Pathogenesis. Qg^ 



rounding- tissues. These serous infiltrations occur particularly 

 in the lungs, both in the perivascular connective tissue and in 

 the bronchial walls; the bacilli may then pass through to the 

 surface of the mucous membrane and be discharged to the 

 exterior with the catarrhal secretions (Nocard & Leclainche). 

 On the other hand they are aspirated into the alveoli with the 

 secretions w^here they give rise to catarrhal processes which 

 are followed by the development of broncho-pneumonic foci 

 which, as a result of the glanderous nature, undergo early 

 central softening. 



According to the investigations of Schuetz glanders nodules develop in the 

 lungs as miliary fibrinous inflammatory foci, in which the chromatin of the nuclei 

 breaks up into fine granules as the process of necrosis advances (Unna's nucleus 

 degeneration or chromatotexis), while calcification is said never to take place (?). 

 Similarly, Csokor, in harmony with the views of other authors (Eoloff, Eabe), is of 

 the opinion that the primary glanders nodule is the result of swelling, coalescence 

 and subsequent fatty-granular degeneration of the alveolar endothelium following 

 aerogenic infection. According to Nocard, on the other hand, the primary pul- 

 monary lesions of glanders consist in the development of hyaline tubercle-like 

 nodules, as had already been observed by Loeffler and Schuetz in the lungs of 

 horses that had been infected experimentally by subcutaneous and intranasal 

 administration of cultures: viz., fresh, gray nodules varying in size from a millet 

 seed to that of a hemp seed and surrounded by a red area. More recently these 

 nodules have been regarded as of particular importance, especially through the 

 experimental investigations of Nocard, who frequently demonstrated them to be 

 present as the only pathological lesions in naturally infected horses that were con- 

 demned and killed upon the evidence of a reaction to the mallein test, and in 

 horses that had been infected experimentally by the alimentary administration of 

 small quantities of virus, in all cases the glanderous nature of the nodules having 

 been demonstrated by experimental inoculation of laboratory animals. Coremans 

 and Priesz express similar opinions in regard to the nature of these nodules, having 

 demonstrated the presence of glanders bacilli in them by microscopical examination 

 as well as by culture. On the other hand Schuetz as well as Olt and AngelofP 

 deny the glanderous nature of these nodules. According to their views they are 

 the result of infection with embryonic filaria (nodules of this character consist for 

 the most part of eosinophile cells which absolutely do not occur in glanders nod- 

 ules) ; in addition to this the aforementioned authors maintain that the encapsu- 

 lated and frequently calcified foci are also due to the presence of these parasites. 

 Kitt and Johne, however, have succeeded in demonstrating virulent glanders bacilli 

 in partially calcified foci, and it seems, therefore, that the many conflicting observa- 

 tions and views on this question are evidently due to the fact that different investi- 

 gators have investigated structures of a different nature. 



According to Hutyra's histological investigations of the lungs of infected 

 horses and guinea pigs, nodules due to hematogenic infection are caused by bacil- 

 larj emboli, followed by the formation of thrombi and the development of an 

 almost simultaneous vasculitis and perivasculitis in the peribronchial and inter- 

 lobular connective tissue which cause the formation of sharply circumscribed groups 

 of round cells which appear macroscopically as glassy, hyaline nodules (in a few 

 instances glanders bacilli could be demonstrated within these nodules, but in no 

 instance could filaria be found). As the cell groups enlarge, the inflammatory 

 process extends to the neighboring alveolar walls, which may, however, be involved 

 from the beginning as a result of the lodgment of bacilli in the interalveolar capil- 

 laries. In either case a miliary fibrinous inflammation is the result. Finally the 

 nodules which develop in the walls of the small bronchioles may perforate their 

 lumen and discharge their contents into them, producing an inflammation of their 

 mucous membranes, which is followed by bronchopneumonic processes. The coales- 

 cence of neighboring pneumonic foci results in the formation of larger nodes, and 

 the fusion of diffuse inflammatory areas in the interlobular septa results in the 

 formation of so-called glanderous growths. In both instances thrombus formation 

 in the bloodvessels of the affected area goes hand in hand with the inflammatory 



In regard to local susceptibility, the various organs show 

 considerable difference. After the lungs, the mucous membranes 



