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Studies on Influenza in the Pandemic of 1957-1958. Ii. Pulmonary Complications of Influenza

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Studies on Influenza in the Pandemic of 1957-1958. Ii. Pulmonary Complications of Influenza STUDIES ON INFLUENZA IN THE PANDEMIC OF 1957-1958. II. PULMONARY COMPLICATIONS OF INFLUENZA Donald B. Louria, … , Edwin D. Kilbourne, David E. Rogers J Clin Invest. 1959;38(1):213-265. https://doi.org/10.1172/JCI103791. Research Article Find the latest version: https://jci.me/103791/pdf STUDIES ON INFLUENZA IN THE PANDEMIC OF 1957-1958. II. PULMONARY COMPLICATIONS OF INFLUENZA * t By DONALD B. LOURIAt HERBERT L. BLUMENFELDt JOHN T. ELLIS, EDWIN D. KILBOURNE, AND DAVID E. ROGERS (From the Departments of Medicine, Pathology, and Public Health and Preventive Medicine, The New York Hospital-Cornell Medical Center, New York, N. Y.) (Submitted for publication July 10, 1958; accepted August 7, 1958) Influenza presents a paradox. To the clinician edge of influenza derived from modern virologic practicing medicine in 1918, influenza was a fear- studies of the epidemic (interpandemic) disease some disease attended by frequent and often fatal must be applied with caution to the 1918-19 pan- pulmonary complications. To the student of in- demic. In the new pandemic in 1957, certain old terpandemic influenza in the last quarter century, questions remained unanswered: the disease is an acute, temporarily incapacitating 1. What is the etiologic agent of pandemic in- infection of the upper respiratory tract which is fluenza? benign except on the rare occasion when bacterial 2. Is the pandemic disease more severe than the pneumonia supervenes. This contrast in the mani- interpandemic form or only more widespread? festations of influenza has led to speculation that 3. Is bacterial pneumonia the major cause of the disease of 1918 was either a different disease fatalities in pandemic influenza; if so, may fatali- entity or caused by an agent of greater virulence ties be prevented by modem antimicrobials? than influenza viruses now encountered. 4. May influenza virus induce fatal disease in The microbiologic and pathologic evidence ac- the absence of bacterial pathogens? cumulated during the 1918-19 pandemic estab- The first question has been unequivocally ans- lished the probable bacterial etiology of most in- wered. A virus biologically indistinguishable from fluenza fatalities. There were, however, many viruses previously isolated from cases of epidemic clinicians who insisted that certain patients died influenza may cause pandemic disease. The etio- of fulminating illness unassociated with known logical agent of the 1957-58 pandemic, the so- bacterial pathogens. This impression received called Asian strain of influenza virus, differs anti- support in the studies of Goodpasture who pre- genically from previously isolated viruses, but is sented pathologic evidence of a diffuse hemor- nonetheless a strain of influenza A virus. Fur- rhagic pneumonia in two patients which was un- thermore, recent serologic studies suggest anti- associated with the demonstrable presence of bac- genic similarity of the virus of the 1957 pandemic teria (2). to the agent of the pandemic of 1889 (4). The pandemic of 1918-19 antedated the first The definitive answer to the second question recognition of the influenza A virus (Smith, An- must await analysis of data from the present pan- drewes and Laidlaw, 1933 [3]). Thus, knowl- demic, but preliminary evidence suggests that * This work was supported in part by Traineeship pandemic influenza does not differ clinically from Grant E-6 and Research Grants E-2162 and E-1078 from the epidemic disease (5, 6). the National Institute of Allergy and Infectious Diseases, Partial answers to the final questions are sub- Public Health Service; The Research and Development jects of the present paper. This investigation of Division, Office of the Surgeon General, Department of influ- the Army under contract number DA-49-007-MD-703; patients with pulmonary complications of and by grants from Chas. Pfizer & Co., Brooklyn, N. Y.; enza was organized in the fall of 1957 as a pro- The Upjohn Co., Kalamazoo, Mich.; and Wyeth Labora- spective study of disease in the new pandemic. tories, Philadelphia, Pa. The results represent a collaborative integration of t A preliminary report of a part of this investigation laboratory and bedside investigations. has been presented before the Association of American more Physicians and has been published in the Transactions of During the 1957-58 influenza pandemic that society (1). than 50 patients with influenza and evidence of t Research Fellows in Medicine. lower respiratory tract involvement were admitted 213 214 LOURIA, BLUMENFELD, ELLIS, KILBOURNE, AND ROGERS to The New York Hospital. Extensive clinical selected cases. In patients dying during the course of and laboratory