Pneumocystosis: an overview

Pneumocystosis (pneumocystosis, pneumocystis pneumonia) is an opportunistic infectious disease caused by Pneumocystis jiroveci (formerly known as Pneumocystis carinii), characterized by the development of pneumocystis pneumonia. In connection with the possible defeat of other organs and systems, the term "pneumocystosis" is more justified.

P. Jiroveci (formerly P. Carinii) is a common cause of pneumonia in immunodeficient patients, especially in HIV-infected patients. Symptoms of pneumocystosis include fever, dyspnoea and cough. Diagnosis requires the identification of an organism in a sputum sample. Treatment of pneumocystis is carried out with antibiotics, usually trimethoprim-sulfamethoxazole or pentamidine and glucocorticoids in patients with PaO2 less than 70 mmHg. Art. The prognosis is generally favorable with timely treatment.

[1], [2], [3], [4], [5], [6], [7]

Epidemiology

Among opportunistic infections in AIDS, pneumocystis is one of the most common diseases. Pneumocystis is diagnosed throughout the year, but the greatest number of diseases falls on the winter-spring period with a peak in February-April.

The primary reservoir in the nature of pneumocyst is not known. Pneumocysts are widespread in all regions of the world and are found in virtually all animals: wild, synanthropic and agricultural. A wide spread of pneumocystis among people was also revealed. Infection with pneumocystis occurs aerogenically from a person (patient or carrier). In the study of nosocomial pneumocystosis outbreaks, the dominant role of medical personnel as a source of infection has been demonstrated. In the department for patients with HIV infection, a wide spread of pneumocyst among patients (92.9%) and personnel (80%) was revealed.

Most researchers believe that the mechanism of a clinically pronounced disease is mainly associated with the activation of a latent infection. People become infected in early childhood - even before the age of 7 months, and in 2-4 years already 60-70% of children are infected. On the other hand, cases of group diseases with pneumocystis and outbreaks of intra-biliary infection are well known not only in children, but also in adults (in preterm infants, young children with CNS pathology, in hemoblastosis departments, in a tuberculosis hospital). Cases of family infection are described (sources of infection were parents, and their weakened children became ill). The development of relapses of pneumocystis pneumonia in patients with HIV infection is most likely due not to the activation of a latent infection, but to a new infection.

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

[8], [9], [10], [11], [12], [13]

Causes of the pneumocystis

P. Jiroveci is a ubiquitous organism transmitted by airborne droplets that does not cause any diseases in immunocompetent patients. Patients with HIV infection and CD4 + count <200 / μL, patients after organ transplantation, with hematologic oncological diseases and patients taking glucocorticoids, are at risk of developing P. Jiroveci-pneumonia.

[14], [15], [16]

Risk factors

Pneumocystosis has a risk group - people with HIV infection, premature babies, weakened infants and children of early age with agammaglobulinemia or hypogammaglobulenemia, rickets, hypotrophy, leukemia patients, oncological diseases, organ recipients receiving immunosuppressants. Elderly people from nursing homes, sick with tuberculosis.

[17], [18], [19], [20], [21], [22],

Pathogenesis

The pathogenesis of pneumocystis pneumonia is associated with mechanical damage to the walls of the interstitium of the lungs. The entire life cycle of pneumocysts passes in the alveolus, to the wall of which they are very tightly attached. To develop pneumocysts, a large amount of oxygen is needed. Gradually multiplying, they fill the entire alveolar space, capturing all large areas of the lung tissue. With close contact of trophozoites with the walls of the alveoli, the pulmonary tissue deteriorates, the extensibility of the lungs gradually decreases, and the thickness of the alveolar walls increases 5-20 times. As a result, the alveolar-capillary block develops, which leads to severe hypoxia. The formation of atelectasis sites aggravates the violation of ventilation and gas exchange. In patients with immunodeficiency states, a marked decrease in the number of CD4 + lymphocytes (less than 0.2 × ^{10 9} / L) is critical for the development of PCP.

[23], [24], [25], [26], [27], [28]

Symptoms of the pneumocystis

Most have fever, dyspnea and a dry, unproductive cough that develops subacutely (more than a few weeks, HIV infection) or acutely (for more than a few days, other causes that damage cellular immunity). Chest X-ray diffusion shows diffuse, bilateral infiltrates in the roots, but 20-30% of patients have normal x-rays. Investigation of arterial blood gases reveals hypoxemia, with an increase in the alveolar-arterial gradient of O2, and lung function studies show an altered diffusion capacity (although this is rarely done for diagnosis).

Diagnostics of the pneumocystis

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

The diagnosis is confirmed by the detection of a microorganism after treatment with methenamine silver, Giemsa, Wright-Giemsa, Grocotte modification, Weygert-Gram, or immunochemical staining using monoclonal antibodies. To obtain sputum samples, an induced collection or bronchoscopy is usually performed.

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

[29], [30], [31]

Treatment of the pneumocystis

Pneumocystis is treated with trimethoprim-sulfamethoxazole (TMP-SMX) 4-5 mg / kg intravenously or orally 3 times a day for 14-21 days. Treatment can be initiated before confirmation of the diagnosis, as P. Jiroveci cysts persist in the lungs for many weeks. Undesirable effects, more often occurring in AIDS patients, include skin rashes, neutropenia, hepatitis and fever. Alternative regimens include pentamidine 4 mg / kg intravenously once a day, or 600 mg per day aerosol, atovahon orally 750 mg twice daily, TMP-SMX orally 4 times a day at a dose of 5 mg / kg with dapsone 100 mg orally 1 time per day or clindamycin 300-900 mg intravenously every 6-8 hours with primaquine basally at a dose of 15-30 mg per day, also for 21 days. The use of pentamidine limits the high incidence of toxic adverse effects, including renal failure, hypotension and hypoglycemia. Additional glucocorticoid therapy is required for patients with Pa02 less than 70 mm Hg. Art. The scheme of oral administration of prednisolone 40 mg twice a day (or its equivalent) during 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 a day for prolonged treatment.

HIV-infected patients who had pneumonia P. Jiroveci or if CD4 + <200 / μL should receive prophylaxis of TMP-SMX 80/400 mg once a day; when this drug is intolerant, prescribe dapsone in a dose of 100 mg orally 1 time in swizzes or aerosol pentamidine 300 mg once a month. These prophylactic regimens can also be shown for patients without HIV infection, but with the risk of P. Jiroveci pneumonia.

Forecast

Pneumocystis has an unfavorable prognosis. On average, the number of surviving patients after advanced pneumocystis pneumonia is 75-90%. Relapses survive about 60% of patients.

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

[32], [33], [34], [35]