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Toxoplasmosis hepatitis.
Last reviewed: 05.07.2025
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Congenital toxoplasmic hepatitis is a disease caused by toxoplasma acquired by the fetus antenatally from a mother with toxoplasmosis.
Spreading
Toxoplasmosis is one of the most pressing health problems. In the structure of opportunistic diseases in Russia, toxoplasmosis ranks third after tuberculosis and cytomegalovirus infection.
The causative agent of toxoplasmosis is widespread in nature, and through contact with domestic and farm animals, the population is infected with it - from 6 to 90%. For example, in the German Autonomous Okrug, toxoplasmosis infection was detected in 36.3% of residents, and in the Kamchatka Region - in 13%.
In England, the seroprevalence rate for Toxoplasma is 9.1%.
Women predominate among those infected with toxoplasma, which is apparently explained by their greater involvement in food preparation and contact with raw meat.
The presence of toxoplasmosis in pregnant women is detected with a very high frequency: for example, in Sweden, seropositivity for toxoplasmosis among pregnant women was found in 18% of cases.
In Russia, antibodies to toxoplasma are detected in pregnant women with a frequency of 10 to 40.6%. Infection of newborns with toxoplasma reaches significant levels - from 17.3 to 26.3%.
In fetuses and newborns who died from congenital malformations, intrauterine infection with toxoplasma is detected in 1.7% of cases, and the simultaneous presence of intrauterine infection caused by toxoplasma and the herpes simplex virus is detected in 11.5%.
Causes of Toxoplasma Hepatitis
The causative agent of toxoplasmosis - Toxoplasma gondii - belongs to the type Protozoa, class Sporozoa, order Coccidia. There are proliferative forms of toxoplasma, or endozoids (taxizoids), cysts and oocytes (the resting stage of the pathogen in the intestine of the final host). Cysts are formed in the body of the intermediate host (humans, cattle). They are localized mainly in the brain, eyes, myocardium and muscles. Toxoplasma also reproduces inside the cysts. Then they leave the cysts, penetrate into the host's cells, where they begin to reproduce. This occurs during relapses of toxoplasmosis in humans. Viable parasites in cysts can persist in the infected organism for life. Toxoplasma is not transmitted from person to person. In the case of primary infection caused by toxoplasma that occurs during pregnancy, the pathogen is transmitted to the fetus. In a woman who has already been infected and therefore is not immune, a fresh toxoplasmosis infection is accompanied by parasitemia, at least short-term, and endozoa (proliferative forms of the pathogen) can be carried by the bloodstream into the mother's placenta. Then, if the barrier function of the trophoblast layer of the chorion is impaired, the parasite penetrates the fetal bloodstream. The probability of transplacental transmission of toxoplasma (from 10 to 80%) depends on the gestational age of the fetus. The severity of fetal lesions becomes less with increasing gestational age, but the risk of fetal infection increases.
Toxoplasma infection of the fetus causes acute or chronic forms of the disease, causes developmental abnormalities, and can cause damage to various organs and systems.
[ Morphology
In congenital toxoplasmosis hepatitis, lesions of other organs are also described with greater frequency. For example, meningoencephalitis, myocarditis, pneumonia, pyelonephritis, enterocolitis, etc. are observed.
The liver is usually enlarged. Histological examination reveals preservation of the lobular structure, discomplexation of the liver beams, and the presence of lymphohistiocytic infiltration. Hyaline and vacuolar dystrophy is detected in hepatocytes, centrilobular necrosis of hepatocytes and necrosis along the periphery of the lobules are observed, and cholestasis is present. Toxoplasma cysts are detected in lymphohistiocytic infiltrates, and the formation of small granulomas from lymphoid and monocytic cells with an admixture of epithelioid cells is noted.
Symptoms of toxoplasmic hepatitis
Most children with congenital toxoplasmosis hepatitis are born full-term, have an Apgar score of 7-8 points. The condition is assessed as moderate, in some newborns it can be severe. Intoxication is observed in the form of lethargy, refusal to eat, regurgitation. Jaundice appears on the 2-3rd day of life - from mild to intense. An increase in the size of the liver, compaction of its consistency are noted in all children. The liver is palpated below the costal arch by 3-5 cm; the edge is rounded, the surface is smooth. Splenomegaly is recorded in 30-40% of patients, while the spleen protrudes from the hypochondrium by 1-2 cm. Exanthema may appear in the form of a maculopapular rash in the inguinal and gluteal regions. Lymphadenopathy is present in 35-40% of cases. Changes in the heart are expressed in the presence of systolic murmur and muffled heart sounds in 30% of newborns.
