Epidemic Respiratory Disease: The pneumonias and other infections of the repiratory tract accompanying influenza and measlesOpie, Eugene L. (Eugene Lindsay)
History
Epidemic Respiratory Disease: The pneumonias and other infections of the repiratory tract accompanying influenza and measles
The term interstitial bronchopneumonia has been used by MacCallum to
designate a lesion which he has found in association with measles at
Fort Sam Houston. This name he states does not describe accurately the
early stage of the lesion, for its interstitial character is not evident
at first. In his monograph on “Epidemic Pneumonia in the Army Camp,”
published in 1919, MacCallum describes and pictures instances of the
lesion which we have designated interstitial suppurative pneumonia and
classifies them as interstitial bronchopneumonia. We have shown that
this lesion, which is the result of infection of the lymphatics with S.
hemolyticus, bears no necessary relation to the lesion which is
characterized in its early stage by peribronchiolar pneumonia and in its
later stages by chronic inflammation with mononuclear infiltration and
proliferation of the peribronchial, perivascular and interalveolar
tissue. At Fort Sam Houston, nearly every patient with measles was
infected with hemolytic streptococci; we observed, following influenza,
similar prevalence of hemolytic streptococci in certain wards in the
base hospital at Camp Pike. Among the cases at Fort Sam Houston there
were doubtless instances both of interstitial suppurative pneumonia
caused by hemolytic streptococcus and of chronic bronchopneumonia not
referable to this microorganism.
Studying pneumonia following influenza at Camp Lee, Va., and later at
Camp Dix, N. J., during the fall of 1918, MacCallum reached the
conclusion that “interstitial bronchopneumonia” following influenza was
caused by B. influenzæ of Pfeiffer. This lesion attributed to B.
influenzæ differed from that previously referred to hemolytic
streptococcus in the following characters: the lymphatic channels in the
bronchial walls and widened interlobular septa are inconspicuous and
none are found distended with exudate; there is no intense infection of
the pleura, and polynuclear leucocytes are inconspicuous in the alveolar
exudate and in the walls of the bronchi. It seems probable these
differences are explained by the absence of hemolytic streptococci which
tend to invade lymphatics and produce severe inflammatory changes in the
pleura.
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