Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness

In the paper

“The pandemic caused a “W-shaped” age-specific mortality curve, which exhibited peaks in infancy, between about 20–40 years of age, and in elderly individuals [3, 21].”

What the sources say

• ?Not checked — no full text of the sourcecites [3] Morens DM Fauci AS The 1918 influenza pandemic: insights for the 21st century J Infect Dis 2007 195 1018 28 17330793 source
• Supported

  The passage labeled Abstract describes the 1918 pandemic’s age-specific death rates as a W-shaped curve: peaks in the very young and very old, plus a third peak at approximately ages 20–40. The Figure 2 caption identifies the plotted mortality curve as being for the 1918 pandemic year. (LLM, conf=0.95)

  cites [21] Taubenberger JK Morens DM 1918 influenza: the mother of all pandemics Emerg Infect Dis 2006 12 15 22 16494711 PMC3291398 source

In the paper

“The viruses that caused the 1957 and 1968 pandemics were descendants of the 1918 virus in which 3 (the 1957 virus) or 2 (the 1968 virus) new avian gene segments had been acquired by reassortment [21].”

What the sources say

• Partly supported

  The passage headed “What Was the Animal Host Origin of the Pandemic Virus?” says the 1957 and 1968 viruses arose by reassortment between an avian virus and the previously circulating human H1N1 strain; another passage describes the reassorted pandemic viruses as descendants of the 1918 virus. Our copy does not give the claimed counts of three new avian gene segments in 1957 and two in 1968. (LLM, conf=0.88)

  cites [21] Taubenberger JK Morens DM 1918 influenza: the mother of all pandemics Emerg Infect Dis 2006 12 15 22 16494711 PMC3291398 sourceExperimental — accuracy not yet measured

In the paper

“Staphylococcus aureus, a relatively minor cause of the 1918 fatalities, was predominant in the culture results from 1957–1958 [21, 57-61], and negative lung tissue cultures were more common, possibly as a result of the widespread administration of antibiotics [57, 58, 61].”

What the sources say

• ?Could not verify

  The paper discusses 1918 influenza mortality and complicated respiratory infections (Abstract; no page given), but the passages found do not identify Staphylococcus aureus as a relatively minor cause of 1918 deaths. Searches for Staphylococcus aureus, 1957–1958 culture results, negative lung cultures, and antibiotics found no passage addressing those claims. (LLM, conf=0.76)

  cites [21] Taubenberger JK Morens DM 1918 influenza: the mother of all pandemics Emerg Infect Dis 2006 12 15 22 16494711 PMC3291398 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [57] Mark DD The pathology of 1957 (Asian) influenza Am Rev Tuberc Pulmon Dis 1959 79 440 9 13650115 source
• ?Not checked — no full text of the sourcecites [58] Robertson L Caley JP Moore J Importance of Staphylococcus aureus in pneumonia in the 1957 epidemic of influenza A Lancet 1958 2 233 6 13564806 source
• Partly supported

  The Discussion (page unavailable) says bacteria were almost invariably isolated from fatal 1918–19 cases and that S. aureus was the associated pathogen in a majority of the fatal influenza pneumonias it discusses from later years. It does not establish that staphylococci were a relatively minor cause of 1918 fatalities. More importantly, its section on primary influenza virus pneumonia argues that antibiotics were unlikely to have made the culture-negative lungs in its cases sterile, contrary to the proposed explanation. (LLM, conf=0.86)

  cites [59] Louria DB Blumenfeld HL Ellis JT Kilbourne ED Rogers DE Studies on influenza in the pandemic of 1957–1958. II. Pulmonary complications of influenza J Clin Invest 1959 38 213 65 13620784 PMC444127 sourceExperimental — accuracy not yet measured
• Partly supported

  The Pleural Effusion discussion reports that Staphylococcus aureus was common in pathological series of 1957 influenza deaths, supporting its prominence in those results. The paper does not establish that it was a minor cause of 1918 fatalities or that negative lung-tissue cultures were more common in 1957–1958 because of antibiotics; its discussion of antibiotic use does not link it to negative cultures. (LLM, conf=0.85)

  cites [60] Oswald NC Shooter RA Curwen MP Pneumonia complicating Asian influenza Br Med J 1958 2 1305 11 13596593 PMC2027396 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [61] Oseasohn R Adelson L Kaji M Clinicopathologic study of thirty-three fatal cases of Asian influenza N Engl J Med 1959 260 509 18 13632920 source

