Sexually Transmitted Diseases - I. I. Mavrov 2005

Urogenital diseases caused by protozoa
Toxoplasmosis

Toxoplasmosis is a parasitic disease belonging to the group of protozoan zoonoses. It is characterized by A wide variety of clinical manifestations, yet it often proceeds asymptomatically and frequently remains undiagnosed. A warm and humid climate fosters the spread of the infection. In certain patient groups, including newborns and individuals with AIDS, toxoplasmosis poses a life-threatening risk.

Etiology. The causative agent is Toxoplasma gondii, an obligate intracellular parasite classified among the Protozoa of the phylum Apicomplexa, subclass Coccidia. It is widespread globally and infects various animals and birds without causing disease in them. Definitive hosts of the parasite are various feline species, within whose bodies toxoplasmas complete their life cycle, analogously to the malaria parasite's cycle in mosquitoes. Other animals and humans serve as intermediate hosts. Within the host Organism, the parasite can exist in one of three forms: tachyzoites, cysts, and oocysts. Tachyzoites are rhombus-shaped or round Cells measuring 3x7 µm with a well-defined Nucleus. At this stage, the parasite is capable of invading virtually all cells. Inside The Cell, the parasites multiply rapidly, leading to the rupture of The cell membrane and their subsequent dissemination. Eventually, the host organism begins to produce Antibodies against the parasites, which destroy the tachyzoite forms.

Only the parasites located intracellularly survive. With the appearance of antibodies, the parasites transition into another stage, forming cysts that reside in the Tissues. Tissue cysts are typically round or spindle-shaped and may contain up to 3,000 parasites.

Epidemiology and general pathology. In many cases, human infection and the subsequent Development of the disease occur asymptomatically. Its Diagnosis is critically important in obstetric practice, as a disease that is asymptomatic in the mother can affect the unborn child. According to Wilson et al. (1980), congenital toxoplasmosis is observed annually in 3,500 children in the USA, and its severe course with fetal involvement accounts for approximately 1 case per 8,000 individuals.

Congenital infection is frequently the cause of stillbirth, as well as chorioretinitis, The Development of intracerebral calcifications, psychomotor disorders, Hydrocephalus, or microcephaly. Such complications are observed when the mother is infected during Pregnancy.

Perinatal toxoplasmosis causes blindness and damage to other Organs in the child. Maternal infection During the first 3 months of pregnancy typically leads to fetal demise (stillbirth) or the development of severe Central Nervous system anomalies.

Toxoplasmas exhibit a pronounced tropism toward parenchymal cells and Cells of the reticuloendothelial system.

Cysts can form in any organ as early as 8 days post-infection and persist throughout the host's life. Tissue cysts most frequently form in skeletal Muscles, the Brain, and ocular tissues. The appearance of tissue cysts indicates the onset of the latent phase of infection.

Domestic cats and other members of the feline family contract toxoplasmosis by consuming the cyst-containing meat of their prey, such as rats, mice, and birds. These cysts are resistant to the action of gastric digestive Enzymes.

In the Small Intestine, tachyzoite forms are released from the cysts and undergo developmental stages within the intestinal epithelial cells. The end result is The formation of oocysts, which are excreted into the external environment via feces. Under favorable Temperature and humidity conditions, oocysts complete their maturation within 3-4 days, becoming infectious to humans.

Oocysts can remain viable for several months and are resistant to many chemical agents, including standard disinfectants. Desiccation, heat Treatment, and freezing destroy them.

Modes of transmission. The portal of entry consists of the digestive tract organs (the lower section of the small intestine). For a long time, it was widely accepted that infection occurred primarily transplacentally. In recent years, The Role of cats in parasite transmission has been established. Viable cysts can be carried by flies and cockroaches. Transmission of the infection is also possible via Blood transfusion and organ transplantation. Laboratory personnel can contract toxoplasmosis through careless handling of infected material. Intrauterine fetal infection plays a major role. Infection of a pregnant woman with acute toxoplasmosis carries the risk of transplacental fetal infection.

