Part 2 — THE PATHOLOGY OF EPIDEMIC INFLUENZA (continued 3)

The extensive hemorrhage and inflammatory œdema of the lung are striking during the early stages of the lung involvement. The mononuclear infiltration which appears early and remains for a variable time, until the purulent process is well under way, is also unique. The hyaline deposit in the lung alveoli; the capillary thrombosis and necrosis of the alveolar walls and bronchi are important; while the tendency to abscess, infarct, gangrene and incomplete resolution with fibrosis differentiates this type of pneumonia from the common lobar variety.

As an organic evidence of the acute intoxication, none stands out more prominently than the degeneration of the voluntary muscles. These resemble the waxy degeneration of other bacterial intoxications, and particularly that of typhoid fever. The finding of these acute degenerations does not assist us in arriving at a conclusion as to the nature of the poisonous body, whether a true exotoxin. The presence, however, of such widespread degenerative lesions in cases showing no naked eye change suggests, at least, that the peculiar muscle weakness associated with pain has its origin in this definite process and not in primary nerve lesions.

Very interesting it is that the different muscular structures are not equally affected by the intoxication. This is particularly noteworthy in the heart and intestine. In neither of these structures have we met with lesions comparable to those in the voluntary muscles. Wherein this immunity resides we cannot state. In our own series, as well as in the majority of others, there was an unusual absence of evidence of myocardial weakness. In most of those dying during the acute illness, the heart muscle was found firm and the cavities not dilated. This finding was in striking contrast to that found in acute lobar pneumonia where dilatation of the right ventricle and auricle, along with muscle degeneration, is almost the rule. In but one case of the present series did we find myocardial degeneration leading to dilatation of the cavities and causing death. And in this particular case the intoxication was due to a streptococcus septicæmia arising as a late sequel from the middle ear. The heart in influenza withstands remarkably well the effects of an intoxication from 292the disease and carries the extra load imposed upon it by the involved lung with little evidence of fatigue.

It is also worthy of attention to note that the kidney suffers so little in this severe disease. Bacterial localization with inflammatory concomitants does not occur, and there is no lasting damage upon its structure. As in so many conditions of bacterial poisoning, tubular degeneration, varying from a cloudy swelling to a more acute damage, is to be found in a percentage of cases, but complete restoration is rapidly obtained in convalescence. It is unusual to find such severe renal damage to incapacitate function to a degree to endanger life.

Finally we can add our evidence, gained from a study of the pathology of epidemic influenza, that the primary disease induced by the invasion of the B. influenzæ opens the way for secondary infections of a variety of kinds, whose subsequent effect may be more serious than initial lesions. The many late complications which arise in this manner we have not investigated.

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