* Week of the influenza epidemic.
** Regarding the details, compare with our influenza lectures (pp. 5 and 36-42), together with the corresponding instructive curves.
We will now briefly consider the croupous pneumonia caused by influenza. We will consider the clinical and pathologic characteristics together, as only in this way can a correct picture be obtained.
The fibrinous pneumonias occurring with influenza frequently differ markedly in their pathologic and clinical characteristics from the typical picture of genuine croupous pneumonia. The inflammatory areas are frequently only lobular (partially lobar) and only gradually become lobar. The pneumonia is often bilateral and is occasionally multiple. The infiltration not uncommonly forms a flabby, indistinctly granular hepatization. The lobar infiltrations occasionally still show the structure of lobular areas at various stages, in that in one and the same lobule there occur red and gray areas of hepatization side by side, but evidently of a granular character.
The stage of inflammatory engorgement often exists for some time before compact infiltration occurs (for this reason there are at first only relative dulness and permanent crepitations without bronchial breathing). The initial rigor is frequently absent, since the pneumonia gradually develops from the influenza. The fever curve occasionally shows marked remissions and even intermissions corresponding to the progression, by stages, of these pneumonias. The typical rusty sputum is often absent, a purulent sputum taking its place, because the diffuse grippal bronchitis which exists at the same time causes so much purulent secretion that the pneumonic sputum is not apparent. The accompanying influenzal capillary bronchitis is characterized, frequently from the beginning, by dyspnea and cyanosis, which are quite disproportionate to the slight amount of the pneumonic infiltration. From the onset of the pneumonia there is marked weakness of the heart, with tachycardia and a small pulse. Resolution is rarely by crisis, but by lysis. Seropurulent or purulent pleural effusions frequently occur, occasionally even at the onset of the pneumonia, but usually at the height of the affection. We shall in the next section (Clinical Characteristics and Course of the Influenza Pneumonias) call attention to several other atypical characters of the pneumonia.
Nevertheless, in this description of atypical forms of croupous pneumonia in influenza we must not lose sight of the fact that the disease often runs the characteristic normal type (onset with chill, acute lobar infiltration, rusty sputum, crisis, etc.), and the typical picture of croupous pneumonia is also frequently found at the autopsy.
The above mentioned clinical and pathologic characteristics of the croupous influenza pneumonia are by no means typical of this form alone. Pneumonia occurs in the very same manner, that is to say, with all the mentioned anomalies, as a primary disease, and has long been known by different names, e. g.: atypical, asthenic, typhoid malignant, contagious, and infectious pneumonia. It occurs commonly in the small epidemics or groups (house, family, prison epidemics), and frequently has a markedly contagious character. In an article,* now apparently forgotten, upon these asthenic pneumonias, as I called them at that time, I said, in the year 1874, therefore before the time of bacteriology, that these pneumonias were different from the ordinary croupous pneumonias, and were probably due to an infection with other, more malignant, causes of disease.
But upon the basis of further clinical, pathologic, and bacteriologic investigation I have, in the course of the last twenty years, arrived at a different opinion, that all these atypical pneumonias are only varieties of the endemic epidemic croupous pneumonia resulting from a combination of its specific micro organism with pyogenic cocci, especially streptococci. In this opinion I am strengthened by the fact, which I pointed out in 1874,** that during the time of such atypical epidemics, for example, in a malignant epidemic, one or more cases in a house or institution may run a normal course of croupous pneumonia, and a postmortem examination show the classic picture, including the diplococci of true croupous pneumonia.
The opinion which we hold regarding atypical croupous influenza pneumonia and primary atypical pneumonia is then as follows: Croupous pneumonia becomes atypical, asthenic, malignant, etc.-(1) By the combination of the specific cause of genuine pneumonia, either from the onset or in the course of the disease, with other cocci, generally with streptococci, to cause a mixed infection; this occurs at all times, frequently in small local epidemics. (2) By the combination of the specific cause of croupous pneumonia with the bacilli of influenza, primarily or secondarily, to produce a mixed infection. This occurs only when influenza coexists. The clinical pathologic result of these etiologically different mixed infections is the same. In both cases the same manifold clinical pathologic deviations from the clinical picture of the pure genuine croupous pneumonia arise.
With the previously described forms, with the catarrhal bronchopneumonia, the fibrinous and the serofibrinous pneumonia, the varieties of inflammations of the lungs occurring in influenza are by no means exhausted. We must also call attention to a rare but clinically important form of pneumonia, which belongs to the previously mentioned variety of cellular pneumonia and is generally thus classified, but nevertheless, both clinically and pathologically, requires an individual description. This variety is by no means peculiar to influenza. It occurs frequently, as I pointed out long ago,* in other infectious diseases, such as scarlet fever, whooping cough, measles, etc. In the following lines we will briefly discuss the most important clinical pathologic features of this variety of pneumonia.
*"Upon Asthenic Pneumonias," "Volkmann's Sammlung klin. Vortrage," 1874, No. 82.
** Loc. cit., pp. 30, 31.
It often arises acutely, like a croupous pneumonia, and attacks immediately a whole lobe, generally the upper lobe. Clinically, as we pointed out in our influenza lectures, it gives the impression of a croupous lobar pneumonia, until the postmortem examination discloses its true character. The cut surfaces of the lung are entirely smooth, homogeneous, of a fleshy red to a bluish red color, of a fleshy, elastic consistence, and totally devoid of air. Neither fluid nor air can be expressed, nor do drops of pus flow from the severed bronchi. It is, as I have remarked in my lectures, a great error to assume that these acutely arising lobar infiltrations are formed by the confluence of lobular areas or result from an ordinary bronchopneumonia. They belong neither clinically nor pathologically to the latter. Histologically, the pneumonia is characterized by extreme vascularity. The alveolar septa are broad and the seat of round cell infiltration; the lumina of the alveoli are filled with cells, but only traces of fibrin can be detected. The cells consist of a small number of red blood cells, the larger number of leukocytes, but notably large epithelioid cells, which we believe to represent desquamated alveolar epithelium. This peculiarity differentiates it, from a purely histologic point of view, from the usual catarrhal pneumonia, which, on account of the large number of leukocytes, represents pus formation "in optima forma," as Pfeiffer terms it. The acute lobar desquamative pneumonia described by Buhl, which has unjustly been forgotten, is clinically and pathologically almost identical with the form which we are now considering, namely, "the acute lobular cellular pneumonia." On account of the flesh like consistence of the infiltrated lobe we have in the past (1882) used the expression "inflammatory carnification." We must, however, now withdraw this name, as Weichselbaum and Kundrat have lately used, it to designate something quite different, namely, chronicindurative processes. Rusty sputum is never seen. The appearance of this sputum alone makes the differential diagnosis from croupous pneumonia possible; no other sign is absolutely pathognomonic. The form of pneumonia just described arises only secondarily in the course of influenza and other infectious diseases, such as scarlet fever, measles, whooping cough, etc. It has absolutely nothing to do with the so called "primary streptococcus pneumonia." Bacterio logically, divers other cocci are found, and, as usual, in all other kinds of inflammatory areas, especially streptococci. The presence of the influenza bacillus in this variety of pneumonia has not yet been demonstrated.