Pneumomycoses

PNEUMOMYCOSIS (from Greek pneumon- lung and mykes- fungus), a term proposed in 1856 by Virchow to designate lung diseases caused by mold fungi (so-called typhomycetes). Subsequently, diseases caused by other fungi closely related to molds were also included in this group, namely various species of actinomycetes, Oidium, and blastomycetes. All these microorganisms are not only not obligatory parasites of humans and animals, but on the contrary become such only under conditions particularly favorable for their fixation and multiplication in living tissues, for which reason such diseases are observed comparatively rarely, despite the colossal distribution of these fungi in the human environment. Among the species mentioned, the ability to a parasitic mode of life is most easily acquired by various representatives of the class of ray fungi (actinomycetes). (For diseases caused by them, see Actinomycosis and Bronchomycoses.) Among proper mold fungi, representatives of all three main genera have been described as facultative parasites, namely: the genus Aspergillus, the genus Penicillium, and the genus Mucor. The most frequently encountered and of greatest importance in the pathology of humans and animals is pneumomycosis aspergillina, the causative agents of which can be many species of Aspergillus having an optimum of growth more or less close to that of the animal body's temperature (mainly A. fumigatus, more rarely A. niger, A. flavescens, A. malignus, etc.-see Aspergillus). A much rarer form is represented by pneumomycosis mucorina (as causative agents, Mucor corymbifer and Mucor rhizopodiformis have been described), and finally an extremely rare form-pneumomycosis penicillina (4 cases in the world literature; in one, Penicillium bicolor was found, in two-Penicillium glaucum, and in one-the species was not determined). In general, cases of human infection with mold fungi are described in the literature as 64. Of these, 40 cases fall aspergilloses, among which 34 are pulmonary (p. aspergillina), 20-infection with Mucor (of which 8 are pulmonary), and 4 with p. penicillina. In view of the fact that initially mold fungi were found in man mainly in such places in the lungs where there were already marked changes arising under the influence of disease processes of a completely different nature (e.g., in tuberculous cavities, foci of caseous pneumonia, bronchiectatic cavities, gangrenous foci, infarcts, cancerous nodes, etc.), Virchow and many subsequent authors considered these fungi as saprophytes growing on the dead, disintegrating organic substrate of these areas of the organ. However, later studies by a number of French and German scientists established that these fungi, even if they appear in tissues as a secondary infection, nevertheless possess an independent, pathogenic role; in some cases, however, they can apparently become fixed in the lungs primarily, causing there the development of a prolonged disease process very similar in its course to benign forms of tuberculosis. The rarity of cases of primary P. is explained, besides the low virulence of mold fungi, by their predominant tendency to develop in acidic media, as well as by their great need for free oxygen. Therefore, for the initial fixation of the fungus, the presence of special conditions is required, consisting either in a very weakening of the body's resistance (resp. of a given organ) under the influence of some recently undergone or continuing diseases, such as dysentery, gastro-intestinal catarrhs, tuberculosis, putrid bronchitis, cancer, especially diabetes (apparently due to the tissue acidosis it causes), or in a very long and abundant introduction (inhalation) of the corresponding infectious material, as occurs in some professions, e.g., in mass feeding of pigeons, in cleaning hair, in working with flour or grain (millers, bakers), in joinery and turning work with certain types of wood, etc. (see Aspergillus-aspergillosis). However, some still consider it necessary for the development of these professional diseases some preliminary damage to the respiratory apparatus in the form of dust bronchitis, influenza, etc. The morphological picture of P., whatever species of mold fungi they are caused by, is in general outline the same; among them, aspergillomycoses are the best studied due to their more frequent occurrence in humans, their significant distribution in animals (horses, sheep, dogs, bulls, deer, rabbits, mice and especially birds, particularly pigeons), and numerous experimental studies. Therefore, the description that follows will mainly refer to the picture of aspergillosis.