The pathology of influenzaWinternitz, M. C. (Milton C.)
Science
The pathology of influenza
Winternitz, M. C. (Milton C.)
Influenza
In the interpretation of this necrotization, the only helpful analogy is
offered by the acute respiratory lesions following the inhalation of
poisonous gases. With the aid of vital stains, it has been demonstrated
that chlorine quickly initiates necrosis due to the direct action of the
gas. Since necrosis also occurs with phosgene,—in the decomposition of
which hydrochloric acid is probably liberated,—there is presumptive
evidence that the halogen is responsible for the process. Studies are
now in progress to determine the relation of the acid-producing
properties of the different strains of organisms to the type and fate of
the pneumonic exudate.
E. THE ORGANIZATION PROCESS
The similarity between the acute lesions of influenzal pneumonia and
those following the inhalation of poisonous gases led to the prediction,
in the early studies, that if the process were not terminated by death,
the bronchiolar and alveolar changes would not result in a restoration
of the tissue to normal, but in an organization which would in its turn
bring about mechanical changes in the pulmonary tissue. This prediction
has been fulfilled; obliterating bronchiolitis (Figs. XI and XLVIII),
bronchiectasis (Figs. L and XII), and organizing pneumonia (47, 92, 156,
162) (Figs. XXXIX, XL, XLI, XLIV, XLV) have been encountered despite the
fact that the time interval for fatalities from extraneous or subsidiary
causes has been short.
[Illustration:
FIG. XLIV. THE ALVEOLAR WALLS ARE IN PART OBLITERATED. THE ALVEOLAR
EXUDATE IS ORGANIZED BUT THE FIBROUS TISSUE STRANDS ARE SPREAD APART
BY EDEMA.
]
[Illustration:
FIG. XLV. AUTOPSY NO. 163. ORGANIZATION OF THE ALVEOLAR EXUDATE AFTER
THE SUBSIDENCE OF THE ACUTE PROCESS. COMPARE FIGURE XLIV.
]
Resolution of the exudate in pneumonia, with the restoration of the
tissue to normal, is a result at such variance with the usual fate of an
inflammatory exudate, that it has attracted a great deal of attention.
Perhaps the most striking results of the study of this subject have been
published recently by Kline (69). Arguing from previous experiments (70)
in which it was demonstrated that the circulation of the pneumonic lung
is impaired, and that for this reason sufficient serum cannot reach the
exudate to inhibit the proteolytic action of leucocytic ferments, Kline
introduced normal serum into the consolidated lung by the tracheal
route, and showed conclusively that this resulted in an organization of
the alveolar exudate. This, of course, might explain resolution, but it
is difficult to see without further study how serum can reach the
exudate to inhibit autolysis, and in this way stimulate organization, in
one case of pneumonia and not in another.
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