Toxoplasmosis: symptoms

In accordance with the "International Statistical Classification of Diseases and Problems related to Health", adopted by WHO in 1995, the following nosological forms of toxoplasmosis are distinguished: toxoplasmosis oculopathy (B.58.0), toxoplasmosis hepatitis (B.58L), toxoplasmosis meningoencephalitis (B. 58.2), pulmonary toxoplasmosis (B.58.3), toxoplasmosis with damage to other organs (B.58.3): toxoplasmosis myocarditis and toxoplasmosis myositis; toxoplasmosis, unspecified (B.58.9), and congenital toxoplasmosis.

Toxoplasmosis oculopathy proceeds according to the type of chorioretinitis or granulomatous uveitis, cataract. It can also be combined with CNS and heart damage. Eye damage is chronic, with recurrences, foci of pigmentary degeneration, atrophic foci on the retina of the eye, atrophy of the optic nerve disk, leading to progressive deterioration of vision, blindness develop gradually.

Toxoplasmosis hepatitis is characterized by the presence of the main symptom - enlargement of the liver, which can be painful on palpation. However, as a rule, no significant violations of liver function are observed. Often recorded and an increase in the spleen. Toxoplasmosis hepatitis develops during a chronic course of infection.

Toxoplasmosis meningoencephalitis has nonspecific symptoms of toxoplasmosis: general intoxication, high fever, severe headache, impaired consciousness, convulsions. An important diagnostic value is the investigation of cerebrospinal fluid, in which toxoplasm can be detected.

Pulmonary toxoplasmosis usually develops in the acute stage of the disease when the infection is generalized. Pneumonia is often bilateral, interstitial, has a prolonged course. After the extinction of the acute process in the lungs remain small dispersed calcifications.

Toxoplasmosis myocarditis is diagnosed when the heart disease is the dominant symptom of the disease. However, it should be emphasized that the clinical picture is not significantly different from the myocarditis of another etiology.

Toxoplasmosis myositis is characterized by pain in the muscles. When X-ray examination, they detect calcifications.

By the nature of the course of infection, acute, chronic and latent forms are isolated. In the acute form of toxoplasmosis after the prodromal period (up to 2 weeks), during which weakness, fatigue, muscle pains are noted, the most characteristic symptom is the appearance of enlarged lymph nodes (in the cervical, occipital, submandibular and axillary regions) . Calcifications, enlarged liver and spleen, myocarditis and pneumonia, as well as severe CNS lesions (encephalitis, meningoencephalitis) can be observed. The incubation period is from 3 to 14 days. Treatment of toxoplasmosis in acute form is the most effective.

The chronic form of the disease most often does not have any symptoms of toxoplasmosis, but patients can also complain of weakness, rapid fatigue, sometimes headaches, and subfebrile temperature. When the CNS is affected, encephalitis, meningitis, and arachnoiditis can develop; when the organ of vision is damaged - chorioretinitis, uveitis, iridocyclitis, atrophy of the optic nerve. There may also be lesions of the musculoskeletal system, myocarditis, hepatitis and endometritis.

Chronic acquired toxoplasmosis is characterized by a prolonged course with periodic exacerbations. Disease toxoplasmosis is not severe, with the exception of neurotoxoplasmosis. Treatment of chronic toxoplasmosis is advisable to conduct during periods of exacerbation.

With a latent form, the infection proceeds secretly, without clinical symptoms.

The incubation period of toxoplasmosis lasts from several weeks to several months. Depending on the mechanism of infection, the acquired and congenital toxoplasmosis is isolated.

Also distinguish acquired and congenital toxoplasmosis.

Acquired toxoplasmosis

Acquired toxoplasmosis does not have any symptoms (up to 99% of all cases of T. Gondii infection). These are healthy people, usually with a low level of antitoxoplasma antibodies, which do not need any medical supervision or treatment. In persons with a normal immune response, in most cases, toxoplasmosis proceeds in a latent form. Manifest toxoplasmosis occurs in acute (up to 0.01% infected) and chronic (1-5%) form, with a tendency to relapse and exacerbation.

[1], [2], [3], [4], [5], [6], [7], [8]

Acute acquired toxoplasmosis

In individuals with a normal immune response, the disease is often not clinically apparent. Infection is indicated by the presence in their blood of specific IgM antibodies with an increase in their level in dynamics 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. There are such symptoms of toxoplasmosis as: fever, intoxication syndrome, lymphadenopathy, lymphocytosis; there are rashes on the skin, diarrhea. The defeat of skeletal muscles is manifested by myalgia. Joint pains often occur. Expressed hepatolyenal syndrome and signs of CNS damage. Catarrhal manifestations, pneumonia, myocarditis are possible.

