ABSTRACT
The influence of T. canis larvae migration on the lung tissue of paratenic host (inbred mice, strain C57BL6/J) was evaluated. First macroscopic manifestation was already observed on day 2 in the time of the highest larval recovery. Larvae entering the lung tissue caused numerous small extravasations. Their migration from the lungs was manifested from day 6 with an increase in the number and extent of extravasations. The lungs assumed tiger spot appearance (Fig. 1). The larval recovery was decreasing. From day 14 the expressiveness of macroscopic changes was declining. Areas of emphysema and atelectasis were observed on the lungs. The genesis and the process of elimination of extravasations were studied histologically. In the first period, the primary extravasations, caused by larvae migrating to the lung tissue (Fig. 2), were eliminated by monocytes and eosinophilic granulocytes in increasing numbers (Fig. 3). Immunohistochemically macrophages and dendritic cells were already observed in the lungs on day 1 (Fig. 4). Acid phosphatase activity was increasing from day 1 and its highest level was observed on day 84. Alkaline phosphatase activity on days 2-4 was not observed in the areas of extravasations although within the larvae themselves it was high. The extravasations of the second period (caused by larval migration from the lungs) from day 5-6 were eliminated with humoral monocytes and cells of perivascular and peribronchial tissue. Eosinophils were not active in this process. Strong exudation was observed here. The humoral part of extravasations was eliminated primarily. The cytoplasmic volume of activated cells was enlarging. Multinuclear symplasms were originated (Fig. 5). The activities of alkaline phosphatase and nonspecific esterase were increased. Macrophages and dendritic cells were still present in high numbers and from day 14 aggregations of T and B lymphocytes were observed (Fig. 6). Reparative processes were frequently observed on the blood vessels altered by the leaving larvae (Fig. 7). Changes on the lungs caused by migration of larvae always ended in functional regeneration of the lung tissue. On the other hand dead larvae stimulated proliferative forms of inflammatory reactions which led to induration (Fig. 8).
Subject(s)
Lung/parasitology , Toxocara canis , Toxocariasis/parasitology , Animals , Larva , Lung/pathology , Mice , Mice, Inbred C57BL , Toxocariasis/pathologyABSTRACT
The pathomorphological changes in the lungs of hare (Lepus europaeus Pallas, 1778) provoked by the parasite P. commutatus (Diesing, 1851) are macroscopically manifested as layer and nodular changes. With regard to the fact that the layer changes are suggesting the hatching nodules of protostronglyoses of small domestic ruminants, we have decided to rate them separately because of the differentiation. The layer changes on the surface of hare's lungs become evident as areas of emphysema, inflammation and induration. The emphysematous changes are macroscopically evident in the form of lobular formation (Fig. 1). Histologically, it was found out that the emphysematous effect was limited by an area of compressed lungs structures without perspicuous signs of the development of atelectatic changes (Fig. 2). The emphysematous changes are causing prominent exudative inflammatory processes in the bronchi and bronchioli provoked by unfertilized and disintegrating eggs of parasites. Inflammatory layers are macroscopically evident as solid brown-reddish areas (Fig. 3). Their macroscopic manifestation is transient. It is qualified by the stages of the inflammation itself. It is possible to put down the stage of manifestative development of the changes in the inflammatory areas only by continual examinations of hare's lungs all year round. Unfertilized eggs and grounded, disintegrating larvae of protostrongylus are provoking the inflammatory reactions which may lead in the layer changes to the obliteration of bronchioli (Fig. 6), which is macroscopically evident as induration (Fig. 7). The bronchioli are obliterated so that the phagocytic ability of monocytes is transformed to a reparative ability.(ABSTRACT TRUNCATED AT 250 WORDS)