In the paper

“Bacillus influenzae tended to appear early in symptomatic influenza in association with diffuse bronchitis and/or bronchiolitis, sometimes infiltrating the bronchiolar submucosa [35]; it caused seroconversion [56] and was then typically replaced by other secondary organisms.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [35] Reckford FFD Acute alveolar and interstitial emphysema in influenza bronchopneumonia Pennsylvania Med J 1920 23 379 87
• Partly supported

  Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [56] Wollstein M Pfeiffer’s bacillus and influenza: a serological study J Exp Med 1919 30 555 68 19868377 PMC2126671 sourceExperimental — accuracy not yet measured

In the paper

“in one study of approximately 9000 subjects who were followed from clinical presentation with influenza to resolution or autopsy [40], researchers obtained, with sterile technique, cultures of either pneumococci or streptococci from 164 of 167 lung tissue samples.”

What the sources say

• Partly supported

  The Introduction (p. 594) reports 9,037 hospital admissions during the epidemic, and the postmortem investigation plan (approximately p. 596) calls for culturing exudates from consolidated lung tissue. The passages in our copy do not establish that all patients were followed to resolution or autopsy, or report 164 positive cultures among 167 lung samples with no negative results. (LLM, conf=0.86)

  cites [40] Hirsch EF McKinney M An epidemic of pneumococcus bronchopneumonia J Infect Dis 1919 24 594 617 sourceExperimental — accuracy not yet measured

In the paper

“In rhesus monkeys, human influenza viruses given intranasally were not pathogenic, but could be made so by nasopharyngeal instillation of otherwise nonpathogenic bacteria [69].”

What the sources say

• Supported

  The Discussion (p. 211) says normal rhesus monkeys remained relatively asymptomatic after intranasal administration of influenza A virus or group C streptococci alone. It then reports (p. 213) that serious infection occurred more often when streptococci were given after influenza virus: five of eleven monkeys became ill, and two developed fatal septicemia. (LLM, conf=0.88)

  cites [69] Wilson HE Saslaw S Doan CA Woolpert OC Schwab JL Reactions of monkeys to experimental mixed influenza and Streptococcus infections. An analysis of the relative roles of humoral and cellular immunity, with the description of an intercurrent nephritic syndrome J Exp Med 1947 85 199 215 19871608 PMC2135694 source

In the paper

“As reviewed recently by McCullers [75], a body of experimental research during the last 3 decades has identified possible mechanisms by which coinfection with the influenza virus and bacteria might affect pathogenicity. These include viral neuraminidase (NA)–induced exposure of bacterial adherence receptors; bacterial NA-induced upregulation of influenza infection; interleukin 10–induced suscept”

What the sources say

• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [75] McCullers JA Insights into the interaction between influenza virus and pneumococcus Clin Microbiol Rev 2006 19 571 82 16847087 PMC1539103 sourceExperimental — accuracy not yet measured
• Partly supported

  The introduction (p. 1) says excessive IL-10 was critically involved in bacterial outgrowth during postinfluenza pneumococcal pneumonia in mice; the Discussion (p. 6) also reports that neutralizing IL-10 reduced bacterial loads. The paper does not establish the claimed neuraminidase mechanisms or IL-10-induced susceptibility to staphylococci, although it mentions staphylococci as a cause of postinfluenza pneumonia. (LLM, conf=0.86)

  cites [76] van der Sluijs KF Nijhuis M Levels JHM Influenza-induced expression of indoleamine 2,3-dioxygenase enhances interleukin-10 production and bacterial outgrowth during secondary pneumococcal pneumonia J Infect Dis 2006 193 214 22 16362885 sourceExperimental — accuracy not yet measured
• ?Not checked — no full text of the sourcecites [77] Navarini AA Recher M Lang KS Increased susceptibility to bacterial superinfection as a consequence of innate antiviral responses Proc Natl Acad Sci U S A 2006 103 15535 9 17030789 PMC1622858 source

In the paper

“The 1968 influenza pandemic was mild, and autopsy studies were uncommon [21].”

What the sources say

• ?Could not verify

  Our copy discusses archival autopsy materials from 1918 (Abstract, page unavailable), but does not address how common autopsy studies were during the 1968 pandemic. Searches for 1968, autopsy studies, and related terms found no passage supporting that point. (LLM, conf=0.75)

  cites [21] Taubenberger JK Morens DM 1918 influenza: the mother of all pandemics Emerg Infect Dis 2006 12 15 22 16494711 PMC3291398 sourceExperimental — accuracy not yet measured

In the paper

“The 1968 influenza pandemic was mild, and autopsy studies were uncommon [21].”

