In the other group, where there is not only a free ingress to the pulmonary parenchyma by the bacteria of the mouth, but where there is, in all probability, also a simultaneous or preliminary pulmonary damage furnishing a proper medium for relatively innocuous organisms, the lesion of response will surely depend upon other factors as much as upon the infecting organism. Among these obscure factors, the most important, unquestionably, is the extent of the damage to the lung tissue before the entry of the organisms, or simultaneously with it, into this area. The systemic capacity to compensate also must be considered.
FIG. LI. AUTOPSY NO. 194. A LUNG IN WHICH INFLUENZAL PNEUMONIA AND PULMONARY TUBERCULOSIS ARE ASSOCIATED. THERE IS A CIRCUMSCRIBED, OLD, TUBERCULOUS FOCUS IN THE UPPER LOBE. COMPARE FIGURES XXXIX AND XL. ]
The portal of entry of the inciting cause is likewise undetermined.
The respiratory lesions, whether primary or secondary, are responsible for the high mortality of the disease.
The lesions of the respiratory tract peculiar to this disease and most frequently encountered are:
An acute tracheobronchitis associated with diffuse involvement of the pulmonary parenchyma.
Hyalinization of the epithelium of the air passages, and necrosis of the alveolar walls with extensive interstitial emphysema and occasionally with pneumothorax.
Aplastic serofibrinous, and hemorrhagic, pneumonic exudates.
Necrotizing and organizing bronchiolitis, and pneumonia: lobar, lobular, peribronchial, interstitial.
The sequelæ—obliterating bronchiolitis and bronchiolectasis.
Proliferation of alveolar and bronchiolar epithelium.
The extrarespiratory lesions of influenza are neither constant nor characteristic. Irrespective of localization, they have the same fundamental pathology characterized by:
A basis for the interpretation of the respiratory lesions of influenza is offered by the analogous changes in the respiratory tract initiated by the inhalation of poisonous gases.
The respiratory lesions are dependent primarily upon the damage produced by the true etiological agent and the systemic capacity to compensate, and only secondarily upon invasion by the bacterial flora of the mouth and inspired air.