[9], [10], [11], [12], [13], [14]

Chronic acquired toxoplasmosis

Chronic form of acquired toxoplasmosis can develop primarily or as a result of the acute form of the disease. In the manifest cases, chronic toxoplasmosis has polymorphic symptoms. The onset is gradual, with mildly expressed manifestations of a general nature: headache, general weakness, increased fatigue, memory loss, neurosis-like changes, sleep disturbances. Holding a long time subfebrile body temperature. The majority of patients are diagnosed with lymphadenopathy, myositis, and arthralgia. When the myocardium is affected, patients notice such symptoms of toxoplasmosis as: dyspnea, palpitation, pain in the heart area. ECG data indicate the development of myocarditis or myocardial dystrophy. Possible interstitial pneumonia, chronic gastritis, enterocolitis, biliary tract and female reproductive system disorders (menstrual disorders, salpingoophoritis, endometritis, infertility).

An important role in the acquired chronic toxoplasmosis is played by the defeat of the nervous system: the brain, its membranes, hypothalamus, peripheral nerves. Detect meningoencephalitis, encephalitis, cerebral arachnoiditis, diencephalic and mental disorders, convulsive syndrome.

When the eyes are affected, pathological changes are possible in all the membranes, lesions of the optic nerve, external muscles of the eyeball occur. In combination with chorioretinitis and other changes, keratoscleritis or keratouveitis is sometimes noted.

In people with immunodeficiency status (for example, AIDS, malignant lymphomas, conditions due to the use of pmunodepressants), the latent current of toxoplasmosis or new infection, as in other opportunistic infections, passes into a generalized process with damage to the brain, myocardium, lungs and other tissues and organs. Activation of latent toxoplasmosis in HIV-infected patients occurs with a CD4 + lymphocyte content of 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 affects the central nervous system - develops severe necrotic encephalitis. Cerebral toxoplasmosis is detected in different countries in 3-40% of AIDS patients. The clinical picture is dominated by symptoms of focal encephalitis, which indicate the damage to the cerebral hemispheres, cerebellum or brainstem (hemiparesis, aphasia, disorientation, hemianopia, convulsive syndrome and other changes) and often combined with encephalopathy. Extra-cerebral 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 (heart, lymph nodes, bone marrow, liver , pancreas, genitourinary system, etc.). Lung infection occurs in 2% of cases.

In children with HIV infection, the disease occurs in a latent form. Among the clinical forms more often reveal cerebral, ophthalmic, pulmonary, myocarditis, lymphonodular, and also damage to the digestive organs.

[15], [16], [17], [18], [19], [20]

Congenital toxoplasmosis

Occurs only when a woman is infected during pregnancy. In women with HIV infection, a latent, pre-pregnancy infestation can be reactivated. Congenital toxoplasmosis in 25-30% of cases has typical symptoms of toxoplasmosis, in other cases - latent. Depending on the timing of infection of the mother during pregnancy, congenital toxoplasmosis in the child can be expressed in various forms.

[21], [22], [23], [24], [25], [26], [27], [28], [29]

Acute congenital toxoplasmosis

The acute form of toxoplasmosis develops with infection in late pregnancy. It proceeds as a severe generalized disease with severe intoxication, fever, rashes on the skin, ulcers on the mucous membrane of the nasopharynx, jaundice, edema, hepatosplenomegaly. Later there is toxoplasmosis encephalitis. Defeat the eyes and other organs. If the child carries the acute form in utero, it can be born with signs of chronic congenital toxoplasmosis: with the consequences of encephalitis in the form of hydrocephalus, oligophrenia, convulsive syndrome, with eye damage (up to micro- and anophthalmia). Gradually the process passes into a secondary chronic form with residual phenomena.

[30], [31], [32]

Chronic congenital toxoplasmosis

In chronic congenital toxoplasmosis (residual phenomena in children and adolescents), residual effects from the CNS and vision organs are revealed: mental and physical developmental lag, hydrocephalus, microcephaly, paresis and paralysis, epileptiform seizures, microphthalmus, microcornea, chorioretinitis, optic nerve atrophy, cataract, strabismus, nystagmus.

