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Toxoplasmosis - Symptoms.
Last reviewed: 04.07.2025

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According to the International Statistical Classification of Diseases and Related Health Problems adopted by WHO in 1995, the following nosological forms of toxoplasmosis are distinguished: toxoplasmic oculopathy (B.58.0), toxoplasmic hepatitis (B.58L), toxoplasmic meningoencephalitis (B.58.2), pulmonary toxoplasmosis (B.58.3), toxoplasmosis with damage to other organs (B.58.3): toxoplasmic myocarditis and toxoplasmic myositis; unspecified toxoplasmosis (B.58.9), as well as congenital toxoplasmosis.
Toxoplasmosis oculopathy occurs as chorioretinitis or granulomatous uveitis, cataracts. It can also be combined with damage to the central nervous system and heart. Eye damage is chronic, with relapses, foci of pigment degeneration, atrophic foci on the retina of the eye, atrophy of the optic nerve head gradually develop, leading to progressive deterioration of vision, blindness.
Toxoplasmic hepatitis is characterized by the presence of the main symptom - an enlarged liver, which can be painful upon palpation. However, significant liver dysfunctions are usually not observed. An enlarged spleen is also often recorded. Toxoplasmic hepatitis develops during chronic infection.
Toxoplasmic meningoencephalitis has non-specific symptoms of toxoplasmosis: general intoxication, high temperature, severe headache, impaired consciousness, convulsions. Of great diagnostic importance is the study of cerebrospinal fluid, in which toxoplasms can be detected.
Pulmonary toxoplasmosis usually develops in the acute stage of the disease with generalization of the infection. Pneumonia is most often bilateral, interstitial, and has a protracted course. After the acute process subsides, small scattered calcifications remain in the lungs.
Toxoplasmic myocarditis is diagnosed when the dominant symptom of the disease is heart damage. However, it should be emphasized that the clinical picture does not differ significantly from myocarditis of other etiologies.
Toxoplasmic myositis is characterized by muscle pain. X-ray examination reveals calcifications in the muscles.
According to the nature of the infection, acute, chronic and latent forms are distinguished. In the acute form of toxoplasmosis, after the prodromal period (up to 2 weeks), during which weakness, increased fatigue, muscle pain are observed, the most characteristic symptom is the appearance of enlarged lymph nodes (in the cervical, occipital, submandibular and axillary regions), and an increase in temperature is also possible. The formation of calcifications, enlargement of the liver and spleen, myocarditis and pneumonia, as well as severe CNS damage (encephalitis, meningoencephalitis) may be observed. The incubation period is from 3 to 14 days. Treatment of toxoplasmosis in the acute form is the most effective.
The chronic form of the disease most often does not have any symptoms of toxoplasmosis, but patients may also complain of weakness, rapid fatigue, sometimes headaches, and subfebrile temperature. If the central nervous system is affected, encephalitis, meningitis, arachnoiditis may develop; if the organ of vision is affected, chorioretinitis, uveitis, iridocyclitis, optic nerve atrophy may develop. Damage to the musculoskeletal system, myocarditis, hepatitis, and endometritis may also be observed.
Chronic acquired toxoplasmosis is characterized by a long course with periodic exacerbations. Toxoplasmosis is not a severe disease, with the exception of neurotoxoplasmosis. Treatment of chronic toxoplasmosis is advisable to carry out during periods of exacerbation.
In the latent form, the infection proceeds covertly, without clinical symptoms.
The incubation period of toxoplasmosis lasts from several weeks to several months. Depending on the mechanism of infection, acquired and congenital toxoplasmosis are distinguished.
A distinction is also made between acquired and congenital toxoplasmosis.
Acquired toxoplasmosis
Acquired toxoplasmosis has no symptoms (up to 99% of all cases of T. gondii infection). These are healthy people, usually with a low level of antitoxoplasma antibodies, who do not need medical supervision or treatment. In people with a normal immune response, toxoplasmosis in most cases occurs in a latent form. Manifest toxoplasmosis occurs in acute (up to 0.01% of infected) and chronic (1-5%) forms, with a tendency to relapse and exacerbation.
Acute acquired toxoplasmosis
In people with a normal immune response, the disease often does not manifest itself clinically. Infection is indicated by the presence of specific IgM antibodies in the blood with an increase in their level over time and subsequent change to IgG. With the development of the manifest form of acute acquired toxoplasmosis, the incubation period lasts from several days to weeks. The following symptoms of toxoplasmosis appear: fever, intoxication syndrome, lymphadenopathy, lymphocytosis; skin rashes and diarrhea occur. Damage to skeletal muscles is manifested by myalgia. Joint pain often occurs. Hepatosplenic syndrome and signs of CNS damage are expressed. Catarrhal manifestations, pneumonia, myocarditis are possible.
