The histological pattern of changes in the lungs was polymorphic. It was caused mainly by changes in the blood vessel walls, perivascular and interstitial tissues. The walls of the bronchi were spasmodic or obturated with thick mucus in the form of mucous plugs. The swelling of the mucous membrane was detected with an exponential thickening of the basal membrane. Although, there was a thick infiltration in all layers of the bronchi, around this area eosinophils, lymphocytes, histiocytes and plasma cells were also observed. Additionally, fungal cells were detected in thickness of these layers. Mucous plugs were contained cells of the desquamated bronchial epithelium, eosinophils, macrophages and spherules of the Paecilomyces fungus.
In the same visual fields of pulmonary parenchyma, an uneven thickening of the interalveolar septum was found, together with pronounced plethora of blood vessels (Fig. a) and individual foci of hemorrhage. Also, vessel walls were thickened. There was evidence of swollen vascular endothelium and desquamation of endothelial cell as well as fragmented internal elastic membrane and increased permeability of vascular walls and perivascular edema (Fig. b). There were fungal cells found in erythrocyte thrombi, vascular walls and the perivascular space. In the lumen of the alveoli, it was observed a pale pink transparent liquid with an admixture of desquamated epithelium and leukocytes. Minor macrophage-histiocytic infiltrates were found in the tissues around the vessels and bronchi, which contained round-oval corpuscles with a two-contour capsule with dimensions of 5.0 × 5.0 to 29 × 30 µm and even larger, which gave a positive color to fungi (Fig. c). In other visual fields, the interalveolar stroma was thickened; its infiltration from cells was more pronounced. Separate walls of small arteries and veins were seen in the form of fibrinoid swelling or fibrinoid necrosis. The changes in the walls of small and medium vessels were characterized by a pattern of destructive-productive vasculitis at different stages from endovasculitis to panvasculitis. This happened with increased permeability of their walls and efflux of fungal cells into the perivascular space. The cellular composition of infiltration around fungal cells was represented by activated eosinophils, lymphocytes, histiocytes and plasma cells. In three cases, a lymphatic and histiocytic infiltration with formation of granulomas without signs of caseous decay was revealed. The structure of granulomas was represented by single giant polynuclear cells, in which cytoplasm contains tissue forms of fungi or their cytoskeletons with granular contents. These were surrounded by epithelioid cells, macrophages and lymphocytes or by a thin layer of histiocytes and lymphocytes. In addition, areas of pulmonary parenchyma with connective tissue growth and stroma were observed around the vessels in peribronchial space as well as in the walls of the alveoli. Cellular response developed in lung tissues where fungal cells existed. This had a profile of alterative and productive inflammation with a tendency to a protracted course, resulted in sclerosis of the affected area, which caused limitation in the further spread of fungal cells into the organ tissues (Fig. d). It should be noted that along with pronounced histological changes in the lungs, there were areas where morphological disorders were minimal or completely absent, which indicated a disseminated nature of the lesion.
The generalized spread of Paecilomyces infection caused dissemination of the Paecilomyces pathogen in the tissues of various organs through the affected vessel walls which were mainly in small and medium caliber.
Histological sections of the heart muscle revealed changes in different times. In some visual fields, there was an edema of the interstitial stroma with the separation of fibers and necrosis of separate muscle fibers. In the lumen of the vessels, fungal tissue cells at different stages of development were observed (Fig. e). In other visual fields, focal infiltrates around small and medium vessels with destruction of the vascular walls were evident in the form of fibrinoid swelling or fibrinoid necrosis and pronounced lymph-plasmocytic infiltration in the perivascular area. Additionally, some areas with the growth of fibrous tissue between the muscle fibers and vessels up to their complete obliteration were observed (Fig. f).