Toxoplasmosis Hepatitis
Last reviewed: 23.04.2024
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Congenital toxoplasmosis Hepatitis is a disease caused by toxoplasm obtained by the fetus antenatally from the mother with toxoplasmosis.
Spread
Toxoplasmosis is one of the most urgent 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 agricultural animals, it infects people - from 6 to 90%. For example, in the German Autonomous District, infection with toxoplasma was detected in 36.3% of residents, and in the Kamchatka region - in 13%.
In England, seropositivity for toxoplasma is 9.1%.
Among those infected with toxoplasm, women predominate, which is probably due to their greater involvement in cooking 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 is found in 18% of cases.
In Russia, antibodies to toxoplasma in pregnant women are detected at a frequency of 10 to 40.6%. Infection of newborns with toxoplasm reaches significant values - from 17.3 to 26.3%.
In fetuses and newborns that 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 herpes simplex virus is 11.5%.
Causes of toxoplasmosis hepatitis
Pathogen of toxoplasmosis - Toxoplasma gondii - belongs to the Protozoa type, Sporoviki class, to the order of Coccidia. There are proliferative forms of toxoplasm, or endozoids (taxozoids), cysts and oocytes (resting stage of the pathogen in the intestine of the final host). Cysts are formed in the organism of the intermediate host (man, cattle). They are localized mainly in the brain, eyes, myocardium and muscles. Inside the cysts there is also a multiplication of toxoplasm. Further, they exit from the cysts, penetrate into the host cells, where their multiplication begins. This occurs with relapses of toxoplasmosis in humans. Viable parasites in cysts can be preserved in the infected organism for life. From person to person toxoplasm is not transmitted. With the primary infection due to toxoplasm, which occurred during pregnancy, the causative agent is transmitted to the fetus. Already infected earlier, and therefore, a non-immune woman, a fresh toxoplasmosis infection is accompanied by parasitemia, at least briefly, while endoids (proliferative forms of the pathogen) can be introduced into the placenta by blood flow. Further, if the barrier function of the trophoblastic 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 the fetal lesions increases with the duration of pregnancy, but the risk of infection of the fetus increases.
Infection with fetal toxoplasma causes acute or chronic forms of the disease, causes developmental abnormalities, can cause damage to various organs and systems.
[Morphology
With congenital toxoplasmosis, hepatitis with greater frequency also describes the damage of other organs. For example, meningoencephalitis, myocarditis, pneumonia, pyelonephritis, enterocolitis and others are observed.
The liver is usually enlarged. Histological examination indicates the preservation of the lobular structure, the discomplexation of the hepatic beams, and the presence of lymphohistiocytic infiltration. In hepatocytes, hyaline and vacuolar dystrophy is detected, centrolobular necrosis of hepatocytes and necrosis are observed along the periphery of the lobes, cholestasis is present. In lymphohystiocytic infiltrates, toxoplasmic cysts are detected, small granulomas are formed from lymphoid and monocytic cells with an admixture of epithelioid cells.
Symptoms of toxoplasmosis hepatitis
In the majority of children with congenital toxoplasmosis hepatitis are born full-term, they have an Apar scores of 7-8 points. The condition is estimated as of moderate severity, in some newborns it can be severe. There is intoxication in the form of lethargy, refusal to eat, regurgitation. Jaundice appears on 2-3 days of life - from weak to intense. Increase in liver size, seal 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 registered in 30-40% of patients, while the spleen protrudes from the hypochondrium for 1-2 cm. Exanthema may appear in the form of a patchy-papular rash in the inguinal and gluteal regions. In 35-40% of cases there is lymphadenopathy. Changes in the heart are expressed in the presence of systolic murmur and muffled heart tone in 30% of newborns.
In the biochemical analysis of blood; 2-3-fold increase in the level of total bilirubin, approximately equal to the content of conjugated and non-conjugated pigment fractions; very weak, mainly in 2 phases, increased activity of ALT, ACT, LDH.
In the syndrome of cholestasis, pronounced icterism of the skin and sclera are noted, an increase in the serum concentration of total bilirubin by a factor of 8-10 with some predominance of the conjugated fraction. At the same time, the level of activity of alkaline earth metals and GGTP increases 2-2.5 times. Children have anxiety, itching of the skin. Hemorrhagic syndrome (petechial rash, hemorrhage at the injection site) occurs more often when a cholestatic variant of hepatitis occurs.
With ultrasound, there is an increase in echo-density of the liver in almost all children with congenital toxoplasmic hepatitis. With the cholestatic variant there is a thickening of the gallbladder walls. Pancreatopathy is registered in 43% of cases.
Variants of flow
The course of congenital toxoplasma hepatitis is acute. Gradually, for 2-3 months, the condition of children improves: intoxication decreases, jaundice disappears; with a cholestatic variant of the disease, jaundice can last up to 4-5 months. At the same time, the biochemical parameters of cholestasis are normalized.
These children die, who, in addition to hepatitis, show severe damage to other organs and systems (meningoencephalitis, pneumonia, myocarditis, etc.).
Chronic course of congenital toxoplasmosis hepatitis occurs in isolated cases. Children are observed about changes in the nervous system (muscle hypotension and hypertension, motor disorders, hydrocephalus), as well as the organ of vision, may be a developmental lag.
Diagnosis of toxoplasmosis hepatitis
In the presence of congenital hepatitis, it is necessary to differentiate toxoplasmosis with other congenital infections, accompanied by the development of hepatitis. This nitomegalovirus infection, hepatitis B, Epstein-Barr infection, listeriosis, etc. The main significance is the detection of serological markers of the current infection. Currently, the diagnosis of congenital toxoplasmosis is established on the basis of the detection in children of the first months of life of anti -toxoplasma antibodies (antti-toxo) of IgM class, IgA class by ELISA, 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, for several months, up to 1 year of life, anti-tooth IgG is formed in accruing titles.
In recent years, new approaches to the early diagnosis of congenital toxoplasmosis have appeared, including with asymptomatic infection at birth.
One of them is the use of recombinant T. Gondii antigens, which currently number 6. It is shown that in children with congenital toxoplasmosis in the first two months of life in 97% of cases antibodies to recombinant antigens of toxoplasm of IgM class are detected.
Another method, more laborious and not always effective, is based on the detection in the blood serum or other biological substrates of the genome of toxoplasma DNA in newborns with congenital toxoplasmosis, as well as in the amniotic fluid of the fruit. The effectiveness of this method of identifying toxoplasmosis is estimated at 60-70%.
Treatment of toxoplasmosis hepatitis
Etiotropic therapy: children are prescribed pyrimethamine (chloride) 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 administered at a dose of 0.2 g per 1 kg of the child's body weight for 7 days. To prevent the side effect of pyrimethamine (chloridine), folic acid is prescribed in a daily dose of 1-5 mg for 30 days. Used hepatoprotectors.
Prophylaxis of toxoplasmosis hepatitis
It is necessary to conduct sanitary education work with pregnant women. To recommend to wash hands thoroughly after contact with fresh meat, with domestic animals, carefully wash vegetables, greens, berries. Specific prophylaxis of toxoplasmosis has not yet been developed.