Pulmonary toxoplasmosis



Overview.

Pulmonary toxoplasmosis is a respiratory disease, lung inflammation caused by Toxoplasma gondii, which is a zoonotic disease. Clinical manifestations include headache, myalgia, dry cough, etc. Cough is paroxysmal, and a few cough a lot of mucus sputum or mucus blood sputum. Chest X-ray shows diffuse fuzzy or fine nodular infiltrating shadow. The drugs of choice for treatment are acetamiprid and sulfadiazine. Spiramycin and clindamycin can also be used, either alone or in combination with pyrimethamine or sulfadiazine.

Causes

Pulmonary toxoplasmosis is caused by Toxoplasma gondii of the genus Toxoplasma gondii in the order Sporozoa, Coccidioidea. The terminal host is the cat or certain felines, and there is a wide range of intermediate hosts, including mammals (pigs, sheep, dogs, cows, rats, rabbits), birds (chickens, ducks, pigeons, etc.) and humans. There are five different developmental stages, namely trophozoites, envelopes, cleistothecia, gametophytes and vesicles. In humans, it is mainly found in intermediate hosts, but can also be found in terminal hosts.

Symptoms

The clinical manifestations of pulmonary toxoplasmosis may be acute in onset or chronic in duration. In acute onset, most of the initial symptoms are similar to those of the upper senses, such as headache, myalgia, dry cough, etc. The cough is paroxysmal, and a few cough up a lot of mucus sputum or mucus blood sputum. The chronic course may have clinical manifestations similar to chronic bronchitis, wheezing bronchitis or bronchial asthma attacks. It may be combined with pleurisy, heart failure, and pericarditis.

Acquired immunodeficiency syndrome (AIDS) combined with pulmonary toxoplasmosis is often diffuse lung inflammation, which may be characterized by high fever, cough, cyanosis, and dyspnea, or symptoms of rash, lymph node enlargement, and meningitis.

Congenital pulmonary toxoplasmosis is most often due to acute maternal infection in late pregnancy. Newborns may be born with retinochoroiditis, hydrocephalus or microcephaly, cerebral malformations, convulsions, psychomotor disorders, and hepatosplenomegaly. If the carrier state is present after birth, symptoms gradually appear over weeks to months, with neurologic abnormalities, mainly strabismus, insomnia, seizures, psychomotor or mental retardation or associated pneumonia.

Examination

1. Pathogenetic testing

Direct light microscopy: Specimens of blood, cerebrospinal fluid, bone marrow, anterior chamber fluid, sputum, urine, saliva, other exudates, as well as lymph nodes, muscle tissues or other biopsies can be used as direct smears or prints. Toxoplasma gondii trophozoites, typically crescent-shaped, can be seen inside and outside the cells by Giemsa or Ritter staining. Toxoplasma gondii can also be pear-shaped or ovoid in tissue cells.

2. Immunological examination

Staining test: According to Sabin in 1948, fresh Toxoplasma gondii mixed with normal serum stains darkly with alkaline methylene blue, while mixed with immune serum stains lightly or does not stain, which suggests that the sensitivity and specificity of this test is high. Other tests such as indirect fluorescent antibody, indirect hemagglutination, complement binding test, all have certain diagnostic reference value, and intradermal test also has high specificity.

3. Imaging examination

Lung X-ray shows four types of changes: bronchopneumonia, atypical pneumonia, pleurisy and combined cardiovascular lesions. Bronchopneumonia type: the lesions are distributed along the bronchial tubes in the two middle and lower lung fields, with uneven density, patchy inflammatory shadows with fuzzy edges, and widened hilar shadows. This type is mostly seen in children and elderly patients. Atypical pneumonia type: patchy flocculent shadow of peribronchial mesenchyme with lighter density and blurred edges, mainly located in the middle and lower lung fields; pleurisy type: signs of pleural effusion. Combined cardiovascular pathology type: there may be X-ray signs of heart failure and pericardial effusion.

Diagnosis

Diagnosis should be made by combining the results of history, clinical manifestations, staining test, immunologic examination, and intradermal test. The diagnosis can be confirmed by finding Toxoplasma gondii in sputum, pleural fluid, cerebrospinal fluid and other body fluids, or biopsy. Positive staining tests, complement binding tests, intradermal tests, or serum antibody tests are diagnostic references.

Treatment

Ethylaminopyrimidine and sulfadiazine, both of which interfere with folate metabolism in Toxoplasma gondii, thereby inhibiting the division and reproduction of Toxoplasma gondii trophozoites, are ineffective drugs against encapsulation. Both drugs can pass the blood-brain barrier, and have a definite effect on potential or symptomatic Toxoplasma meningitis. They are often used in combination or alone. Sulfamethoxazole/metronidazole (compound sulfamethoxazole) is also available. Spiramycin and clindamycin can be used alone or in combination with ethamidopyrimidine or sulfadiazine.

Prevention

Do not eat uncooked meat, eggs, dairy and other foods, and wash your hands before meals. It is best to eat well-done meat.