Evidence againstHelicobacter pyloriBeing Related to Childhood Asthma

carried in the upper respiratory tract, a phenomenon we referred to as “copathogenesis.” The mechanism(s) by which such potentiation may have occurred are unknown. We speculated that the 1918 virus may have had increased tropism for or have been unusually cytopathic for tracheobronchial cells, facilitating access of bacteria to the peripheral bronchopulmonary tree and leading to massive diffuse bacterial bronchopneumonia that was poorly responsive to therapies of the time. Dr. Kilbourne joins us in noting the remarkable measles epidemics in US Army training camps during the winter of 1917–1918, less than a year before the influenza pandemic. The measles epidemics were the result of an unfortunate “natural experiment”inwhichyoungmenfromremoterural areas, many of whom had escaped measles virus infection in childhood, were brought together incrowdedbarracksduringthewinter/ springseasonofmeaslescirculation.Although in years prior to 1918 measles had generally been a less deadly disease than influenza would prove to be a year later, the case fatality rate for measles was, paradoxically, much higher. Deaths in these cases resulted largely from streptococcal or pneumococcal bronchopneumonias pathologically indistinguishablefromthosecausedbypandemicinfluenza several months later [3]. Thus, copathogenic properties of the 1918 influenza virus may have been generic and not specific to the 1918 virus or to influenza viruses in general.