Pneumocystosis: causes and pathogenesis

Causes of pneumocystosis

The cause of pneumocystosis is P. Jiroveci - a microorganism whose taxonomic position is not defined. Most researchers attribute it to the simplest (subtype Sporozoa, class Haplospora). But in recent years, information has accumulated that, according to nucleotide sequences of ribosomal RNA, pneumocysts are closer to fungi. It is an extracellular parasite with a predominant tropism to the lung tissue that affects the first and second order pneumocytes. Only one species of P. Jiroveci was identified, but antigenic differences were found between strains isolated in humans and in some animals.

There are disagreements in the evaluation of the staging of pneumocyst development. Some authors distinguish four morphological forms, others consider that there are only three morphological forms. The first form, trophozoite, is an oval or amoeboid cell 1-5 microns in size, outgrowths on its surface with the help of which the trophozoites adhere tightly to the lung epithelium, so it is difficult to detect them in the sputum. The second form, a pre-cyst, is an oval cell measuring 2-5 microns that does not have outgrowths. The wall of the prets consists of three layers, in the cytoplasm there are several lumps (fissile nuclei). The third form, cyst, is a cell measuring 3.5-6 microns, its walls also consist of three layers. In the cytoplasm, up to 8 intracystic corpuscles with a diameter of 1-2 μm are detected. Having a two-layered shell. Intra-corpuscular bodies emerge upon the destruction of cysts and become extracellular trophozoites, starting a new life cycle of the pathogen. Pneumocysts do not penetrate into host cells during replication, but attach to their surface. Data on the production of toxins by pneumocysts are not available. Pneumocysts are not cultivated on nutrient media.

The duration of preservation of pneumocysts on environmental objects has not been studied, however, in the air of the premises where the patients are, there is DNA of the pathogen. Pneumocystis are sensitive to sulfonamides (sulfamethoxazole) in combination with pyrimidines (trimethoprim), sulfones (dapsone), some antiprotozoal agents (pentamidine, metronidazole), nitrofuranam (furazolidone).

[1], [2], [3], [4], [5], [6], [7], [8]

Pathogenesis of pneumocystosis

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.

In pneumocystis pneumonia, three stages of the pathological process are distinguished in the lungs: edematous (lasts 7-10 days), atelectective (1-4 weeks), emphysema (duration varies). At autopsy, the lungs are enlarged, dense, heavy, pale violet; the tissue of the lungs is easily torn, on the cut it has a marbled appearance with a grayish-cyanotic hue, separated by a viscous shade.

At histological examination in an edematous stage in a lumen of alveoli and terminal bronchioles foam-cellular masses containing congestions of pneumocysts around which neutrophils, macrophages and plasma cells accumulate are found out. Such frothy alveolar exudate is not found in other diseases - it is the pathognomonic sign of pneumocystis. In the atelectatic stage, there is fullness, cell infiltration of interalveolar septa, followed by their destruction, which is most pronounced in the recurring course of the disease in HIV infection. If the recovery comes in the last stage, the process is gradually reversed. When relapses in AIDS patients, fibrocystic changes in the lungs can occur.

In AIDS, pneumocyst dissemination occurs in 1-5% of cases: almost any organ can be affected. It is possible to develop an isolated focus of extrapulmonary pneumocystis or a combination of pulmonary and extrapulmonary lesions.