694 



Glanders. 



and bright red mucous membrane is covered with a purulent 

 secretion, occasionally studded with small nodules and ulcers, 

 the bronchial walls thickened and here and there distended. 

 In affection of the superficial areas of the lungs the ad- 

 jacent visceral layer of the pleura 

 'is indurated while wide strands 

 of yellow gelatinous tissue radiate 

 between the pulmonary lobules. 

 In very rare cases serous or sero- 

 fibrinous exudate may be prescTit 

 in one or both pleural cavities. 



The lesions of glanders of the 

 upper air passages and especially 

 of the trachea, the larynx, the nose 

 and the nasal sinuses are essen- 

 tially similar. The beginning of 

 the morbid process is manifested 

 by the appearance of gray or yel- 

 lowish, prominent nodules as large 

 as millet seeds (rarely larger) and 

 surrounded by a tumefied and 

 brightly reddened area. The ul- 

 cers resulting from the breaking 

 down of the nodules are at first 

 round, reg-ular, and smoothly bor- 

 dered, but subsequently, as a re- 

 sult of progressive tissue destruc- 

 tion, they become irregular with 

 raised borders, ragged edges, pale 

 yellow lardaceous base covered 

 with pus and detritus or, even- 

 tually, a brown scab. Larger ul- 

 cers are formed by the coalescence 

 of small ones and these are usually 

 surrounded by fresh nodules and 

 ulcers (Fig. 117). On the other 

 hand, ulcers that have "healed" 

 are replaced by irregular star- 

 shaped, either smooth white or 

 prominent reddish or white callous 

 cicatrices, which may, in some rare 

 cases, extend over the entire sur- 

 face of one side of the nasal sep- 

 tum. In addition to this scar-like 

 Fig. 117. Glanderous Ulcers on the ^Tlanderous growths of Connective 

 Nasal Septum. tissuc nature may form without 



previous ulcerative processes. 



According to Johne, glanderous proliferations which may subsequently break 

 down, completely or pi^rtially, are products of attenuated bacilli, the toxins of 

 which are no longer able to produce coagulation necrosis of the proliferated con- 



