Pulmonary Edema in Influenzal Pneumonia of the Mouse and the Relation of Fluid in the Lung to the Inception of Pneumococcal Pneumonia

Abstract

In a preceding study (2) concerning the mechanism by which influenza viral infection of the mouse induces susceptibility to secondary pneumococ~l pneumonia evidence was presented that this susceptibility is associated with the appearance of the lesion produced by the virus. The studies reported in the present paper indicate that pulmonary edema is a component of the influenza viral lesion in the mouse and that the presence of fluid in the lung is an important factor in the inception of pneumococcal pneumonia in this animal. In addition, evidence is presented that the chief action of fluid under these circumstances is to furnish a culture medium for growth of pneumococci. Methods and MaterialsDetails of techniques have been described in earlier papers (2, 3). Mice were infected with the Weiss strain of influenza virus and the A5 strain of Type I pneumococcus. 1 The intrabronchial method of inoculation was used not only for the virus but also for introducing fluids or cultures into the lung. In addition, mice were allowed to inhale fine droplets containing pneumococci and were observed for survival or were killed and the pneumocoecal content of the left lobe of the lung determined by grinding the tissue in a mortar and preparing poured blood agar plates.Although pulmonary fluid could be seen in microscopic sections stained with hematoxylin and eosin, other staining procedures rendered fluid more easily and certainly visible. Iron hematoxylin (5) and phloxin with methylene blue (6) were used for this purpose and some undifferentiation of the latter was permitted. Pneumococci in the lung were visualized well with eosin and methylene blue (6) or Giemsa (6).Reexpansion of lungs with fixative was carried out as before in order to see the structure of the lung adequately (7). However, because of the possibility that introduction of fixative into

Defect in intracellular killing of Staphylococcus aureus within alveolar macrophages in Sendai virus-infected murine lungs.

“…The finding that some areas of consolidation did not contain extracellular bacteria or focal areas of bacteria-containing macrophages suggests that edema and consolidation, as proposed by others (17,18), are not the cause of suppressed bactericidal mechanims but rather may be the effect of enhanced bacterial proliferation.…”

“…Male Swiss albino mice (CD 1 strain, [18][19][20] g) were used in these experiments. The animals were housed in filter-topped cages and fed food and water ad libitum.…”

Early bacterial clearance from murine lungs. Species-dependent phagocyte response.

“…Early studies using bacteria presented as a bolus to the distal lung uniformly reported the presence of PMN in the alveoli within a few hours of the introduction of the bacteria (26)(27)(28)(29). Some investigators felt that the granulocytes were primarily responsible for the killing of the bacteria (30,31), whereas others attributed this function to the alveolar macrophage (32). More recent research (33)(34)(35) has focused on bacteria presented to the lungs in the form of a diffuse aerosol rather than a bolus, allowing large numbers of animals to receive a uniform dose of bacteria and permitting meaningful statistical evaluation of bacterial clearance kinetics.…”

Pulmonary Alveolar Macrophage DEFENDER AGAINST BACTERIAL INFECTION OF THE LUNG

“…The pathogenesis of this impairment is unclear. Ozone causes edema formation (23), and previous studies suggest that phagocytic mobility is hindered by intra-alveolar fluid (24). Because the histologic assessment of edema is a crude measureinent, it is possible that sufficient amounts of undetected edema fluid were present to hinder phagocvtosis.…”