The relation of B. influenzæ to the bronchitis of influenza indicates that it has a part in the production of the pulmonary sequelæ of influenza. The microorganism has been found by a single culture from the bronchial passages in 80 per cent of instances of bronchitis with fatal pneumonia following influenza and is probably constantly present, usually in immense number, in the bronchial mucus. It is obtained from the pneumonic lung in only about 40 per cent of instances, and microscopic examination of prepared tissue shows that a bacillus with the morphology of B. influenzæ is often demonstrable in the bronchial passages but seldom in the alveoli of the lung. The microorganism is well adapted to multiply under conditions present in the bronchi but doubtless readily disappears from the alveoli which are the site of an inflammatory reaction. The microorganism has an important part in the production of the associated mucopurulent and hemorrhagic inflammation of the bronchi, but it is rarely if ever found in pure culture, being associated with a considerable variety of pyogenic cocci and occasionally bacilli. Infection of the bronchi with B. influenzæ in immense numbers offers an explanation of the severity of the inflammatory process within the bronchi, and of the subsequent dilatation and other chronic changes which occur in them. The presence of the microorganism and the accompanying injury to the ciliated epithelium and mucous glands are important factors in lowering the resistance of the bronchial passages to secondary bacterial infection.
We have obtained no evidence that B. influenzæ alone is capable of causing pneumonia. Its occurrence in less than half of all pneumonic lungs is explainable, in part at least, by its presence in the terminal bronchi which are cut across whenever the lung is punctured for culture. B. influenzæ alone has been found only once among 153 pneumonic lungs from which cultures were made, and in this instance (Autopsy 487) S. hemolyticus present in the blood of the heart, pleural cavity and bronchus doubtless had a part in the production of the associated pneumonia. Pfeiffer maintained that the lesion we have designated hemorrhagic peribronchiolar consolidation was characteristic of infection with his microorganisms. With this lesion B. influenzæ has been found in the lungs in slightly more than half of our autopsies but never alone, pneumococci being found in a third, hemolytic streptococci in more than a half and staphylococci in a fourth of the lungs examined.
B. influenzæ has relatively little capacity to penetrate from the bronchi into the lung tissue and rarely penetrates into the pleural cavity (once with Pneumococcus III, once with S. hemolyticus and once in pure culture), and only once has it been found in the blood of the heart, in this instance in company with S. hemolyticus. Capacity of the microorganism to penetrate from the bronchi into other tissues, both in man and as our experiments have shown in the monkey, is increased by association with pyogenic cocci.
Pneumococcus.—Lobar pneumonia following influenza, like lobar pneumonia in civil life unassociated with influenza, has been caused by pneumococci, but there is the notable difference that the pneumococci usually found are those types which are commonly present in the mouths of healthy men, namely, Types IV, III and atypical II and not the so-called fixed types, namely, Types I and II, which represent the usual cause of lobar pneumonia unassociated with influenza. It appears that influenza increases susceptibility to lobar pneumonia, so that it is frequently caused by microorganisms which under other conditions are less capable of producing this lesion. The association of the pneumococci usually found in the mouth with the lobar pneumonia of influenza does not exclude the possibility that pneumococci transmitted from one individual to another, when newly recruited troops are brought together, have an important part in the production of pneumonia.
Bronchopneumonia is frequently caused by pneumococci and the types which are recovered from the lung and blood do not differ from those found with lobar pneumonia, those usually present in the mouth being predominant, but the incidence of pneumococci with bronchopneumonia has been much less than with lobar pneumonia. Both lobar and bronchopneumonia caused by pneumococci have undergone secondary infection with hemolytic streptococci in a large proportion of instances and both pneumococci and streptococci are often recovered at autopsy. Nevertheless, the bacterial flora of the bronchi and lungs is much more varied with broncho than with lobar pneumonia, and it is evident that microorganisms other than pneumococci are capable of causing bronchopneumonia.
In instances of bronchopneumonia associated with pneumococci, fibrin has been abundant in the alveolar exudate.
The pneumococcus exhibits a notable tendency to produce an inflammatory process which extends through the bronchial walls and from one alveolus through the alveolar walls to those adjacent, for in 6 instances in which the bronchi were surrounded by pneumonic consolidation recognizable at autopsy, pneumococci were uniformly the causative agent, Pneumococcus Type II, otherwise rarely found, being present in half of these cases.
Pneumonia caused by one type of pneumococcus does not necessarily confer immunity from other types of pneumococci, and with somewhat limited opportunity we have observed a number of instances in which, following recovery from pneumonia caused by one type of pneumococcus, a second attack of pneumonia, usually fatal, has been associated with pneumococci of a different type. This recurring pneumonia in a considerable proportion of the relatively small number of instances observed has been produced by Pneumococcus Type II which otherwise has been seldom found among the cases which we have studied. The virulence of this microorganism doubtless explains its ability to cause recurrent pneumonia.
Streptococcus Hemolyticus.—Secondary infection with S. hemolyticus is a common event during the course of lobar pneumonia following influenza. It is noteworthy that this streptococcus infection of the lung has almost invariably occurred in the stage of red hepatization, whereas with gray hepatization, when the alveoli are filled with polynuclear leucocytes, S. hemolyticus rarely invades the lung. It is possible that infection with S. hemolyticus tends to prolong the stage of red hepatization.
The most significant change produced in the pneumonic lung by streptococci is necrosis. When after death with lobar pneumonia hemolytic streptococci, usually associated with pneumococci, are found both in the lungs and blood of the heart, the lung contains patches of necrosis recognized microscopically, in which the alveolar walls and exuded cells have uniformly lost their nuclei. Microscopic examination demonstrates the presence of chains of streptococci in immense number in these necrotic foci; elsewhere chains of streptococci occur but are much less abundant. In some instances streptococci exhibit a tendency to enter lymphatics and to cause acute lymphangitis with lymphatic thrombosis and edema of the adjacent interstitial tissue.