cysts present in undercooked meat, or in unheated meat products (raw ham, salami);
- Ingestion of oöcysts excreted by infected cats with feces: from the litter box, from the environment contaminated with cat feces, either directly, for example during gardening, via the hands, or with vegetables or via water;
- Infection in utero from the primary infected pregnant woman (vertical transmission);
- Transplantation of organs containing tissue cysts (very exceptionally via blood products).
Cats defecate in the environment in a variety of places and generally hide their feces. This can also be the case in sandboxes, planters and gardens. A well-covered sandbox outside can also contain cat feces. (Jan93) It is not known whether sandboxes with infectious oöcysts play a role in the transmission of Toxoplasma.
In animals that act as a food source for humans, tissue cysts are mainly found in pigs, sheep and goats. To a lesser extent in chicken, rabbit, horse, pigeon, hare. Although cattle are thought to develop tissue cysts less frequently, recent research shows that beef may 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 eating tissue cysts in prey or meat (waste). Cats can also be infected congenitally (via milk or transplacental) with tachyzoan food. Although cats are less susceptible, they can be infected by oral ingestion of infectious ocysts. Intermediate hosts such as cows or sheep can be infected when grazing on pasture infected with ocysts, where cats defecate. Intermediate hosts do not infect each other further.
However, a cat does not need to be present to maintain the non-sexual cycle: pigs can infect themselves by eating dead rodents with tissue cysts, and vertical infection (transplacental or via milk) can also occur in sheep, goats and rodents (Duncansona, 2001). In sheep, T. gondii can also be sexually transmitted from ram to ewe (sheep) (Lopes, 2013).
Binfectiousness
Man is not directly infectious to his environment. The infection can be transmitted from person to person through transplantation of organs containing tissue cysts.
Freshly excreted oöcysts are not directly infectious. After 1 to 24 days the oöcysts have sporulated. The oöcysts survive for a long time (> 1 year) in the environment, and best in moist conditions and at moderate temperatures.
Veterinary
Infectious period in animals
The cat excretes large amounts of oöcysts intermittently for 1 to 3 weeks 3 to 10 days after infection. Primary infection usually occurs in young cats when they just go outside and hunt. It was initially thought that felines would no longer excrete ovarian cysts after reinfection. Laboratory research shows that cats that were experimentally infected at a young age can still secrete oöcysts again if they are exposed to the parasite again years later. (Dub95), or when the immune system decreases (old age, Feline Immunodeficiency Virus, Feline Leukemia Virus). Such cats may show signs of illness, but they do not excrete oöcysts at that time (incubation period 21 days, oöcysts are excreted after 3 to 10 days after ingestion of tissue cysts).
Bij andere diersoorten dan katachtigen ontstaan een week na opname van oöcysten weefselcysten. Deze zijn direct infectieus en kunnen levenslang in hart, spier- en hersenweefsel aanwezig blijven. In geval van abortus of geboorte bij een geïnfecteerd schaap of geit, kunnen tachyzoïeten vrijkomen in geboorteproducten en vaginale uitvloeiing (tot 3 weken post partum).
Diagnostics
With the cooperation of the NVMM.
See also Diagnostic Vademecum Toxoplasma gondii.
Microbiological diagnosis
The diagnosis for toxoplasmosis is divided into two parts: demonstrating the infection in usually symptomatic patients and screening patients (immuno-incompetent persons and pregnant women).
Serology
If toxoplasmosis is suspected, serological testing is usually sufficient, i.e. the demonstration of IgG, IgM and IgA antibodies. 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 was acquired in the intervening period. The presence of specific IgM or IgA antibodies can support the diagnosis of a recent infection. It must be emphasized that IgM determinations are not suitable for determining recent infections because IgM appears to be detectable for a long time, in a significant proportion even 2 years after seroconversion. (Gra04) In practice, this means that if there is a real suspicion, a second serum sample must be examined to clarify seroconversion or a significant increase in titer.
If it is important to gain insight into the duration of the infection, the avidity of IgG can be determined. In the beginning of an infection, avidity is low and increases during the course of the infection. (Sen06) With high avidity, the infection has existed for at least more than 4 months. The advantage is that with the help of a single serum, a statement can be made about the chance that it concerns an older infection. This means that for the majority of patients it quickly becomes clear what is going on. However, this method has some limitations. For example, a number of patients do not develop high-avid antibodies: these patients are therefore wrongly suspected of having a recent infection. In addition, the method is not useful for low IgG titers (< 10 U). Importantly, pregnancy and treatment with spiramycin influence the development of avidity. (Lef06, Lef07)
Molecular techniques
In addition to serology, it is also possible to demonstrate DNA of the parasite. (Con91, Coz98, Wal99, Rom01, Tha05) The PCR (polymerase chain reaction) can detect Toxoplasma DNA in amniotic fluid, placenta, tissue biopsies, liquor, eye fluid and blood. As a result, a resurgence of a latent infection can be detected in immuno-incompetent persons and the existence of an intrauterine infection in pregnant women.