What the sources say

• Supported

  The paper identifies the 1968 pandemic virus as a descendant of the 1918 virus (Abstract, page unavailable) and says that all apparent descendants caused substantially milder human disease. This supports the quoted claim about 1968, although the paper expresses mildness relative to 1918. (LLM, conf=0.84)

  cites [21] Taubenberger JK Morens DM 1918 influenza: the mother of all pandemics Emerg Infect Dis 2006 12 15 22 16494711 PMC3291398 source

In the paper

“During the 1940s, additional studies in ferrets, mice, and rats established that the influenza virus in combination with any of several pneumopathic bacteria acted synergistically to produce either a higher incidence of disease, a higher death rate, or a shortened time to death [70-73]; these effects could be mitigated or eliminated if antibiotics were given shortly after establishment of combined”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [70] Glover RE Spread of infection from the respiratory tract of the ferret. II. Association of influenza A virus and Streptococcus group C Br J Exp Pathol 1941 22 98 107
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [71] Schwab JL Blubaugh FC Woolpert OC The response of mice to the intranasal inoculation of mixtures of Streptococcus hemolyticus and influenza virus J Bacteriol 1941 41 59 60
• ?Not checked — no full text of the sourcecites [72] Francis T Vicente de Torregrosa M Combined infection of mice with H. influenzae and influenza virus by the intranasal route J Infect Dis 1945 76 70 7 source
• Partly supported

  Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

  cites [73] Harford CG Smith MR Wood WB Sulfonamide chemotherapy of combined infection with influenza virus and bacteria J Exp Med 1946 83 505 18 20983719 sourceExperimental — accuracy not yet measured

In the paper

“in certain experimental animal models [e.g., 89], some strains have induced severe pathology that differs from the findings associated with circulating human influenza viruses (which, in these models, cause disease resembling self-limited seasonal influenza in humans [90])”

What the sources say

• Supported

  The Results section (‘Model system for evaluation of pathogenicity in ferrets and mice’; page unavailable) reports severe lung, liver, and brain pathology in ferrets infected with the H5N1 strain VN1203. The paper also describes ordinary human influenza viruses as causing acute respiratory illness in ferrets. The more specific self-limited seasonal-influenza comparison is attached to citation [90], not this source. (LLM, conf=0.88)

  cites [89] Salomon R Franks J Govorkova EA The polymerase complex genes contribute to the high virulence of the human H5N1 influenza virus isolate A/Vietnam/1203/04 J Exp Med 2006 203 689 97 16533883 PMC2118237 source
• ?Not checked — no full text of the sourcecites [90] Reuman PD Keely S Schiff GM James N Assessment of signs of influenza illness in the ferret model J Virol Methods 1989 24 27 34 2760163 source

In the paper

“The postmortem samples we examined from people who died of influenza during 1918–1919 uniformly exhibited severe changes indicative of bacterial pneumonia.”

• Also stated in: § Histologic examination of lung tissue from 1918 victims · hedged

  “The examination of recut lung tissue sections from 1918–1919 influenza case material revealed, in virtually all cases, compelling histologic evidence of severe acute bacterial pneumonia, either as the predominant pathology or in conjunction with underlying pathologic features now believed to be associated with influenza virus infection [10, 24] (figure 1).”

In the paper

“The majority of the cases examined demonstrated asynchronous histopathological changes, in which the various stages of development of the infectious process, from early bronchiolar changes to severe bacterial parenchymal destruction, were noted in focal areas.”

In the paper

“Of 2007 pneumococcal isolates, 874 (43.5%) were serotyped by agglutination. Type I was isolated from 124 (14.2%) of 874 subjects; type II from 163 (18.6%); type IIa from 26 (3.0%); type III from 184 (21.1%); and type IV, a category containing diverse and, at the time, untypeable organisms, from 377 (43.1%).”

In the paper

“Cultures of blood samples in 30 military and 12 civilian series, which examined a total of 1887 subjects (table 2), had positive results in 70.3% of cases and typically contained either pneumococci or streptococci in pure culture.”