Chronic acquired toxoplasmosis
Chronic acquired toxoplasmosis may develop primarily or as a result of an acute form of the disease. In manifest cases, chronic toxoplasmosis has polymorphic symptoms. The onset is gradual, with mild general symptoms: headache, general weakness, increased fatigue, memory loss, neurosis-like changes, sleep disturbances. prolonged subfebrile body temperature. Most patients have lymphadenopathy, myositis, arthralgia. In case of myocardial damage, patients note such symptoms of toxoplasmosis as: shortness of breath, palpitations, pain in the heart. ECG data indicate the development of myocarditis or myocardial dystrophy. Interstitial pneumonia, chronic gastritis, enterocolitis, lesions of the biliary tract and female reproductive system (menstrual irregularities, salpingo-oophoritis, endometritis, infertility) are possible.
An important role in acquired chronic toxoplasmosis is played by damage to the nervous system: the brain, its membranes, hypothalamus, peripheral nerves. Meningoencephalitis, encephalitis, cerebral arachnoiditis, diencephalic and mental disorders, convulsive syndrome are detected.
When the eyes are affected, pathological changes are possible in all membranes, lesions of the optic nerve and external muscles of the eyeball occur. In combination with chorioretinitis and other changes, keratoscleritis or keratouveitis are sometimes noted.
In people with immunodeficiency (e.g. AIDS, malignant lymphomas, conditions due to the use of immunosuppressants), latent toxoplasmosis or a new infection, as with other opportunistic infections, turns into a generalized process with damage to the brain, myocardium, lungs and other tissues and organs. Activation of latent toxoplasmosis in HIV-infected people occurs when the content of CD4+ lymphocytes is less than 0.1x10 9 cells per liter of blood. In this case, the disseminated process develops in 25-50% of patients with specific antibodies. Most often, the central nervous system is affected - severe necrotic encephalitis develops. Cerebral toxoplasmosis is detected in 3-40% of AIDS patients in different countries. The clinical picture is dominated by symptoms of focal encephalitis, indicating damage to the cerebral hemispheres, cerebellum or brainstem (hemiparesis, aphasia, disorientation, hemianopsia, convulsive syndrome and other changes) and often combined with encephalopathy. Extracerebral localization of toxoplasmosis in AIDS is detected in 1.5-2% of cases, most often in the form of eye damage (50%), manifested by focal necrotizing chorioretinitis without an inflammatory reaction, but other organs can also be involved (heart, lymph nodes, bone marrow, liver, pancreas, genitourinary system, etc.). Lung damage occurs in 2% of cases.
In children with HIV infection, the disease occurs in a latent form. Among the clinical forms, cerebral, ocular, pulmonary, myocarditic, lymphonodular, as well as damage to the digestive organs are most often detected.
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Congenital toxoplasmosis
Occurs only when a woman is infected during pregnancy. In women with HIV infection, latent invasion that arose before pregnancy can be reactivated. Congenital toxoplasmosis in 25-30% of cases has typical symptoms of toxoplasmosis, in other cases - latent. Depending on the timing of the mother's infection during pregnancy, congenital toxoplasmosis in the child can be expressed in various forms.
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Acute congenital toxoplasmosis
Acute toxoplasmosis develops when infected in the late stages of pregnancy. It occurs as a severe generalized disease with severe intoxication, fever, skin rashes, ulcers on the mucous membrane of the nasopharynx, jaundice, edema, hepatosplenomegaly. Toxoplasmic encephalitis occurs later. Damage to the eyes and other organs is detected. If a child suffers from the acute form in utero, he may be born with signs of chronic congenital toxoplasmosis: with consequences of encephalitis in the form of hydrocephalus, oligophrenia, convulsive syndrome, with damage to the eyes (up to micro- and anophthalmia). Gradually, the process turns into a secondary chronic form with residual phenomena.
Chronic congenital toxoplasmosis
In chronic congenital toxoplasmosis (residual phenomena in children and adolescents), residual effects on the part of the central nervous system and visual organs are detected: mental and physical developmental delays, hydrocephalus, microcephaly, paresis and paralysis, epileptiform seizures, microphthalmos, microcornea, chorioretinitis, optic nerve atrophy, cataracts, strabismus, nystagmus.
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Toxoplasmosis and pregnancy
The relevance of the toxoplasmosis problem determines the serious consequences of primary infection of women during organogenesis, in the early stages of pregnancy (death of the fetus, deformities, etc.). Therefore, all women planning pregnancy and pregnant women (preferably in the early stages) should be examined for the presence of antibodies to toxoplasma in the blood serum. The study is also necessary in the event of symptoms of lymphadenopathy, fatigue, mononucleosis-like diseases. Pregnant women who arrived from regions with high rates of toxoplasmosis, or who ate undercooked meat during pregnancy, or had contact with infected cats are also subject to testing.
