Chapter XIV: Part 14

Epidemic influenza is an acute infectious process of the respiratory tract, usually localizing in the upper respiratory system, but often and in a fairly constant percentage of cases extending into the lower portion of the same system and causing a type of broncho-pneumonia. Accompanying the initial invasion there is a marked systemic intoxication with lesions of degeneration arising in a variety of tissues. These lesions of degeneration are to be seen both locally in the respiratory system as well as in distant parts, as in the muscles, kidney and liver. The primary damage arising in the respiratory organs, and which we believe to be the result of infection by the B. influenzæ, facilitates attacks by such other bacteria as are available and pathogenic to man. The secondary invaders are not constant in type, but we find variations according to the localities where the epidemic takes place. Just as there is a difference in the bacterial flora which constitutes the secondary invasion, so, too, there is a variation in the picture of the inflammatory process which appears in the lungs. The occurrence of the miliary streptococcal broncho-pneumonia has been met with in certain localities much more frequently than in others; lobular and confluent pneumonia has been the prevailing type in certain regions, while a lobar purulent pneumonia with abscess and gangrene was most frequent with others. There does not appear to be an individual and constant character in the mode of distribution of the pneumonia in the lungs. That the pneumonias were not the usual type otherwise seen, is fairly agreed upon by all. The most astonishing feature presenting itself to us was the frequency of death occurring in the early stages of the inflammatory process and before the gray stage had definitely developed. The gray stage of influenza pneumonia is a purulent pneumonia which often also constitutes an acute interstitial pneumonia.

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 the 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.

BIBLIOGRAPHY

Abrahams, Hallows and French Lancet., 1919; i, p. 1. Advisory Board to the D. G. M. S Brit. Med. Jour., 1918; ii, p. 505. Blanton and Irons Jour. A. M. A., 1918; lxxi, p. 1988. Boggs Johns Hop. Bull., 1905; xvi, p. 288. Brooks and Cecil Brit. Med. Jour., 1918; ii, p. 496. Chickering and Park Jour. A. M. A., 1919; lxxii, p. 617. Christian Jour. A. M. A., 1918; lxxi, p. 1565. Cole Brit. Med. Jour., 1918; ii, p. 566. Cole Canadian Med. Assoc. Jour., 1919; ix, p. 41. Dever, Boles and Case Jour. A. M. A., 1919; lxxii, p. 265. Fildes, Baker and Thompson Lancet., 1918; ii, p. 697. Fletcher Lancet., 1919; i, p. 104. Friedlander, McCord, Sladen and Wheeler Jour. A. M. A., 1918; lxxi, p. 1652. Goodpasture and Burnett U. S. Naval Med. Bull., 1919; xiii, No. 1. Hall, Stone and Simpson Jour. A. M. A., 1918; lxxi, p. 1986. Hunt Lancet., 1918; ii, p. 419. Keegan Jour. A. M. A., 1918; lxxi, p. 1051. Kuskow Virchows Archiv., 1895; cxxxix, p. 406. Le Count Jour. A. M. A., 1919; lxxii, p. 650. Lord Boston Med. and Surg. Jour., 1905; cl, p. 537. Lyon Jour. A. M. A., 1919; lxxii, p. 924. MacCallum Jour. A. M. A., 1919; lxxii, p. 720. MacCallum Monog. Rock. Inst. for Med. Res., 1919; No. 10. Muir and Wilson Brit. Med. Jour., 1919; i, p. 3. McMeans Archives of Int. Med., 1917; xix, p. 709. Nuzum, Pilot, Stangl and Bonar Jour. A. M. A., 1918; lxxi, p. 1562. Oertel Canadian Med. Assoc. Jour., 1919; ix, p. 339. Opie, Freeman, Blake, Small and Rivers Jour. A. M. A., 1919; lxxii, p. 556. Speares Boston Med. and Surg. Jour., 1919; clxxx, p. 212. Stone and Swift Jour. A. M. A., 1919; lxxii, p. 487. Symmers Jour. A. M. A., 1918; lxxi, p. 1482. Synnott and Clark Jour. A. M. A., 1918; lxxi, p. 1816. Torrey and Grosh Amer. Jour. Med. Sci., 1919; clvii, p. 170. Weber British Med. Jour., 1919; i, p. 8. Wittingham and Sims Lancet., 1918; ii, p. 865.

EXPLANATION OF PLATES

Fig. i. Cyanosis of head and neck.

Fig. ii. Acute tracheitis with desquamation of epithelium and
superficial necrosis.

Fig. iii. Acute serous and hemorrhagic pneumonia.

Fig. iv. Acute serous pneumonia with massive hemorrhage.

Fig. v. Acute hemorrhagic and purulent lobular pneumonia. The
purulent process is seen to be advancing from the focal
type to the more diffuse lobar by fusion of the
neighboring lobules.

Fig. vi. Acute purulent pneumonia.

Fig. vii. Lobular fibrosing pneumonia. In this specimen the patches of
new scar tissue formed irregular islands. The final stage
of contraction of the scar had not taken place.

Fig. viii. Acute serous pneumonia with some infiltration by mononuclear
cells.

Fig. ix. Acute hemorrhagic pneumonia.

Fig. x. Hyaline deposits upon alveolar walls. In some areas the wall
itself has suffered necrosis.

Fig. xi. Acute purulent pneumonia. In other areas of the same lung
the interstitial infiltration by leucocytes was more
intense.

Fig. xii. Acute lymph adenitis, showing the unusual numbers of
endothelial cells while leucocytes are relatively
infrequent.

Fig. xiii. Rupture of abdominal rectus muscle with hemorrhage. The
degeneration antecedent to the rupture is shown in the
belly of the muscle.

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TRANSCRIBER’S NOTES

1. Silently corrected typographical errors and variations in spelling. 2. Anachronistic, non-standard, and uncertain spellings retained as printed. 3. Footnotes have been re-indexed using numbers. 4. Enclosed italics font in _underscores_.