observations were made on 33 their disease, specimens of lung tissue removed at au- individuals in this group in whom influenza virus topsy were frozen and stored at -68° C. until virus studies could be performed. infection could be clearly documented. As these Acute serum specimens were drawn at the time of ad- studies progressed it became apparent that four mission on all patients. Subsequent convalescent sera pulmonary syndromes could be differentiated on were obtained on one or more occasions 7 to 35 days later the basis of history, physical examination, the ap- on patients who survived their illness. Sera were tested pearance of chest X-rays, bacteriologic and viro- for the presence of hemagglutination-inhibiting and/or complement fixing antibody to the Asian strain of influ- logic studies and the subsequent course of the ill- enza A virus by techniques detailed in the preceding ness. These syndromes have been categorized as paper (5). follows: The following criteria were arbitrarily established as 1. Influenza virus infection with physical signs definitive evidence of recent infection with the Asian of strain of influenza A virus: lower respiratory tract involvement without in- 1. A fourfold or greater rise in complement fixing filtrates detectable by roentgenography. antibody between acute and convalescent sera using the 2. Influenza virus infection followed by sec- Japan 305 strain of influenza A virus as the test (viral) ondary bacterial pneumonia. antigen. 3. An acute, rapidly progressive pneumonia 2. An initial complement fixing antibody titer of 1: 128 or greater against the Japan 305 strain in patients apparently produced by influenza virus infection seen on or after the seventh day of influenza symptoms. alone. These titers were felt to represent clear evidence of in- 4. Concomitant viral and bacterial pneumonia. fluenza infection after study of a series of 55 normal indi- The present paper describes and defines these viduals revealed none with baseline serum titers of com- clinical entities. Included in this report are the re- plement fixing antibody above 1: 64. 4. Bacteriologic studies. Specimens of sputum, blood, sults of laboratory and physiologic studies, the and swabs from the nasopharynx and throat were cul- course of illness, the therapy employed and the tured from all patients. In many instances, duplicate microbiologic and histologic studies of tissues ob- cultures were performed within the diagnostic bacteri- tained post mortem. ology laboratory of The New York Hospital and the laboratories of the Division of Infectious Disease. Sputum specimens were plated on blood and chocolate MATERIALS AND METHODS agar plates and inoculated into liver dextrose and thio- All 33 patients were hospitalized at The New York glycollate broth. Particular attention was directed to iso- Hospital. Thirty patients were studied on the medical lation of coagulase positive staphylococci, pneumococci, wards. Three pregnant women were studied on the Hemophilus influenzae and beta hemolytic streptococci. obstetrical service. Microorganisms were identified by appropriate subcul- 1. Clinical studies. Each patient was initially exam- ture, biochemical reactions, staining characteristics and ined by the house staff. When the clinical history was serologic studies. compatible with influenza, the patient was re-examined In many instances, 1 ml. of emulsified sputum was also and evaluated by a member of the influenza study group. inoculated intraperitoneally into white mice. When ani- During the acute phase of illness, each patient was exam- mals died, the peritoneal cavity was washed with 1 ml. ined at least once daily by members of the study group of sterile saline and the peritoneal exudate examined by who kept detailed records on symptoms, physical find- Gram stain and inoculated upon blood agar plates and ings and the course of the illness. into appropriate liquid media. Animals which survived 2. Routine laboratory studies. Certain routine stud- sputum inoculation were killed several days later and the ies were performed serially on all patients. These in- peritoneal washings subjected to the same procedures. cluded hematocrit determinations, total and differential In fatal illnesses, postmortem cultures of lung and leukocyte counts, erythrocyte sedimentation rates, uri- heart's blood were obtained from all but one patient. nalyses, chest roentgenograms, blood urea nitrogen, ve- Specimens of lung tissue were plated directly on blood nous carbon dioxide combining power and serum sodium, agar plates and inoculated into beef heart infusion broth, serum potassium and serum chloride determination. liver dextrose broth, and beef heart infusion broth con- 3. Virologic studies. The procedures used for the iso- taining five per cent defibrinated rabbits' blood. Speci- lation of influenza virus are presented in detail in the mens of lung from
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