Epidemic Respiratory Disease / The pneumonias and other infections of the repiratory tract accompanying influenza and measles

by Eugene L. Opie; Francis G. Blake; Thomas M. Rivers; James C. Small

There is no reason for believing that the influenza which prevailed in this country differed in any essential feature from that of previous epidemics and particularly of the pandemic of 1889–90. Our studies have shown that an organism with the morphologic and cultural characters of B. influenzæ of Pfeiffer has been constantly found in association with the disease, and so frequently demonstrated in association with its pulmonary complications that there is little doubt of its constant presence. The bronchial and pulmonary complications of influenza present characters which, while varied, are not usually observed in the absence of epidemic influenza, and in this pandemic agree with those of the former pandemic so far as it is possible to determine from the descriptions available.

Especially noteworthy is the severity of the changes within the bronchial passages. Clinical studies have shown that purulent bronchitis has occurred in 36 per cent of instances of influenza. The sputum with this condition has contained B. influenzæ in all instances, but although there were no signs of pneumonia it has been constantly associated with other microorganisms, namely, pneumococci (in 11 of 13 instances), S. hemolyticus, S. viridans, M. catarrhalis, etc.

Identification of the bacteria which have been present in the bronchi of those dead with pneumonia following influenza have determined what microorganisms have penetrated into the lower respiratory passages. B. influenzæ has been found so frequently (80 per cent) that there is good reason to believe that it has been constantly present and has not been isolated in every instance because it has been overgrown by other microorganisms on the plates or after long continued illness has disappeared from the bronchi. Mixed infections of B. influenzæ and other microorganisms are constantly found in the inflamed bronchi; combinations of B. influenzæ and pneumococci, B. influenzæ and hemolytic streptococci or these combinations with staphylococci or the four organisms together are common. Other microorganisms such as B. coli, S. viridans, M. catarrhalis and diphtheroid bacilli are not infrequently associated with those which have been mentioned.

Purulent bronchitis has been found in 137 of 241 autopsies; its bacteriology differs in no respect from that which has just been described and indeed no line can be drawn between this condition and the bronchitis invariably present with the pneumonias of influenza. Other evidence of profound injury to the bronchi is the frequent occurrence of hemorrhage in a zone ensheathing the smaller bronchi, and the common occurrence of bronchiectasis when the fatal disease has lasted more than two or three weeks.

Microscopic study demonstrates that the changes in the bronchial walls are such as destroy the defences against invasion by microorganisms. The bronchial epithelium undergoes destruction which is not infrequently limited to the superficial ciliated cells, but often complete loss of epithelium occurs. The mucous glands of the larger bronchi exhibit a special susceptibility to injury, and in the early stages of the lesion profound degenerative changes are found in the secreting cells, whereas at a later stage chronic inflammatory changes are almost invariably present.

Pneumonia following influenza is in most instances bronchopneumonia, but typical lobar pneumonia has been found in autopsies representing 40.7 per cent of pneumonias of influenza. Lobar pneumonia is frequently accompanied by purulent bronchitis, and in a considerable number of autopsies (34 of 98 with lobar pneumonia) lobar and bronchopneumonia have occurred in the same individual.

Statistics based upon the clinical diagnosis of lobar and bronchopneumonia following influenza are so inaccurate that they have little if any value. Notwithstanding careful study of the symptomatology of the disease, lobar and bronchopneumonia following influenza are not accurately distinguishable by the means usually employed, and an erroneous diagnosis has been recorded on the patient’s history in 36.6 per cent of 227 fatal cases with autopsy. A diagnosis of suppurative pneumonia is rarely if ever made. The difficulties of diagnosis are in part explained by the frequent association of lobar pneumonia with purulent bronchitis, with bronchopneumonia or with both, and by the occurrence of bronchopneumonia with confluent lobular consolidation involving a large part of a lobe or whole lobes.

There are many defects in the present knowledge of the symptomatology of the pneumonias under consideration. The symptoms of suppurative pneumonia are not clearly defined. Many of these deficiencies might be supplied by further application of the time-honored method of comparing the clinical course of the disease with the changes found at autopsies, supplemented by bacteriologic studies made during life and confirmed after death.

With peribronchial pneumonia bronchi of medium size, on the cut surface of the lung, are surrounded by sharply defined zones of pneumonic consolidation perhaps 0.5 cm. in radius, and this lesion furnishes conclusive proof that the inflammatory process can extend directly through the bronchial wall reaching all alveoli within a limited distance for these alveoli bear no relation to the distribution of the terminal bronchi of the affected bronchus. This peribronchial pneumonia is usually characterized by fibrinous exudate, and pneumococcus has been found either in the blood of the heart or in the lung in all of 6 instances in which peribronchial consolidation has been recognized at autopsy; in half of these autopsies Pneumococcus Type II has been isolated and this relationship is especially noteworthy because Type II has been uncommonly associated with the pneumonias of influenza.

Lobar Pneumonia.—The distribution of lobar pneumonia has repeatedly furnished evidence that the process spreads like the peribronchial lesion directly through the tissue of the lung and is not necessarily disseminated by way of the bronchial tree. Pneumococci doubtless enter the lung by way of the bronchi; the occurrence of lobar pneumonia in frequent association with influenza which exhibits a peculiar capacity to destroy the defences of the lower respiratory passages is in harmony with this view. The presence of pneumococci in the blood furnishes no evidence that infection is hematogenous, for bacterial infections, particularly at their onset, are frequently accompanied by bacteriemia. The wave-like spread of lobar pneumonia may be indicated by a narrow zone of red hepatization separating a large patch of firm, gray consolidation from engorged but air containing lung tissue. A semicircular patch of consolidation not infrequently extends from the left lower lobe into the upper lobe at the site where the interlobular cleft is absent. This patch may be firm and gray in continuity with similar consolidation in the lower lobe but surrounded over its convex surface by a zone of red hepatization.