The pleura is protected by several tissue boundaries of differing degrees of strength. Penetration of the pleural space by mediastinal infection occurs more easily than from the lung, which in turn occurs more easily than through the diaphragm or chest wall. Infectious organisms of all classes, including bacteria, viruses, fungi, and protozoa are capable of causing pleural infection. The basic tissue response in the pleura is similar to that seen in other tissues but is modified by the peculiar anatomy of the pleura, flat serosal surfaces in constant motion against each other. Most pleural infections are initiated in the lung. Some of the most spectacular pathologic lesions are caused by aspergillus where vasculoinvasive fungi cause infected infarcts that result in round visceral pleural lesions. These in turn result in "kissing lesions" of the parietal diaphragmatic surfaces which are of the same size and shape as the visceral pleural lesions, indicating attachment and splinting of the pleural surfaces in these loci. Studies in rabbit demonstrate rapid resolution of experimental empyema with a standardized series of pathologic responses. In uncomplicated empyema, the end result is an extremely thin, almost undetectable scar. Thick fibrotic pleural lesions suggest a complicated course with continuing infection.