Clinical Features. The clinical manifestations of toxoplasmosis in adults are extremely diverse and can mimic various diseases, particularly those of viral origin, such as infectious mononucleosis or cytomegalovirus infection.

Humans are relatively resistant to infection. Contamination may occur imperceptibly and remain undetected, although moderately pronounced lymphadenopathy, malaise, fever, and occasionally a Skin rash may develop.

The posterior cervical and supraclavicular Lymph Nodes are most frequently affected, though unilateral involvement is also possible. Enlarged nodes are firm and typically tender.

The disease in a pregnant woman is rarely pronounced. The clinical picture depends on which Organ Systems are affected. Symptoms may include headache, depression, myalgia, Pneumonia, hepatitis, myocarditis, encephalitis, and even convulsions.

Fetal involvement. Toxoplasmas most commonly affect the fetus during primary maternal infection during pregnancy—in approximately 1/3 of such cases.

If maternal infection occurs prior to pregnancy, the infection is rarely transmitted to the fetus. The degree of risk of fetal infection also depends on the trimester of pregnancy in which maternal infection takes place.

If maternal infection occurs during the first half of pregnancy, the fetus is affected less frequently, but the disease runs a more severe course in the newborn. When infection and the acute phase of toxoplasmosis occur during early Cytology/cytology/21.html">Stages of intrauterine development, the child may be born with signs of meningoencephalitis or encephalomyelitis. Variations in the clinical manifestations in newborns may result from the immaturity of the fetal immune system. When the fetus is infected in the third trimester of pregnancy, the child may be born with symptoms of acute disease (fever, hepatosplenomegaly, jaundice, skin rash, cyanosis, edema, iridocyclitis, chorioretinitis).

In the most severe cases, intrauterine toxoplasmosis leads to fetal demise. Sometimes, however, signs of fetal damage may be so subtle that the child appears completely healthy at birth. Intrauterine damage manifests later as chorioretinitis, mental retardation, Hearing loss, or other neurological defects.

Toxoplasmosis and Spontaneous Abortion. There is a widespread belief that acute toxoplasmosis during the early months of pregnancy frequently leads to spontaneous abortion, although the exact correlation between toxoplasma infection and abortion has not yet been definitively established.

Currently, it is difficult to determine the frequency of abortions caused by toxoplasmosis. On the one hand, a higher incidence of spontaneous abortions is observed in women with anti-toxoplasma antibodies compared to those without them; on the other hand, a clear correlation between the presence of toxoplasma antibodies and a history of abortions is not evident.

An association between chronic toxoplasmosis and stillbirth or premature delivery has likewise not been established.

Diagnosis. The diagnosis of toxoplasmosis is established based on the medical history, characteristic clinical manifestations, and laboratory test data:

1) isolation of parasites from blood, CEREBROSPINAL FLUID, and other specimens; 2) inoculation of laboratory animals; 3) detection of the parasite via Microscopy; 4) serological tests.

Along with blood and cerebrospinal fluid, various exudates and Bone Marrow are commonly used as test Materials. Biopsies of lymph nodes, palatine Tonsils, and muscles, as well as ventricular fluid (in congenital cases), may also be examined.

On microscopic examination, Toxoplasma can be detected in smears and tissue sections stained with Giemsa. The presence of cysts "packed" with parasites (pseudocysts), predominantly in the brain or other CNS tissues, points strongly toward a chronic infection.

Identification of the causative agents must be confirmed by isolating them using tissue culture techniques or in developing chicken embryos. Toxoplasma can only be cultivated in the presence of living cells, which reveals typical intracellular and extracellular parasites.

The diagnosis of toxoplasmosis is also confirmed by inoculating laboratory animals, a method that plays a crucial role in establishing a definitive diagnosis. Various types of material containing Toxoplasma are administered intraperitoneally to mice, after first ensuring they are free of spontaneous toxoplasmosis. If the animals do not die, they are monitored for 6 weeks, after which blood is drawn from the tail vein or Heart to detect specific antibodies. The detection of cysts in the brain tissue of infected animals confirms the diagnosis.

The Procedure of inoculating experimental animals is time-consuming and is therefore not used by most clinical laboratories. Because the infection is often subclinical, serological Methods are the most effective and widely applied in clinical practice for diagnosing toxoplasmosis.

