Toxoplasmosis is a zoonotic protozoal infection that has a long course and leads to damage to the nervous, lymphatic, visual, muscular systems, myocardium, liver, spleen. Acute toxoplasmosis occurs with feverish intoxication syndrome, lymphadenopathy, hepatosplenomegaly, skin rashes; in severe cases – with the development of myocarditis, encephalitis, encephalomyelitis. The diagnosis of toxoplasmosis is established by bacteriological seeding, PCR, ELISA. Treatment of toxoplasmosis includes taking etiotropic antiparasitic drugs, desensitizing, restorative agents, immunotherapy with toxoplasmin.
Toxoplasmosis is a chronic parasitic invasion caused by intracellular protozoa (toxoplasmas) and accompanied by the development of lymphadenitis, hepatitis, meningoencephalitis, pneumonia, myocarditis, myositis, etc. The infection rate of the population with toxoplasmosis is extremely high: in Europe and North America it is 25-50%; in Africa, South and Latin America – up to 90%.
Toxoplasmosis is a huge danger for pregnant women and people with reduced immunity. In the first case, intrauterine infection of the fetus may occur with spontaneous termination of pregnancy, stillbirth, or the formation of embryonic and fetopathies; in the second, toxoplasmosis acquires a severe manifest course. Given the multiple and diverse clinical manifestations, toxoplasmosis is relevant not only for infectious diseases, but also for neurology, ophthalmology, pulmonology, cardiology.
The infectious agent leading to the disease is Toxoplasma gondii (tocosplasm), belonging to the genus of obligate intracellular microorganisms, the order of coccidia, the class of spores. Toxoplasma has a curved crescent shape, one end of which is pointed, and the other is more rounded, 4-7mkm long and 2-5 microns wide. In its development, the causative agent of toxoplasmosis passes through the phases of sexual and asexual reproduction and the stages of trophozoites, cysts and oocysts.
The sexual cycle takes place in the intestinal epithelial cells of representatives of the feline family (domestic cats, lynx, jaguar, cougar, etc.), which act as the final hosts of toxoplasmas. Here gametocytes are formed, which then differentiate into male and female gametes; when they merge, a zygote is formed, and then an oocyst. With the feces of cats, oocysts are released into the external environment, where they turn into invasive forms – sporozoites.
The asexual reproduction cycle of toxoplasmas occurs in the cells of various tissues (central nervous system, liver, myocardium, placenta, etc.) of humans and warm-blooded animals. In the body, the parasite exists in the form of trophozoites that reproduce by longitudinal division. In the chronic course of toxoplasmosis, pathogens take the form of tissue cysts, which can remain in a “dormant” state for decades and reactivate with a decrease in immunity, causing a relapse of toxoplasmosis. Toxoplasma cysts and oocysts are highly resistant in the external environment (they persist in the soil for more than 1 year) and are resistant to the effects of chemotherapy drugs.
Infection with toxoplasmosis most often occurs by alimentary means when eating foods seeded with oocysts, as well as raw meat of infected animals; less often – by contact through damaged skin. During pregnancy, vertical transmission of infection to the fetus through the placenta is possible. Less often, toxoplasmosis infection occurs parenterally (with blood transfusion or organ transplantation).
Once in the human body through the gastrointestinal tract, oocysts are introduced into the enterocytes of the lower small intestine, from where they penetrate into the mesenteric lymph nodes, causing their inflammation (mesadenitis), necrosis, calcification and the formation of specific granulomas. From the primary lymphatic focus, toxoplasmas enter the bloodstream and are spread hematogenically throughout the body, where they are fixed in target organs: liver, spleen, myocardium, central nervous system, eye membranes, skeletal muscles, causing the formation of necrosis, granulomas, impaired function of the affected organs.
The vital activity of toxoplasmas is accompanied by the release of allergens and toxins, which finds expression in the development of general infectious and allergic syndromes. As specific antibodies are developed, the vegetative forms of toxoplasmas are encysted, which is marked by the transition of toxoplasmosis to a chronic form. With a decrease in the activity of the immune system (in AIDS patients, hematological and oncological patients), reactivation of infection with a generalized course is possible.
Taking into account the nature of infection, congenital and acquired toxoplasmosis are distinguished. Acquired infection can occur in acute, chronic and latent form; in this case, the latent form is divided into primary and secondary, developing after acute or relapse of chronic toxoplasmosis.
Approximately 95-99% of people have toxoplasmosis in the form of a latent infection. In the acute manifest form of toxoplasmosis, the incubation period is 2-3 weeks. Mild and subclinical course of toxoplasmosis is usually diagnosed retrospectively based on positive results of skin tests with toxoplasmin, serological reactions, calcified lymph nodes and other signs.
Clinical manifestations of severe generalized toxoplasmosis develop acutely with sudden fever (t – up to 38-39 ° C) and the phenomena of general intoxication (cognition, decreased appetite, myalgia, arthralgia). It is characterized by an increase in the liver and spleen (hepatosplenomegaly), the development of lymphadenopathy, the appearance of maculopapular rashes on the skin. Most often, the reaction is expressed from the cervical, axillary, inguinal, mesenteric lymph nodes, as well as mediastinal lymph nodes. Skin rashes with toxoplasmosis are located all over the body (except for the scalp, palms and soles), can merge into spots with uneven wavy edges. At the height of the severity of the process, acute myocarditis, encephalitis, meningoencephalitis, encephalomyelitis can develop. Severe forms of acute toxoplasmosis can be fatal.