In the paper

“As was true for the 58 autopsy cases we reviewed (see above), published autopsies for victims of the 1918–1919 pandemic generally showed histopathological asynchrony [20].”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [20] Opie EL Blake FG Rivers TM The pathology and bacteriology of pneumonia following influenza Chapter IV Opie EL Blake FG Small JC Rivers TM Epidemic respiratory disease. The pneumonias and other infections of the respiratory tract accompanying influenza and measles St Louis CV Mosby 1921 107 281

In the paper

“(4) the predominance of bronchopneumonia and lobular pneumonia, as opposed to lobar pneumonia, consistent with diffuse predisposing bronchiolar damage [27-33].”

What the sources say

• ?Not checked — no full text of the sourcecites [27] Goodpasture EW The significance of certain pulmonary lesions in relation to the etiology of influenza Am J Med Sci 1919 158 863 70 19680020 source
• Not checked yetcites [28] Klotz O Members of the Faculty of the School of Medicine, University of Pittsburgh The pathology of epidemic influenza Studies on epidemic influenza comprising clinical and laboratory investigations by Members of the Faculty of the School of Medicine, University of Pittsburgh Pittsburgh University of Pittsburgh 1919 207 294
• ?Not checked — no full text of the sourcecites [29] Lucke B Wight T Kime E Pathologic anatomy and bacteriology of influenza: epidemic of autumn, 1918 Arch Intern Med 1919 24 154 237 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [30] MacCallum WG Pathology of epidemic pneumonia in camps and cantonments in 1918 Med Rec 1919 95 776 84
• Not checked yetcites [31] Tobias JW Anatomía Patológica de la grippe pandémica Rev Med Univ Buenos Aires 1920 17 109 99
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [32] Winternitz MC Wason IM McNamara FP The pathology of influenza New Haven Yale University Press 1920
• Not checked yetcites [33] MacCallum WG Pathological anatomy of pneumonia associated with influenza; 23 plates Johns Hopkins Hosp Rep 1921 20 149 249

In the paper

“The rest of the deaths were associated collectively with either culture of nonpneumopathogenic “other bacteria,” such as nonhemolytic and viridans streptococci, “green-producing streptococci” [54], probably largely corresponding to α-hemolytic streptococci, uncharacterized diplostreptococci, Micrococcus (Moraxella) catarrhalis, Bacillus (Escherichia) coli, Klebsiella species, and complex mixed b”

What the sources say

• ?Not checked — no full text of the sourcecites [54] Tunnicliff R Observations on green producing cocci of influenza J Infect Dis 1920 26 405 17 source

In the paper

“(2) the frequency of pneumonia caused by both mixed pneumopathogens (particularly pneumococci and streptococci) and by other mixed upper respiratory–tract bacteria;”

In the paper

“(3) the aggressiveness of bacterial invasion of the lung, often resulting in “phenomenal” [30] numbers of bacteria and polymorphonuclear neutrophils, as well as extensive necrosis, vasculitis, and hemorrhage [20, 32, 33];”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [30] MacCallum WG Pathology of epidemic pneumonia in camps and cantonments in 1918 Med Rec 1919 95 776 84
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [20] Opie EL Blake FG Rivers TM The pathology and bacteriology of pneumonia following influenza Chapter IV Opie EL Blake FG Small JC Rivers TM Epidemic respiratory disease. The pneumonias and other infections of the respiratory tract accompanying influenza and measles St Louis CV Mosby 1921 107 281
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [32] Winternitz MC Wason IM McNamara FP The pathology of influenza New Haven Yale University Press 1920
• Not checked yetcites [33] MacCallum WG Pathological anatomy of pneumonia associated with influenza; 23 plates Johns Hopkins Hosp Rep 1921 20 149 249

In the paper

“These findings reflect rates of bacterial isolation similar to those of the series that reported the predominance of pneumopathogens (above and table 1), but with higher isolation rates for “other bacteria” offsetting the lower isolation rates for pneumococci, streptococci and staphylococci.”

In the paper

“Cultures of pleural or empyema fluid, reported in 23 military and 12 civilian series examining a total of 1245 subjects (table 2), revealed either streptococci or pneumococci as the most commonly recovered organism in all but 7 series: in 4 series mixed pneumopathogens predominated, and in 3 series Staphylococcus aureus predominated.”

In the paper

“From more than 2000 such publications, we carefully examined the 1539 reports that contained human pathologic and/or bacteriologic findings”

In the paper

“109 of which provided useful bacteriologic information derived from 173 autopsy series. These series reported 8398 individual autopsy investigations undertaken in 15 countries”

In the paper

“96 postmortem lung tissue culture series, 42 blood culture series, and 35 pleural fluid culture series.”

