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THE PATHOPHYSIOLOGY OF INFLUENZAL PNEUMONIA IN 1918 KINGSLEY M. STEVENS* During and shortly after the 1918 pandemic, evidence was presented to support the view that the causative agent ofinfluenza wasHaemophilus influenzae [1, 2], although other workers felt that influenza was a virus disease [3]. Cummins, in a Ministry of Health report [4], proposed a possible synergistic role for the bacterium acting with a virus: "Had it not been for these recent observations which have gone so far toward demonstrating the etiological role of a filter-passing organism, the evidence in favour of H. influenzae would probably have been regarded as conclusive . As it is, this bacillus must still be admitted to be the earliest and most constant 'associate' appearing on the scene within the first hours of the attack. To what extent it facilitates the operations of other and more virulent germs still remains to be discovered." In 1931, Shope [5-7] demonstrated that influenza was a virus disease—with the important proviso that severe disease required the presence of both the virus and H. influenzae. His studies were in swine with virus and bacterium of swine origin, although there was considerable evidence that the virus, at least, came from man in the fall of 1918 [8]. Shope [6, 8, 9] therefore proposed that this synergistic combination was probably responsible for influenza in man, consistent with Cummins 's 1920 suggestion. In 1933 Smith, Andrewes, and Laidlaw [10] isolated the first influenza virus from man. This WS strain is now known as a type A virus, as is the swine strain isolated by Shope. It was subsequently shown that either human or swine strains of virus could produce fatal disease in experimental animals without the presence of H. influenzae or other bacteria. Furthermore, H. influenzae did not increase the virulence of influenza viruses, using human strains of the bacterium in swine [11] or mice [12] The author thanks the library staffs of his affiliations for their help. *Medical Service, Veterans Administration Medical Center, Northport, New York 11768; and Department of Medicine, State University of New York at Stony Brook.© 1981 by The University of Chicago. All rights reserved 003 1-5982/82/250 1 -0245$0 1 .00 Perspectives in Biology and Medicine · Autumn 1981 | 115 or strains from swine in ferrets [13]. In a Harvey lecture in 1936 [9] and the Thayer lectures in 1944 [8], Shope carefully organized the data to support his contention that//, influenzae could have played a crucial role in the devastating pandemic of 1918. Yet the verdict of medical science was, and is, that swine influenza was a special case having no applicability to human influenza in 1918. Nonetheless, there remained nagging problems about the pandemic. The morbidity rate was not much higher than in other epidemics [14, 15], but the mortality rate was a great deal higher. The cause of the high mortality was the occurrence of severe pneumonia in 15-20 percent of clinical cases of influenza [4, 14]—much higher than had occurred before or has since. In years of influenza epidemics, there has always been an increase in pneumonia deaths. These "excess" deaths occur primarily in older people [16] and are late deaths due to bacterial pneumonia following the onset of influenza. Experimental models indicate that the bacteria must be introduced a few days after the virus [17-19]. This late increased susceptibility to bacterial pneumonia is due, at least in part, to a decrease in the ability of alveolar macrophages to destroy bacteria [20]. To account for the extraordinarily high mortality in the 1918 pandemic, it was postulated that particularly virulent strains of streptococci, pneumococci, and staphylococci were prevalent in 1918 [21, p. 58]. If this were true, the mortality rate in 1918 should have shown a much greater increase with advancing age than in other epidemics of influenza . In fact, the mortality rate for the 55-65 age group was essentially the same as in the epidemics of 1892 and 1900. The great increase in mortality in 1918 was in the young adult group [4]. Because the relationship between age and mortality was totally inconsistent with secondary bacterial pneumonia, we reviewed the bacterial studies carried out in 1918-1919...


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