Morphology and Life Cycle Stages
The pathogen has a complex life cycle involving several morphological forms:
- Oocysts. Formed in the intestine of definitive hosts (felines) via sexual reproduction. These are oval structures (10–12 µm) containing two sporocysts, each with four sporozoites. They become infectious in the external environment after 3 days and can survive for up to a year.
- Tachyzoites. Rapidly dividing forms characteristic of the acute infection stage. They resemble an orange segment or crescent, measuring 4–7 µm. On Giemsa staining, their cytoplasm turns blue, and the nucleus becomes ruby-red.
- Pseudocysts. Intracellular clusters of tachyzoites (endozoites), for example, within macrophages. They lack a distinct thick wall and are surrounded by the host cell vacuole membrane. A single cell may contain from 10 to 30 organisms.
- Cysts. Formed during the transition to the chronic stage. They have a thick wall enclosing hundreds of slowly dividing parasites (bradyzoites). Cysts can reach up to 1000 µm in size and persist in host tissues for decades.
Epidemiology and Transmission
The definitive host of Toxoplasma gondii is members of the cat family (Felidae), which shed oocysts into the environment. Intermediate hosts include humans, as well as many species of wild and domestic birds and mammals.
Main routes of human transmission:
- Ingestion (primary). Eating undercooked meat containing tissue cysts and pseudocysts, or swallowing oocysts via unwashed vegetables, fruits, and contaminated water.
- Contact. The pathogen can penetrate through damaged skin and mucous membranes.
- Vertical (transplacental). Transmission from mother to fetus during a primary infection acquired in pregnancy.
- Iatrogenic. Rare cases transmitted via blood transfusions or organ transplantation.
Pathogenesis and Clinical Presentation
Upon entering the human intestine, sporozoites emerge from oocysts, penetrate lymphatic vessels, and reach regional lymph nodes, where they actively replicate (tachyzoite stage). The pathogen then enters the bloodstream, disseminates throughout the body, and invades cells of the reticuloendothelial system in various organs (neural tissue, liver, eyes, heart).
In approximately 90% of cases, acquired toxoplasmosis is asymptomatic. In manifest cases (about 10%), the disease presents non-specifically: occipital lymphadenopathy, myalgia, fever, rash, and hepatosplenomegaly are characteristic. Severe manifestations may include myocarditis, pneumonia, and meningoencephalitis.
Congenital Toxoplasmosis
A highly dangerous form resulting from primary infection of a pregnant woman (risk is approximately 3 cases per 1,000 pregnancies). The most severe consequences occur when infection happens during the first trimester.
The infection exhibits a pronounced teratogenic effect. It can lead to fetal demise, spontaneous abortion, or stillbirth. Surviving newborns frequently present with severe central nervous system, hepatic, and splenic lesions accompanied by systemic toxicity, resulting in high perinatal mortality or progression to a severe chronic form.
Diagnosis and Treatment
Immunity in toxoplasmosis is non-sterile, involving cell-mediated and humoral reactions as well as delayed-type hypersensitivity.
Laboratory diagnostic algorithm:
- Serology (primary). Detection of IgM antibodies (acute phase) and IgG. A specific test is the Sabin-Feldman dye test: patient serum antibodies alter the staining of toxoplasma cytoplasm with methylene blue.
- Microscopy. Examination of blood smears, CSF, or tissue aspirates stained with Giemsa.
- PCR. Crucial for detecting congenital toxoplasmosis and severe forms in immunocompromised patients (e.g., HIV).
- Skin test. Intradermal test with toxoplasmin (becomes positive by the 4th week).
Standard therapy includes a combination of pyrimethamine and sulfonamides. However, pyrimethamine is toxic during pregnancy and is therefore replaced by spiramycin, which does not cross the placental barrier and is safe for the fetus.