[33], [34], [35], [36], [37]

Toxoplasmosis and pregnancy

The urgency of the problem of toxoplasmosis causes serious consequences of primary infection of women during organogenesis, in early pregnancy (fetal death, ugliness, etc.). Therefore, all women planning pregnancy, and pregnant (preferably in the early period) should be examined for the presence of serum antibodies to toxoplasm. The study is also necessary in case of symptoms of lymphadenopathy, fatigue, mononucleosis-like diseases. Pregnant women who come from regions with high incidence rates of toxoplasmosis, or who consume half-raw meat during pregnancy, or who have contact with infected cats are also subject to testing.

Laboratory diagnosis of toxoplasmosis in the past, or the detection of an acute infection caused by T. Gondii, in a pregnant woman is performed serologically. Seroconversion is usually monitored by determining IgG or IgM for toxoplasmic antigens in two sets at intervals of two to three weeks. Serologic monitoring during pregnancy is recommended to be carried out with an interval of 1 to 3 months.

When detecting pregnant M immunoglobulins against toxoplasmic antigens, there is a suspicion of an acute infection. An important point of diagnosis in this case is the presence or absence of clinical symptoms of toxoplasmosis (because it is possible that infection occurred several months before pregnancy), and also the results of serological analysis in the dynamics. If the M antibody test is negative and IgG is positive for two paired sera, but no titer changes, then a recent infection is excluded. Women with positive IgG and IgM assays for toxoplasmic antigens in the first sera should be examined again in 2-3 weeks, and the nature of the acquired infection is judged by changing the level of antibodies (increasing or decreasing the titers). Activation of toxoplasmosis in subsequent pregnancy is possible only in the case of severe immunosuppression (for example, in HIV-infected people).

Toxoplasmosis in children

Intrauterine toxoplasmosis occurs as a result of primary infection, with clinical symptoms or asymptomatic infection, in the mother. Symptoms of intrauterine toxoplasmosis in newborns during primary infection in the second half of pregnancy, manifested in the first months of the child's life, most often neurological. Consequences or relapse may occur later in the child's development (chorioretinitis, retinopathy of prematurity, or subclinical symptoms).

Suspicion of toxoplasmosis in newborns occurs in the case of intrauterine growth retardation, hydrocephalus, microcephaly, hepatosplenomegaly, thrombocytopenia, hepatitis and the presence of petechiae.

In addition, evidence of infection can serve as a positive result of ophthalmic examination, analysis of cerebrospinal fluid and computed tomography of the brain at the birth of a child.

Serological evidence of toxoplasmosis in newborns is the positive results of detection of specific immunoglobulins of class M, while infection in the mother is also recorded by the determination of IgM to antigens of toxoplasm. It has been shown that antibodies of class M do not pass through the placenta. To detect specific IgM, serum taken from the umbilical cord is often used. However, one should remember about the possibility of a false positive result due to contamination by the mother's blood. All positive results obtained in the study of umbilical cord blood should be checked by a similar analysis of a blood sample from a vein in a newborn.

Thus, in the detection of specific IgM in the newborn's serum, intrauterine toxoplasmosis is diagnosed in the laboratory. However, the sensitivity of this test is approximately 80%.

When determining IgG for antigens of toxoplasm in newborns, it should be remembered that these antibodies passively pass from the mother and persist until the child's 6-8 month old age. Positive results of serological analysis, indicating the presence of specific antibodies later than this time, confirm a possible intrauterine infection, but in the absence of antibodies, the mother speaks of acquired toxoplasmosis in the child.

It should be noted that in the diagnosis of intrauterine toxoplasmosis, none of the serological tests have absolute sensitivity. Therefore, a comprehensive approach to diagnosis is needed, which includes, along with the assessment of clinical symptoms and serological examination, the detection of a parasite in a clinical material (pieces of placenta, umbilical cord, blood, liquor, etc.).

In the late period of newborns and in older children, suspected toxoplasmosis may occur if there are one or more of the following: developmental retardation, loss of vision or hearing. Proof will also serve to identify pathological changes in the in-depth examination of the organs of sight, hearing, and also in computed tomography of the brain. Positive results of a serological test confirm the presence of an infection that can be both congenital and acquired. Observation of this age group is necessary to be carried out together with specialists of other profiles (oculists, neuropathologists, etc.).

Evaluation of severe form of toxoplasmosis in a child includes:

• analysis of the history of pregnancy in women, history of the disease (lymphadenopathy, fatigue, mononucleose-like condition);
• results of ultrasound of the fetus (if any);
• results of PCR 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 organ of vision;
• general blood analysis;
• determination of indicators of liver function;
• examination of cerebrospinal fluid;
• computer tomography of the brain (with or without contrasting);
• analysis of serum creatinine and the study of kidney function;
• serological examination of the mother and child in dynamics with the determination of the antibody titer.