Toxoplasma infection induces The production of IgM and IgG antibodies. Large IgM molecules do not cross the Placenta, whereas IgG antibodies passively cross it to reach the fetus.

Currently, various serological tests are used to diagnose toxoplasmosis. The most common methods for detecting anti-Toxoplasma IgG antibodies are the Sabin-Feldman dye test, the indirect fluorescent antibody test (IFAT), and the indirect hemagglutination assay.

Recently, enzyme-linked immunosorbent assay (ELISA) has become particularly widespread for detecting toxoplasmosis. This method is relatively simple, highly sensitive and specific, and suitable for screening large populations.

Antibodies detected by serological reactions appear in the blood serum within 1-2 weeks after primary infection, reaching peak titers exceeding 1:1000 in 6-8 weeks. The titer begins to decline in the following months and may persist at a certain level throughout life.

Treatment. Medical treatment for non-pregnant women with toxoplasmosis is indicated only in cases of CNS, cardiac, pulmonary, or other vital organ involvement, or when an acute infection is complicated by immunodeficiency.

An infection acquired well before pregnancy poses no threat to the child and requires neither medical treatment nor Termination of the pregnancy.

Therapy for acute toxoplasmosis in pregnant women can prevent the development of the disease in the fetus. However, if the fetus is already infected, treating the mother with spiramycin (an antibiotic similar in action to erythromycin) is unnecessary, as the drug does not cross the placenta and cannot prevent fetal disease. Currently, there is no conclusive data regarding the efficacy of pyrimethamine (daraprim) and sulfonamides in such cases.

Many physicians do not recommend Chemotherapy during the first trimester of pregnancy. Pyrimethamine is potentially teratogenic and should be avoided during the period of fetal Organogenesis. Spiramycin is less toxic than pyrimethamine, causes no apparent adverse effects on the fetus, and is recommended for patients at various stages of pregnancy. Spiramycin is prescribed at 0.1 g twice daily for 3 weeks.

The standard treatment regimen for adults is pyrimethamine at 25 mg daily for 3 weeks following a loading dose of 50 mg, combined with sulfadiazine at 4.0 g daily in divided doses for 3 weeks. This combination exhibits a synergistic effect against the trophozoite forms of Toxoplasma. Unfortunately, there are currently no effective drugs against the parasite's cysts. Treatment may lead to Folic acid deficiency and maternal bone marrow suppression, resulting in agranulocytosis, thrombocytopenia, and anemia. To prevent this, folic acid (6 mg daily intramuscularly) is recommended throughout the course of pyrimethamine administration. The treatment course is monitored via complete blood counts (twice a week).

Children with congenital toxoplasmosis require treatment regardless of the severity of clinical manifestations. The recommended regimen is pyrimethamine at 1 mg/kg of body weight daily for 3-4 days, followed by 0.5 mg/kg daily as a single dose for 21-30 days. The maximum daily dose should not exceed 25 mg.

Alongside pyrimethamine, sulfonamides should be administered at 100 mg/kg of body weight daily (in 4 divided doses) along with 5 mg/kg of folic acid twice a week. Because these drugs are relatively toxic to children, blood parameters must be monitored twice a week. A repeat course of treatment may be necessary during the child's first year of life (2 or 3 times, depending on the clinical course).

Prevention. The most critical step is breaking the parasite's transmission chain. Physicians treating women of childbearing age should advise them on hygiene practices that minimize the risk of acquiring toxoplasmosis.

Since the primary source of infection is raw or undercooked meat, pregnant women must ensure that any meat they consume is thoroughly cooked to an internal temperature above 66 °C. Freezing meat below -20 °C for 24 hours also destroys the cysts.

Hands must be washed thoroughly after handling raw meat or coming into contact with cats. Pet cats should not be allowed outdoors, where they might hunt birds and mice or feed on refuse. Laboratory personnel working with potentially hazardous (infectious) materials must wear gloves. Fruits and vegetables should be washed meticulously before consumption, as they may be contaminated with Toxoplasma oocysts.