Pneumocystosis - Overview

Pneumocystosis (pneumocystis pneumonia) is an opportunistic infectious disease caused by Pneumocystis jiroveci (old name - Pneumocystis carinii), characterized by the development of pneumocystis pneumonia. Due to the possible damage to other organs and systems, the term "pneumocystosis" is more justified.

P. jiroveci (formerly P. carinii) is a common cause of pneumonia in immunocompromised patients, especially those with HIV infection. Symptoms of pneumocystis include fever, dyspnea, and cough. Diagnosis requires identification of the organism in a sputum specimen. Treatment of pneumocystis is with antibiotics, usually trimethoprim-sulfamethoxazole or pentamidine, and glucocorticoids in patients with a PaO2 less than 70 mmHg. Prognosis is generally good with prompt treatment.

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Epidemiology

Among opportunistic infections in AIDS, pneumocystosis is one of the most common diseases. Pneumocystosis is diagnosed throughout the year, but the greatest number of cases occurs in the winter-spring period with a maximum in February-April.

The primary reservoir of pneumocystis in nature is unknown. Pneumocystis are widespread in all regions of the world and are found in almost all animals: wild, synanthropic and farm animals. Widespread carriage of pneumocystis among humans has been revealed. Infection with pneumocystis occurs through the air from a person (patient or carrier). When studying nosocomial outbreaks of pneumocystis, the dominant role of medical personnel as a source of infection has been proven. In the department for patients with HIV infection, widespread carriage of pneumocystis among patients (92.9%) and personnel (80%) was revealed.

Most researchers believe that the mechanism of clinically expressed disease is mainly associated with the activation of latent infection. People become infected in early childhood - even before the age of 7 months, and by the age of 2-4 years, 60-70% of children are infected. On the other hand, there are well-known cases of group pneumocystosis diseases and outbreaks of hospital-acquired infection not only in children but also in adults (in departments for premature babies, young children with CNS pathology, in departments for patients with hemoblastoses, in a tuberculosis hospital). Cases of family infection have been described (the sources of infection were parents, and their weakened children fell ill). The development of relapses of pneumocystis pneumonia in patients with HIV infection is most likely associated not with the activation of latent infection, but with a new infection.

Impaired cellular and humoral immunity predisposes to the development of the disease, but T-cell immunodeficiency is of primary importance: a decrease in the number of CD4 cells and an increase in the content of cytotoxic cells leads to the manifestation of the disease.

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Causes pneumocystosis

P. jiroveci is a ubiquitous airborne organism that does not cause any disease in immunocompetent patients. Patients with HIV infection and CD4+ counts <200/μL, organ transplant patients, hematologic malignancies, and patients receiving glucocorticoids are at risk for developing P. jiroveci pneumonia.

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Risk factors

Pneumocystis has risk groups - patients with HIV infection, premature, weakened newborns and young children with agammaglobulinemia or hypogammaglobulinemia, rickets, hypotrophy, patients with leukemia, cancer, organ recipients receiving immunosuppressants, elderly people from nursing homes, patients with tuberculosis.

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Pathogenesis

The pathogenesis of Pneumocystis pneumonia is associated with mechanical damage to the walls of the pulmonary interstitium. The entire life cycle of Pneumocysts occurs in the alveoli, to the wall of which they are very tightly attached. Pneumocysts need a large amount of oxygen to develop. Gradually multiplying, they fill the entire alveolar space, capturing ever larger areas of lung tissue. With close contact of trophozoites with the walls of the alveoli, damage to the lung tissue occurs, the extensibility of the lungs gradually decreases, and the thickness of the alveolar walls increases by 5-20 times. As a result, an alveolar-capillary block develops, which leads to severe hypoxia. The formation of atelectasis areas aggravates the violation of ventilation and gas exchange. In patients with immunodeficiency states, a marked decrease in the number of CD4 + lymphocytes (less than 0.2x10 ⁹ /l) is critical for the development of Pneumocystis pneumonia.

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Symptoms pneumocystosis

Most have fever, dyspnea, and a dry, nonproductive cough that develops subacutely (more than a few weeks; HIV infection) or acutely (more than a few days; other causes that impair cell-mediated immunity). Chest radiography characteristically shows diffuse, bilateral hilar infiltrates, but 20% to 30% of patients have normal radiographs. Arterial blood gas studies reveal hypoxemia, with an increased alveolar-arterial O2 gradient, and pulmonary function tests show altered diffusing capacity (although this is rarely done diagnostically).

Diagnostics pneumocystosis

The diagnosis of pneumocystosis is established on the basis of a complex of clinical and laboratory data.

The diagnosis is confirmed by identifying the organism after treatment with methenamine silver, Giemsa, Wright-Giemsa, Grocott modification, Weigert-Gram, or immunochemical staining using monoclonal antibodies. Sputum samples are usually obtained by induced collection or bronchoscopy.

Sensitivity ranges from 30 to 80% with sputum induction and more than 95% with bronchoscopy with bronchoalveolar lavage.

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Treatment pneumocystosis

Pneumocystis is treated with trimethoprim-sulfamethoxazole (TMP-SMX) 4-5 mg/kg intravenously or orally 3 times daily for 14-21 days. Treatment may be started before diagnosis is confirmed because P. jiroveci cysts persist in the lungs for many weeks. Adverse effects, more common in patients with AIDS, include skin rashes, neutropenia, hepatitis, and fever. Alternative regimens include pentamidine 4 mg/kg IV once daily or 600 mg daily by inhalation, atovaquone 750 mg orally twice daily, TMP-SMX 5 mg/kg orally 4 times daily with dapsone 100 mg orally once daily, or clindamycin 300-900 mg IV every 6-8 hours with primaquine 15-30 mg orally initially, also for 21 days. The use of pentamidine is limited by the high incidence of toxic adverse effects, including renal failure, hypotension, and hypoglycemia. Additional glucocorticoid therapy is required in patients with a PaO2 less than 70 mmHg. The suggested regimen is oral prednisolone 40 mg twice daily (or equivalent) for the first 5 days, 40 mg/day for the next 5 days (as a single dose or divided into 2 doses), and then 20 mg once daily for long-term treatment.

HIV-infected patients with a history of P. jiroveci pneumonia or with CD4+ < 200/mm3 should receive prophylaxis with TMP-SMX 80/400 mg once daily; if intolerant, dapsone 100 mg orally once daily or aerosolized pentamidine 300 mg once monthly. These prophylactic regimens may also be indicated for patients without HIV infection at risk for P. jiroveci pneumonia.

Forecast

Pneumocystis has an unfavorable prognosis. On average, the number of patients who survive after suffering from pneumocystis pneumonia is 75-90%. In case of relapses, about 60% of patients survive.

Overall mortality for P. jiroveci pneumonia in hospitalized patients is 15-20%. Risk factors for death may include a history of P. jiroveci pneumonia, advanced age, and CD4+ cell count <50/μL in HIV-infected patients.

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