The degeneration as observed in these cases showed many of the characters like that of waxy degeneration seen in typhoid fever. Similar appearances to these have also been described in connection with the toxic degenerations which occur in the vicinity of infections by the gas bacillus. In fact, all the stages observed in the one can be seen in the other. They differ, however, only in the degree to which final destruction takes place and in the speed with which the degeneration is accomplished. The character of the degeneration is well studied in sections stained with hematoxylin and eosin, eosin-methylene blue, and best of all in the phosphotungstic acid hematoxylin. By the latter method one is able to follow clearly the grade of degeneration as it effects the muscle striations. On the other hand, the peculiar waxy appearance of the early degenerating fibers is best seen in sections stained with eosin or fuchsin, where the striated muscle fibers are found to be changed to a more intensely staining red body of homogeneous character and devoid of all evidence of their original internal architecture. These bland waxy fibers were often of the size and shape like the normal. On the other hand, the fibers are also not uncommonly swollen, stretching the sarcolemma to almost the bursting point. Following this primary bland degeneration the fiber takes on irregular shapes, becoming constricted and collapsed at irregular intervals, so that islands of the waxy contents lie within the sarcolemma, being separated from each other by constricted areas in which the original myoplasm has undergone decomposition and sometimes complete absorption. This irregular destruction of the muscle contents often has a granular stage in which the original muscle substance has become disintegrated. The sarcolemma follows the condition within it, stretching when the fiber is swollen and shrinking, or even becoming collapsed when the inner substance is becoming liquified and absorbed. The sarcolemma does not suffer the degenerative changes of the inner fiber, nor can one observe nuclear changes in this sheath which are significant.
When first studying this process of degeneration it appeared to us that the earliest change was a loss of the transverse striations and the subsequent disappearance of the longitudinal fibrillæ. We have subsequently found that this is incorrect and that the changes observed in the markings of the fibers were not constant. At times the muscle substance would progress through stages of degeneration up to the point of disintegration and dissolution while the transverse striæ were still discernible in the altered fiber. The one constant change that we have observed in the degenerating fibers was the early loss of staining qualities as obtained by the phosphotungstic acid hematoxylin. In such preparations the earliest effect of the intoxication upon the muscle fiber was a change in reaction to this stain. Sometimes within a given fiber small irregular and poorly staining blotches could be observed, while the remaining portion of the fiber was normal in its appearance. Later these poorly staining areas became larger, occupying the entire width of the fiber and being distributed at irregular intervals in its length. Finally the characteristic staining quality was entirely lost, although in the poorly colored cell transverse striations were still discernible and a true waxy stage had not yet taken place.
At times the waxy degeneration advanced into the stage of disintegration by an irregular destruction within the fiber. When this occurred the fragments of waxy substance took on curious coiled and grotesque shapes, while a granular destruction was taking place in their periphery. Neither inflammation, œdema nor a vascular reaction could be determined in these tissues of mild or severe change. The reaction as is indicated in the table occurred quite acutely and was not accompanied by fatty products commonly seen in the slower forms of degeneration.
Gradually the debris of the degenerated fibers is absorbed and the sarcolemma shrinks and collapses upon itself. During this stage a reaction occurs in the sarcolemma with nuclear proliferation. At times the last vestiges of the muscle fiber are seen to be surrounded by a crown of nuclei and cells reminding one of the appearance of the degenerating nerve cells in the Gasserian ganglion in hydrophobia. The involved area becomes active in appearance, showing proliferation of fibroblasts and the appearance of occasional lymphocytes and plasma cells. Scar tissue continues to develop in proportion to the amount of damage done. In areas where hemorrhage had taken place the amount of scar tissue is exaggerated, owing to a process of organization which is taking place quite apart from the muscle degeneration. Thus not a few scars scattered through the voluntary striped muscles are the final outcome of this toxic degeneration occurring in epidemic influenza. Some of these lesions may account for the indefinite pains and symptoms of which the patient complains for so many months after his acute illness. I refer particularly to lesions occurring in the psoas and muscles of the back as possible explanations for the partial invaliding of some individuals.