Cultivation
It is possible to culture the parasite using mouse inoculation or tissue culture. The use of these methods has drastically decreased 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 first performed. IgG and IgM antibodies directed against Toxoplasma are determined, possibly supplemented with an IgG avidity. If there is a serious suspicion (seroconversion or significant titer increase (> 4-fold) or low avidity), amniotic fluid examination using molecular methods is the next step. The amniotic fluid must be collected before starting therapy because medication can negatively influence the sensitivity of the PCR.
Diagnosis of congenital infection in the child
At birth, blood is taken from mother and child. If there is a serious suspicion, the child's serology should be repeated after 10 days and then every 3 months until the child becomes completely negative. An infection can be demonstrated in a neonate by looking at the different 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 at a very low level or delayed, so a negative result does not rule out an infection. (Gil07) IgG antibodies are transferred from mother to child. If the child (in the absence of therapy) becomes seronegative during the first year of life, a congenital infection is excluded.
Serodiagnosis of ocular toxoplasmosis
Serology and the examination of aqueous humor (PCR and antibody determinations on paired blood and ocular fluid samples) are important for the confirmation of ocular toxoplasmosis. (Gro06) Serology is of little value in the event of reactivation of ocular toxoplasmosis. Serology is also not very informative for diagnosing an eye infection in HIV or AIDS patients and highly immunosuppressed transplant patients.
Screening
For a screening question (has the patient ever had contact with T. gondii before), it is usually sufficient to determine IgG antibodies. 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 deal with a pregnant woman who has (had) contact with cats or other exposure and has no complaints. The chance that an infection will occur during a one-off contact or risk behavior is very small. Advice on how to avoid risky behavior and reassure the patient is often preferable to serodiagnosis in these types of situations.
Non-microbiological diagnostics
Diagnosis of ocular toxoplasmosis
Ocular toxoplasmosis presents with chorioretinal lesions and the diagnosis can be suspected based on the clinical ocular symptoms. In (newborn) children, the diagnosis is often made too late, because they cannot express their eye complaints and parents only raise the alarm if visual impairment or blindness exists. A definitive diagnosis is not possible based on clinical symptomatology. (Sta02)
Veterinary
Diagnosis in animals
Fecal examination in cats to detect Toxoplasma eggs is not easy. Cats only intermittently excrete oöcysts for 1 to 3 weeks, which 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 cat at some point in its life
parasite, but a negative result does not guarantee that it is Toxoplasma free. For a risk assessment for an individual person, having IgG or IgM determined in cats is not useful, because most cats only seroconvert after the oöcyst secretion 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
Having a cat or working in a slaughterhouse or veterinary practice (cats) does not increase the risk (Kortbeek, 2004) (Shuhaiber, 2003). Meat processing is indicated as a risk factor (Jones, 2009).
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Labour-related risk groups
High-risk occupations
High-risk professions are:
- Laboratory workers when working specifically with the toxoplasma parasite and when used in laboratory animals (e.g. needlestick accident) (1,2);
- Green or ground workers and employees who professionally clean litter boxes (e.g. animal shelters, home care);
- Veterinarians and other persons working with small ruminants (particularly 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 slaughterers in butchers' shops have a very low risk of transmission with correct information, application of basic hygienic measures and correct use of personal protective equipment (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 event of intrauterine infection early in pregnancy) and immunocompromised people (transplant patients, HIV or AIDS patients or with immunosuppressive therapy).
The Working Conditions Decree (Article 4.109) states that ‘pregnant employees are prohibited from performing work in which they could be exposed to the toxoplasma parasite unless it has been proven that she is immune to this’.
Increased risk of a serious course
In immunocompromised people such as transplant patients and HIV or AIDS patients, the chance of a serious course is also high.
Pregnancy
Intrauterine infections
Intrauterine infections where the infection occurs early in pregnancy have a high risk of a serious course.
Epidemiology
Distribution in the world
Toxoplasmosis occurs everywhere in the world where there are cats or felines.
Occurrence in the Netherlands
The seroprevalence of the Dutch population increases with age from 17.5% in people younger than 20 years to more than 70% in people older than 65 years. The average seroprevalence for the Dutch population was 40.5% in 1996, but this appears to have decreased in recent decades. (Kortbeek 2004)
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Reports of occupational infections
Two reports of an occupational toxoplasmosis infection were made to the Dutch Center for Occupational Diseases (NCvB) (in 2003 and 2007). This says little about occupationally acquired cases; the NCvB has to deal with under-registration and the infection is often not properly recognized.