-In primary P., the initial fixation of the fungus occurs, as in other aerogenous infections, in the vast majority of cases in the small bronchial branches (bronchioles), causing there first a picture of more or less acute catarrh, and subsequently leading to necrosis of one or another part of the bronchial wall. For a long time the process¹ may remain superficial, with the fungus abundantly growing in the lumen of the bronchus, however not extending beyond its limits and often forming here, due to sufficient inflow of free oxygen, numerous fruiting bodies, which give its masses the characteristic color of each species of fungus (greenish, yellowish-brown, grayish-black, etc.). From here the infection spreads, on the one hand, bronchogenically to other parts of the lungs, on the other-hand into the depth of the lung tissue. The latter occurs partly by the penetration of fungal threads through the non-necrotized bronchial wall into the adjacent alveolar parenchyma, and partly per continuitatem due to the growth of mycelium on the mucous membrane to the alveolar passages and alveoli. A characteristic change in lung tissue in P. should be considered the formation of pneumonic foci (also colored greenish-yellow, brownish-yellow or dirty gray), sometimes dense, sometimes with central softening or even cavity. Microscopic examination always establishes in such a focus the presence of central necrosis, in which not only can no tissue structure be distinguished, but very often the fungus itself cannot be found (even elastic tissue is preserved mostly only in fragments). Immediately outward from this necrotic center, where the structure is still distinguishable and the changes are predominantly necrobiotic in nature, there are always abundant masses of mycelium, further peripherally bordering usually with dense accumulations of leukocytes or-in more slowly progressing cases-with a granulation zone consisting mainly of epithelioid elements, sometimes with an admixture of giant cells. Behind this demarcation zone comes the area of perifocal pneumonia with the surrounding zone of collateral edema. Such is the typical scheme of the spread of changes. The central necrotic focus, as already mentioned, very often undergoes autolysis, turning into liquid pus, after removal of which a cavity remains, which may gradually increase in size due to the progression of the process or the fusion of several separate foci. The mycelial threads sometimes pierce the demarcation zone and appear in the pneumonic zone, and it is often possible to observe necrosis of the vessel walls and their penetration by the fungus with subsequent thrombosis of the vessel or its rupture and hemorrhage. On the other hand, at the periphery of the granulations, a process of scarring may begin, isolating the entire focus from the surrounding tissue. If the fungus becomes fixed in a previously formed cavity (cavern, bronchiectasis, etc.), it covers its walls with masses of mycelium characteristic in their coloring, which may grow inward, increasing the destruction of the organ, or-which happens more often-grow mainly in the cavity without affecting the adjacent lung tissue. However, even in this last case, hemorrhage is possible due to the destruction by the fungus of the blood vessels closest to the surface. Whatever the origin of the cavity containing the fungus, i.e., whether it arose under its influence or it developed in it secondarily, a very bright sign distinguishing it from an ordinary gangrenous or bronchiectatic cavity is the complete absence of odor in the contents, even if it accumulates there in large quantities. The same applies to the sputum excreted by such patients during life. In hematogenous mycoses, obtained experimentally by intravenous injection of pure fungal cultures to animals, nodules form in various organs, including the lungs, very similar to tubercles, which under the microscope consist of leukocytes and epithelioid cells (sometimes with an admixture of giant cells) with numerous fungal threads in the center. Subsequently, some nodules scar over, others necrotize, soften and turn into small cavities, in other words, they repeat the same cycle of development as naturally occurring foci.

In general, in humans the process usually proceeds favorably, although it may persist stubbornly for many years, causing the formation of granulomatous nodules, bronchiectases, cavities, scars, etc., and very much resembling in its course and ante-mortem physical findings tuberculosis. Death most often occurs from that primary disease which creates the soil for the development of the fungal infection (diabetes, tuberculosis, cancer, etc.), whereas in cases of so-called primary pneumomycosis, the disease most often ends in recovery, rarely giving fatal outcomes from hemorrhage or marasmus. Pneumomycoses caused by fungi of the species Oidium have been described very little. In all these cases, it was a matter of secondary infection of the lungs in very weakened severely ill patients (pneumonia in diabetes, putrid bronchitis, etc.), mostly children, who had abundant accumulations of the same fungus on the mucous membrane of the mouth and throat (thrush). In the lungs, the fungus was sometimes found only in the bronchi, while in some cases it also grew into the lung tissue, where either foci of pneumonia with mycelial threads in the exudate or cavities of gangrenous type were found, but without a putrid odor and with abundant masses of fungus in the contents. As for Blastomycetes, primary aerogenous infection of the lungs by them has never been observed. Only individual cases of metastatic blastomycosis of the lungs are known with corresponding skin lesions. The morphological picture of changes found here, as far as can be judged from these few descriptions, differs little from the picture of other fungal lesions of the lungs and amounts to the appearance in the lung tissue either of dense nodules with a necrotic center or of cavities filled with semi-liquid, dark, purulent-like mass. Foci of both types contain an abundant number of yeast cells and are surrounded by a zone of inflammatory infiltrate, in which in some forms of experimental blastomycosis in animals, numerous giant cells were found.