Chronic toxoplasmosis is characterized by a long torpid course. Common symptoms include subfebrility, malaise, weight loss, generalized arthralgia, lymphadenopathy. Manifestations of mesadenitis are dyspeptic disorders: nausea, flatulence, abdominal pain, constipation. Specific signs of chronic toxoplasmosis are muscle tissue damage, manifested by myositis. Heart damage causes the development of focal or diffuse changes in the myocardium or pericarditis, manifested by fatigue, palpitations, shortness of breath, cardialgia.
On the part of the nervous system, the phenomena of asthenia and vegetative-vascular dystonia, neurasthenic reactions and phobias are noted. The long-term chronic course of toxoplasmosis leads to the development of epilepsy, mental disorders, and a decrease in intelligence. Endocrine disorders may include impotence, menstrual irregularities, secondary adrenal insufficiency. Eye damage in toxoplasmosis occurs in the form of progressive myopia, uveitis, retinitis and chorioretinitis with optic nerve atrophy.
The course and outcomes of congenital toxoplasmosis depend on the gestational age of the fetus. Infection in the first and second trimester leads to intrauterine fetal death or the formation of intrauterine malformations – blastopathies, embryo- and fetopathies. In the case of a later intrauterine infection (in the third trimester), the child is born with a chronic, subacute or acute form of toxoplasmosis; at the same time, the later the infection occurs, the more severe the symptoms are at the time of birth.
The condition of newborns with an acute form of toxoplasmosis is severe from the first days. There is a febrile body temperature, pronounced intoxication, abundant polymorphic rashes on the skin, generalized lymphadenopathy, hemorrhages in the mucous membranes and sclera. The liver and spleen are usually enlarged, jaundice often develops, dyspeptic disorders. Acute toxoplasmosis in newborns can lead to the development of pneumonia, myocarditis, encephalitis, meningoencephalitis and death. The subacute and chronic course of toxoplasmosis is characterized by hydrocephalus, convulsive syndrome, prolonged jaundice, subfebrility, chorioretinitis.
In the long-term period, persistent irreversible changes due to intrauterine infection are detected. Such consequences can be a lag in physical development, mental and speech development delay (ZPR and ZRR), microcephaly, oligophrenia, epilepsy, microphthalmia, blindness, hearing loss, deafness. These and other disorders are regarded as residual toxoplasmosis. Congenital toxoplasmosis can have a long latent course with clinical manifestation at 2-7 years of life of the child.
In the diagnosis of intrauterine infection, an obstetric anamnesis, the results of the analysis of TORCH infections in the mother and serological reactions in the newborn, the study of amniotic fluid and placenta by PCR are given a big role. Children need the supervision of a pediatrician, a pediatric ophthalmologist, an otolaryngologist, a neurologist; lumbar puncture, CT of the brain, neurosonography. Congenital toxoplasmosis should be differentiated from congenital rubella, herpes, listeriosis, cytomegaly, chlamydia infection, intracranial birth trauma.
Among the clinical manifestations, the combination of lymphadenopathy, hepatosplenomegaly, eye and CNS lesions has the greatest diagnostic value in acquired toxoplasmosis. It is mandatory to consult a patient with a neurologist, ophthalmologist, therapist or cardiologist. The main list of instrumental studies includes EEG, Echo-EG, radiography or CT of the skull, ophthalmoscopy, ECG.
For laboratory confirmation of toxoplasmosis, parasitological and immunological methods are used. The first involve microscopic detection of the pathogen in smears-prints of affected organs, biopsy of lymph nodes, blood or cerebrospinal fluid. It is possible to conduct a biological test with infection of laboratory rodents. Immunological diagnostics of toxoplasmosis includes serological methods (IFT, IFA, ELISA, RPH), as well as an intradermal allergic test with toxoplasmin. In the case of acquired infection, tuberculosis, lymphogranulomatosis, rheumatism, cat scratch disease, infectious mononucleosis, herpesvirus infection are excluded first of all.
Depending on the predominant organ lesions, the treatment of patients with toxoplasmosis is carried out in specialized departments: neurological, therapeutic, cardiological, ophthalmological, etc. Etiotropic therapy for manifest toxoplasmosis is carried out with antiparasitic drugs: more often with chloridine in combination with sulfonamide drugs or tetracycline antibiotics; with contraindications – metronidazole, chloroquine, aminoquinol. Usually, the course of treatment for toxoplasmosis consists of 3 5-10-day cycles, repeated at intervals of 7-10 days. Additionally, antihistamines and general tonic agents, multivitamins are prescribed. In chronic toxoplasmosis, the drug course of treatment is supplemented with immunotherapy – intradermal administration of toxoplasmin. The tactics of management of pregnant women with primary chronic or primary latent toxoplasmosis involves chemoprophylaxis with spiramycin. In the acute form of toxoplasmosis in a pregnant woman, a medical abortion is recommended.
Prevention of human infection includes a complex of veterinary (examination and treatment of pets) and sanitary and hygienic measures. The latter involve avoiding close contact with cats, careful heat treatment of meat, protection of children’s sandboxes from the feces of neglected animals, compliance with personal hygiene measures. Examination of pregnant women for toxoplasmosis is carried out three times, in each trimester.