The pathology of influenzaWinternitz, M. C. (Milton C.)
Science
The pathology of influenza
Winternitz, M. C. (Milton C.)
Influenza
FIG. XXII. AUTOPSY NO. 175. AN ALMOST PURE FIBRINOUS EXUDATE. THE
ALVEOLAR WALLS ARE SLIGHTLY HYALINIZED AND THEIR EPITHELIUM IS
ALMOST ENTIRELY LACKING.
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There are, of course, variations in the extent of the serum, the fibrin,
and the hemorrhage in the exudate of the alveoli, and while these
different types may occur as pure forms, often they are associated. In
still other areas and varying in prominence, one finds as characteristic
an exudate, not only of serum, strands of fibrin, and red blood cells,
but also a diffuse dotting of the exudate with bacteria, singly, in
pairs, clumps, and chains (92, 164) (Fig. XXI). This type of reaction is
uncommon in pulmonary disease. It resembles more closely a streptococcus
cellulitis such as is encountered frequently in the subcutaneous
tissues, for example, a woody phlegmon, or a sero-hemorrhagic exudate
like the avirile response to a rapidly fatal hemolytic streptococcus
serositis. A similar reaction has been reproduced experimentally in
animals which have been rendered aplastic with benzol previous to
pulmonary insufflation, and it is conceivable that the lack of
polymorphonuclear response in the inflammatory exudate may be associated
with some such general destruction or temporary suspension of leucocytic
formation (160).
A more striking picture, however, even than this aplastic alveolar
exudate appears in the terminal bronchioles. In many instances, these
are conspicuous on account of their size, for they are dilated to form
prominent, often irregular, sacs (Fig. XV). The distention of these
terminal bronchioles may be so great that the surrounding alveoli are
compressed. What makes them even more conspicuous is their lining, once
epithelium, but now a swollen, thick, homogeneously staining material,
with complete loss of architecture; the material forms (with hematoxylin
and eosin) a red band limiting the lung tissue and sharply demarcating
it from the exudate within the bronchioles (48, 92). However, this
ribbon of red, often thickened by fibrin deposition, is not always pure,
for bacteria thrive in the dead tissue. They occur singly, paired, in
chains, and also as circumscribed, dense masses which in size and
position, simulate nuclei (162) (Fig. XVI). This same hyalinization of
the epithelium, it will be recalled, occurs in the larger bronchi (Fig.
V), and there, too, bacteria frequently develop in the dead tissue (Fig.
VIII). In the smallest bronchiolar ramifications, acute epithelial
necrosis is not infrequently encountered, even when the surrounding lung
tissue is relatively normal (Fig. XVI). That the process does not stop
with the epithelium, but, as in the larger bronchi, may extend through
the entire structure of the bronchioles, is manifest. Even the alveolar
walls may be involved and frequently homogeneous pink or red bands, now
the phantom of the former viable lung tissue, mark the presence of the
old wall of the alveolus (Fig. XVII). Occasionally, some architecture
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