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A histologic, immunofluorescence, and electron microscopic study of the intracellular parasitism of Coxiella burnetii (the Q fever agent) in mouse lungs after intranasal challenge was undertaken. It was shown that this microorganism invades type I and, rarely, type II pneumocytes as well as pulmonary fibroblasts and histiocytes. The infectious process can be described as a focal intra-alveolar inflammation with the macrophages prevailing in the exudate. It is self-limited, with a complete resolution. The inflammation is associated with atelectases and with increased secretory activity by type II pneumocytes. Alveolar macrophages and granulocytes degrade C. burnetii. This degradation is followed by damage to and eventual disintegration of some macrophages and by damage to some bacterium-free pneumocytes and vascular endothelial cells in the vicinity of macrophages degrading organisms. The cell damage might be caused by lipopolysaccharide released from degraded organisms. The infectious process is also associated with the influx of T cells in the pneumonic foci, T-cell attachment to the macrophages degrading organisms, and fusion of some macrophages. These are considered a morphologic expression of cell-mediated immunity involved in the infectious process.
KHAVKIN et al. (Fri,) studied this question.