In the biochemical blood test; 2-3-fold increase in the level of total bilirubin, approximately equal content of conjugated and unconjugated fractions of the pigment; very weak, mainly 2-fold, increase in the activity of ALT, AST, LDH.
In cholestasis syndrome, marked icterus of the skin and sclera is observed, the total bilirubin concentration in the blood serum increases by 8-10 times with some predominance of the conjugated fraction. At the same time, the activity level of alkaline phosphatase and GGT increases by 2-2.5 times. Children experience anxiety and itchy skin. Hemorrhagic syndrome (petechial rash, hemorrhages at injection sites) often occurs in the cholestatic variant of hepatitis.
Ultrasound reveals increased echo density of the liver in almost all children with congenital toxoplasmic hepatitis. In the cholestatic variant, thickening of the gallbladder walls is noted. Pancreatopathy is recorded in 43% of cases.
Flow options
The course of congenital toxoplasmic hepatitis is acute. Gradually, over 2-3 months, the condition of children improves: intoxication decreases, jaundice disappears; in the cholestatic variant of the disease, jaundice can last up to 4-5 months. At the same time, biochemical indicators of cholestasis normalize.
Those children who die are those who, in addition to hepatitis, have severe damage to other organs and systems (meningoencephalitis, pneumonia, myocarditis, etc.).
Chronic course of congenital toxoplasmic hepatitis occurs in isolated cases. Children are observed for changes in the nervous system (muscle hypotonia and hypertension, movement disorders, hydrocephalus), as well as the organ of vision, there may be developmental delay.
Diagnosis of toxoplasmic hepatitis
In the presence of congenital hepatitis, it is necessary to differentiate toxoplasmosis from other congenital infections accompanied by the development of hepatitis. These are nitomegalovirus infection, hepatitis B, Epstein-Barr infection, listeriosis, etc. Of primary importance is the detection of serological markers of the current infection. Currently, the diagnosis of congenital toxoplasmosis is established based on the detection of anti-toxoplasma antibodies (anti-toxо) of class IgM, class IgA in children in the first months of life using the ELISA method, but not all children with congenital toxoplasmosis are identified with these antibodies. In 30-60% of these children, anti-toxo IgM and IgA are not detected.
Only gradually, over the course of several months, up to 1 year of life, are anti-toxo IgG formed in increasing titers.
In recent years, new approaches to the early diagnosis of congenital toxoplasmosis have emerged, including asymptomatic infection at birth.
One of them is the use of recombinant T. gondii antigens, of which there are currently 6. It has been shown that in children with congenital toxoplasmosis, antibodies to recombinant toxoplasma antigens of the IgM class are detected in 97% of cases already in the first two months of life.
Another method, more labor-intensive and not always effective, is based on the detection of the toxoplasma DNA genome in blood serum or other biological substrates in newborns with congenital toxoplasmosis, as well as in the amniotic fluid of fetuses. The effectiveness of this method of toxoplasmosis identification is estimated at 60-70%.
Treatment of toxoplasmosis hepatitis
Etiotropic therapy: children are prescribed pyrimethamine (chloridine) in a daily dose of 0.5-1 mg per 1 kg of body weight for 5 days. Such 5-day cycles are repeated 3 times, with intervals of 7-10 days. At the same time, sulfadimidine is prescribed in a dose of 0.2 g per 1 kg of the child's body weight for 7 days. To prevent the side effects of pyrimethamine (chloridine), folic acid is prescribed in a daily dose of 1-5 mg for 30 days. Hepatoprotectors are used.
Prevention of toxoplasmic hepatitis
It is necessary to conduct sanitary and educational work with pregnant women. It is recommended to wash hands thoroughly after contact with fresh meat, with domestic animals, to wash vegetables, greens, berries thoroughly. Specific prevention of toxoplasmosis has not yet been developed.