Abstract
The data presented show that cells of Nocardia caviae 112 were converted to cell wall-deficient microbial variants within the intact murine lung after intranasal administration. At the time that these L-phase variants were recovered in large numbers from the lung, there was a correspondingly enhanced inflammation leading to alveolar consolidation and animal death. During the peak of this response (at 1 week after infection), normal nocardial cells were neither isolated from nor seen within the lung. It is suggested that the conversion of these normal nocardial cells to their L-phase variant leads to this extensive pulmonary damage. Furthermore, the L-phase organisms appear to play an active role in this pathological effect since introduction of similar amounts of killed nocardial cells into the lungs of the mice failed to produce a similar response.