The hyalinization of the epithelium lining the ducti alveolares (47, 48)
also merits special attention (Figs. V, XV, XVI). This process may
extend through the wall of the duct and is often seen in the alveolar
walls throughout the involved lung. The entire alveolar wall may be
homogeneous in appearance, but, occasionally, the thrombus alone, which
has formed in its vessels (41), presents this change (Fig. XVII). The
alveolar as well as the bronchiolar wall is thickened by a homogeneous
material in which cell-body and exudate cannot be differentiated. This
acute necrosis, as has been mentioned, is encountered in gas poisoning
but is unusual in other known types of respiratory infection. Doubtless,
it is a precursor to the more destructive lesions commonly found in
later stages of the disease—abscesses which extend through the
bronchiolar walls (Fig. XXXI), necrotizing areas of pneumonia in which
huge clumps of bacteria are found (Fig. XXXII), and true gangrene (Figs.
XXXIII, XXXIV, XXXV). The destruction of the alveolar wall in the early
stages of the disease plays a causal rôle in the production of
subcutaneous emphysema (Figs. XVIII and XIX). This important phase of
the histological change in influenzal pneumonia has received but little
attention and, with one or two exceptions, is not mentioned in the
literature (8, 162).
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.