The material so far presented has dealt with contact infection in cases of pneumonia following influenza. That a similar contact infection in cases of influenza treated in crowded hospital wards is responsible in considerable degree for the development of pneumonia in cases of influenza seems quite probable. It has already been stated that this pneumonia was found in large part to be caused by infection with types of pneumococcus that are found in the mouths of normal individuals. It has been fairly definitely established by Stillman[52] that lobar pneumonia caused by pneumococcus Types I and II is in all probability due to contact infection, and definite instances of such infection by Pneumococcus Type II have been reported above. In a recent communication Stillman[53] has furthermore shown that of the various groups of Pneumococcus II atypical those most frequently associated with pneumonia are rarely found in normal mouths, while those infrequently associated with pneumonia are more commonly found. Whether similar considerations will hold true for pneumococci of Group IV can only be determined by further investigation. It has been stated that certain observations made during the course of this work have suggested that cases of pneumonia which complicate influenza may be due to contact rather than to autogenous infection. The data available are far too limited to establish this fact and it would require a very extensive study to furnish conclusive evidence. Certain general observations have suggested this point of view. It is well recognized that the incidence of pneumonia in patients with influenza has been much higher where overcrowding has existed. It would seem probable that this has been in large part due to the greater opportunity for the dissemination of organisms capable of producing pneumonia and the consequently increased opportunity for secondary contact infection among patients treated under such conditions. The not infrequent occurrence of influenzal pneumonia due to combined infections of the different types of pneumococci, hemolytic streptococci, staphylococci, and other bacteria, instances of which have been cited, is in harmony with this view, especially since pneumonia under ordinary conditions is rarely found to be associated with mixed infections of this nature. It is true that healthy individuals occasionally carry more than one type of pneumococcus simultaneously in the mouth, though this is very infrequent, and autogenous infection occurring in such individuals might account in some instances for the mixed pneumococcus infections encountered. By way of analogy it has been clearly shown in other studies by the Commission on the relation of hemolytic streptococcus carriers to the complications of measles, that secondary infection of the respiratory tract with S. hemolyticus is in very large part due to contact infection, the chronic carrier rarely developing complications due to this organism.