Paflio-.'.H'sis. 93 



develop as a vicarious clironiv' (Miipliysciua of the lungs in various chronie 

 diseases leading to the obstruction of portions of the lungs. This form 

 is of clinical importance only in so far as it increases still further the 

 respiratory difficulties caused by the primary disease. 



Predisposition. The frequency of the disease increases 

 with age. It is exceedingly rare in horses younger than five 

 years, but common in older horses. The frequent occurrence 

 of the disease in older animals finds its explanation in the 

 fact that forced respiration continued over longer periods and 

 due to hard work will produce a detrimental effect; work 

 horses are moreover frequently exposed to affections of the 

 respiratory organs and to disturbances of nutrition in con- 

 sequence of insufficient feeding and of digestive anomalies. 



The influence of insufficient nutrition is seen convincingly 

 in senile atrophy of the lungs, where dilatation of the alveoli 

 is due exclusively to atrophy and thinning out of the inter- 

 alveolar septa. The power of resistance of the pulmonary 

 tissue shows a good deal of individual variability because it 

 would otherwise be unexplainable why some animals contract 

 the disease after a comparatively short exposure to harmful 

 influences and at a comparatively young age, while others 

 remain well under the same conditions or only develop a mild 

 form of the affection late in life. A diminished resistance of 

 the pulmonary tissue may he acquired, congenital or hereditary. 



Pathogenesis. A considerable dilatation of the alveoli 

 occurring again and again innumerable times, perhaps for 

 years, will decrease the elasticity of the pulmonary tissue of 

 itself to a certain degree. Much more important, however, is 

 the circumstance that under the conditions indicated the 

 alveolar pressure becomes increased during expiration or 

 coughing and the interalveolar and interinfundibular septa with 

 their capillaries, are compressed and distorted from both sides. 

 Frequently recurring narrowing of the pulmonary capillaries 

 impedes the free flow of the blood more or less and some 

 capillaries will become impervious, while blood corpuscles are 

 arrested in them. Since there is then no blood-current in some 

 capillaries or at least only a current of blood plasma, the nutri- 

 tion of the pulmonary parenchyma suffers, including that of 

 the compressed and distorted capillaries. For this reason and 

 in consequence of the ever increasing alveolar pressure the 

 capillaries become completely obliterated, the elastic fibers 

 yield to the increased pressure and the alveolar epithelia 

 undergo fatty degeneration. Thus the interalveolar and inter- 

 infundibular' septa gradually become thinner, the interstices 

 l^etween the yielding elastic fibers become lar<?-er, until finally 

 the interalveolar and later also the interinfundibular septa dis- 

 appear entirely so that neighboring alveoli become confluent 

 to form a common cavitv. 