Veterinary
Occurrence in the Netherlands in animals
A seroprevalence of 20% was found among cats in the Netherlands 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 this 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. The vaccine may pose a risk of infection to humans due to the presence of live parasites in the vaccine.
General preventive measures
Preventing ingestion of oöcysts by:
- Wear gloves when gardening and working with soil;
- Wash vegetables and fruit well before consumption;
- Change the litter box every day (due to sporulation of oöcysts). For pregnant women: use gloves or have someone else do it.
- Heat meat thoroughly and do not eat raw meat such as fillet américain or beef sausage. The tissue cysts in meat are not destroyed at normal refrigeration temperatures. At a temperature of 56°c for 10 à After 15 minutes the cysts lose their viability. A freezing treatment (–20°c) of meat for consumption is effective with regard to inactivation, provided it is long enough to reach a sufficiently low temperature throughout the product; (kijl08)
- Wash hands after handling raw meat;
- Clean surfaces and tools that have come into contact with raw meat;
- Meat can be frozen (at least 1 week at –20°c).
Preventing ingestion of vital tissue cysts by: Determining the immune status of donor and recipient with regard to toxoplasmosis during transplantation.
Pregnancy
Prevention in pregnant women
- See general preventive measures above.
- See also brochure Pregnancy and infections.
- See also the toxoplasmosis and pregnancy page with information for professionals.
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Preventive measures at work
- Repeatedly information must be provided, starting upon entry into employment, about the risk of exposure, the transmission route and the symptoms. The importance of general hygiene, cleaning of the environment and protective measures (particularly wearing gloves) should also be repeatedly emphasized. This is particularly important for medically vulnerable employees and should be monitored (1).
- The employer must have a broadly supported Pregnancy Policy for high-risk positions. This must state how the information is organised, how employees of childbearing age/immunocompromised employees have access to the company doctor's consultation hours and for whom and how research into protection (experienced toxoplasmosis) is organised. Adjust work activities for seronegative pregnant women in high-risk professions (8).
See also the general preventive measures mentioned earlier.
Disinfection
Conforms to Standard methods of cleaning, disinfection and sterilization.
Measures
Report obligation
None.
Iinvolvement of other agencies
Not necessary.
Bron detection
Not applicable.
Contact investigation
Not applicable.
Measures regarding patient and contacts
Not applicable.
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Report as an occupational disease
If the disease was (probably) contracted during the course of work, this must be reported to the Dutch Center for Occupational Diseases (www.beroepsverzekeringen.nl).
Exclusion from work, school or daycare
Exclusion from work, school or daycare is not useful from a public health perspective.
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Prohibition from work
Man is not infectious to his environment, so it is not useful to avoid work.
Prophylaxis & Treatment
Prophylaxis
In all seropositive patients with less than 100 – 200 CD4 cells/mm3 and IgG antibodies against toxoplasmosis, prophylaxis with Co-trimoxazole is recommended. The practitioner determines the need for prophylaxis for 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 the infection), but the bradyzoites in the tissue cysts remain vital. Spiramycin has been withdrawn from the market in the Netherlands since 2005. No data from randomized, controlled therapy trials are available.
For treatment, see the guidelines of the Antibiotic Policy Working Group Foundation (SWAB): http://www.swabid.nl/therapie.
Congenital toxoplasmosis
The medication for congenital toxoplasmosis consists of pyrimethamine, sulfadiazine, folinic acid and spiramycin. It is still not clear how many of the congenitally infected patients will eventually still develop symptoms after therapy. The studies in the field of therapy are still too short (< 10 years) to provide clarity about the effect on ocular lesions in the longer term.
A systematic review (SYROCOT: Systematic Review on Congenital Toxoplasmosis) showed that prenatal treatment of T. gondii infection has little effect on transmission, regardless of the time of treatment. There appears to be a clear effect of early treatment on the occurrence of symptoms (Syr07).
Ocular toxoplasmosis
There is no known therapy that will cure an ocular Toxoplasma infection. (Sta03) The treatment is aimed at reducing damage to the eye and limiting visual impairment and blindness. It has been shown that treatment with several weeks of antiparasitic agents can limit damage to the eye. Treatment with anti-inflammatory agents can also prevent the complications of the inflammatory process in the eye. (Rot93, Bos02) Initiating 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. An infection with T. gondii in a rodent was described for the first time in 1908, and the first infection in humans 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 can act as hosts. At the end of the 1960s it was discovered that felines secrete oöcysts and can be regarded as 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.
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