Laboratory diagnostics of past toxoplasmosis or detection of acute infection caused by T. gondii in a pregnant woman are performed by serological methods. Monitoring of seroconversion is usually performed by determining IgG or IgM to toxoplasma antigens in two tests with an interval of two to three weeks. Serological monitoring during pregnancy is recommended to be performed at intervals of 1 to 3 months.
If class M immunoglobulins to toxoplasma antigens are detected in a pregnant woman, an acute infection is suspected. An important diagnostic point in this case is the presence or absence of clinical symptoms of toxoplasmosis (since it is possible that the infection occurred several months before pregnancy), as well as obtaining the results of serological analysis in dynamics. If the results of the analysis for class M antibodies are negative, and IgG are positive for two paired sera, but without a change in titer, then a recent infection is excluded. Women with positive results of the analysis for the presence of IgG and IgM to toxoplasma antigens in the first sera should be examined again after 2-3 weeks, and the nature of the acquired infection is judged by the change in the antibody level (increase or decrease in titers). Activation of toxoplasmosis during a subsequent pregnancy is possible only in the case of severe immunosuppression (for example, in HIV-infected women).
Toxoplasmosis in children
Intrauterine toxoplasmosis occurs as a result of primary, clinically symptomatic or asymptomatic, infection in the mother. Symptoms of intrauterine toxoplasmosis in newborns with primary infection in the second half of pregnancy, manifested in the first months of the child's life, are most often neurological. Consequences or relapse may appear at later stages of the child's development (chorioretinitis, retinopathy of prematurity or subclinical symptoms).
Toxoplasmosis in newborns is suspected in cases of intrauterine growth retardation, hydrocephalus, microcephaly, hepatosplenomegaly, thrombocytopenia, hepatitis and the presence of petechiae.
In addition, positive results of ophthalmological examination, cerebrospinal fluid analysis and CT scan of the brain at birth can serve as evidence of infection.
Serological confirmation of toxoplasmosis in neonates is positive results of detection of specific immunoglobulins of class M, while the infection in the mother is also registered by determination of IgM to toxoplasma antigens. It has been shown that antibodies of class M do not pass through the placenta. Serum taken from the umbilical cord is often used to detect specific IgM. However, one should remember about the possibility of a false-positive result due to contamination with maternal blood. All positive results obtained in the study of umbilical cord blood should be verified by similar analysis of a blood sample from a vein of the newborn.
Thus, when specific IgM is detected in the serum of a newborn, intrauterine toxoplasmosis is diagnosed in the laboratory. However, the sensitivity of this test is approximately 80%.
When determining IgG to toxoplasma antigens in newborns, it should be remembered that these antibodies are passively transmitted from the mother and persist until the child is 6-8 months old. Positive results of serological analysis, indicating the presence of specific antibodies after this time, confirm a possible intrauterine infection, but in the absence of antibodies in the mother, they indicate acquired toxoplasmosis in the child.
It should be noted that in the diagnosis of intrauterine toxoplasmosis, none of the serological tests has absolute sensitivity. Therefore, a comprehensive approach to diagnosis is necessary, including, along with the assessment of clinical symptoms and serological examination, the detection of the parasite in clinical material (pieces of placenta, umbilical cord, blood, cerebrospinal fluid, etc.).
In the late neonatal period and in older children, toxoplasmosis may be suspected if there is one or more of the following symptoms: developmental delay, loss of vision or hearing. Evidence will also include the detection of pathological changes during an in-depth examination of the organs of vision, hearing, and during computed tomography of the brain. Positive results of serological testing confirm the presence of an infection, which can be either congenital or acquired. This age group should be monitored jointly with specialists of other profiles (ophthalmologists, neurologists, etc.).
Evaluation of severe toxoplasmosis in a child includes:
- analysis of the woman's pregnancy history, medical history (lymphadenopathy, fatigue, mononucleosis-like condition);
- ultrasound results of the fetus (if any);
- PCR results of amniotic fluid, anterior chamber of the eye, cerebrospinal fluid, etc. (if it is possible to conduct such a study);
- physical examination;
- in-depth examination of the visual organ;
- general blood test;
- determination of liver function indicators;
- cerebrospinal fluid examination;
- performing a computed tomography scan of the brain (with or without contrast);
- serum creatinine analysis and renal function testing;
- serological examination of mother and child over time with determination of antibody titer.