In a certain number of cases of acute influenza the patients complain of severe abdominal pain, in the absence of any localizing symptoms or evidence of intestinal derangement. Such was the case with a number of the above cases coming to autopsy, and the sole evidence we could offer was muscle degeneration with or without massive hemorrhage. The abdominal pains complained of were more of the nature of dull aches with occasional exacerbations and shooting or lancinating “stitches.” Rarely was the patient able to define the position of the pain, not being able to state whether it was within the abdomen or in the parietes. Most frequently they claimed it was internal. We have on no occasion demonstrated an intra-abdominal lesion which could account for such pains. None of our cases was of the type of “intestinal influenza.” We are, therefore, led to the conclusion that the muscle degenerations of the various degrees, from the slight with few muscle elements involved to the severe with rupture and hemorrhage, account for a proportion of the clinical symptoms of (muscle) pains and aches as well as weakness. We cannot claim that coughing was a necessary factor in inducing rupture of the abdominal recti. In some of the cases with rupture severe coughing had not been observed during the illness.
Upper Respiratory Tract
The pathological changes found in the nose, pharynx and larynx were of relatively slight importance and most variable in their severity and incidence. The majority of individuals had few clinical manifestations of disease in these parts. Some, however, complained of dryness of the pharynx with slight feeling of fullness. An examination of these parts revealed some congestion, varying from a red injected mucosa to a bluish cyanosis. In the nose the reaction was rarely as acute as is seen in infectious coryza, but even where relatively little change was to be seen in the tissues hemorrhage from the erectile tissue was not uncommon during the acute stages. No particular lesion was to be found associated with nose bleed. There was an unusual absence of excessive secretion from nose and pharynx in the majority of cases. One was also struck with the infrequency with which the larynx was involved. A certain number of individuals complained of hoarseness, and in them injection of the vocal cords with some swelling was found. In many others, however, even where an intense infectious process was present in the lower respiratory tract the larynx was almost without change. It was from the level below the larynx that the acute reaction in the respiratory system was found.
In all of our cases the trachea showed definite inflammatory reaction. Of the 32 cases there were 26 having an acute tracheitis, 5 with an acute mucopurulent inflammation and 1 with a reaction in the subacute stage. In the majority of the cases with acute tracheitis there was a thin layer of exudate lying upon the mucosal surface. At times the trachea was filled with a frothy serous fluid, the greater part of which had its origin in the lung. Nevertheless, as we shall point out later, we did obtain microscopical evidence indicating that during the early acute stage of the tracheitis a considerable serous exudate escapes from its mucosa. This serous inflammatory reaction is an important one for all of the mucosal structures upon which the virus of influenza obtains a footing. This we have found true for the trachea, bronchi and alveoli of the lungs. In some cases the exudate was grey and lay in close contact with the injected tissues. At first sight this grey exudate suggested necrosis, but it was readily wiped from the underlying structure. Some leucocytes and cell debris with many bacteria made up the content of this grey exudate.
The macroscopic appearance of the trachea was that of an intensely injected structure which had largely lost its normal lustre. The naked eye could distinguish that anatomical change had occurred in the surface tissue of the trachea and that there was unusual evidence of intensely injected vessels lying in the submucosa. In only one instance was there an appearance of a true necrotic membrane lying upon the surface of this intensely inflamed layer. This apparent membrane was found to consist of a wide patch of desquamated epithelial cells which was lying as a delicate necrotic plate upon the surface. This thin layer was devoid of a meshwork of fibrin threads as usually accompanies a true false membrane of other sources.
The early intense inflammatory reaction of the surface membrane of the trachea was characteristic, and in our experience was never exceeded in intensity by other infections. A desquamation of the lining membrane was also a common finding. Naturally this intense reaction so commonly found in the trachea extended without interruption into the main bronchi and their divisions. The finding of this continuous surface inflammation is good evidence of the mode of spread of the infectious process along these membranes, beginning in the upper portions and by direct continuity involving more and more of the respiratory tubes toward the lung.