In the paper

“cases have tended to occur in elderly individuals, who rarely undergo autopsy.”

In the paper

“The 1918 pandemic and subsequent pandemics differed with respect to the spectrum and extent of secondary bacterial pneumonia (e.g., the switch in prevalence during the antibiotic era to predominantly staphylococcal secondary pneumonia, as opposed to streptococcal, pneumococcal, and mixed secondary pneumonia; and the greatly decreased involvement of Bacillus [Hemophilus] influenzae)”

In the paper

“Influenza pandemic preparedness strategies in the United States [2] assume 3 levels of potential severity corresponding to the 20th century pandemics of H1N1 “Spanish flu” (1918–1919), H2N2 “Asian flu” (1957–1958), and H3N2 “Hong Kong flu” (1968–1969)”

What the sources say

• Not checked yetcites [2] United States Department of Health and Human Services (HHS) HHS pandemic influenza plan Washington, DC US Government Printing Office 2005 Available at: http://www.hhs.gov/pandemicflu/plan/pdf/HHSPandemicInfluenzaPlan.pdf 16 June 2008

In the paper

“Extrapolation from 1918–1919 pandemic data to the current population and age profile has led United States government officials to plan for more than 1.9 million excess deaths during a severe pandemic [2].”

What the sources say

• Not checked yetcites [2] United States Department of Health and Human Services (HHS) HHS pandemic influenza plan Washington, DC US Government Printing Office 2005 Available at: http://www.hhs.gov/pandemicflu/plan/pdf/HHSPandemicInfluenzaPlan.pdf 16 June 2008

In the paper

“The increased fatality rate in the 3 high-risk age groups was predominantly due to the increased frequency of bronchopneumonia, not to increased incidence of influenza or an increased bronchopneumonia case-fatality rate [19].”

What the sources say

• ?Not checked — no full text of the sourcecites [19] Collins SD Age and sex incidence of influenza and pneumonia morbidity and mortality in the epidemic of 1928–29 with comparative data for the epidemic of 1918–19 Public Health Rep 1931 46 1909 37 source

In the paper

“Primary “panbronchitis” [35] was thought to reflect rapidly spreading epithelial cytolytic infection of the entire bronchial tree [32, 35, 36]; this was thought to have led to the secondary spread of enormous numbers of bacteria along the denuded bronchial epithelium to every part of the bronchial tree, following which focal bronchiolar infections broke through into the lung parenchyma.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [35] Reckford FFD Acute alveolar and interstitial emphysema in influenza bronchopneumonia Pennsylvania Med J 1920 23 379 87
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [32] Winternitz MC Wason IM McNamara FP The pathology of influenza New Haven Yale University Press 1920
• ?Not checked — no full text of the sourcecites [36] Roos C Notes on the bacteriology, and on the selective action of B. influenzae Pfeiffer J Immunol 1919 4 189 201 source

In the paper

“Among the ≥60% of individuals who survived such severe pneumonia, severe chronic pulmonary damage was apparently uncommon [37, 38].”

What the sources say

• ?Not checked — no full text of the sourcecites [37] Wynn WH Chronic influenzal fibrosis of the lungs Lancet 1927 2 964 7 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [38] Nuzum JW Pilot I Stangl FH Bonar BE Pandemic influenza and pneumonia in a large civil hospital J Am Med 1918 71 1562 5 12100

In the paper

“It is noteworthy that pneumococcal typing antisera were unavailable in 11 of these 14 studies, and that many of the cultured “other” bacteria were reported as “gram-positive diplococci,” “streptococci,” or “diplostreptococci” (data not shown), consistent with the possibility that in this early era of bacterial typing, some of the unidentified organisms in the culture may have been pneumopathogens.”

In the paper

“The data are consistent with a natural history in which the virus, highly cytopathic to bronchial and bronchiolar epithelial cells, extends rapidly and diffusely down the respiratory tree, damages the epithelium sufficiently to break down the mucociliary barrier to bacterial spread”

• Also stated in: § DISCUSSION · hedged

  “and if able to gain access to the distal respiratory tree—perhaps on the basis of receptor affinity [80]—creates both a direct pathway for secondary bacterial spread and an environment (cell necrosis and proteinaceous edema fluid) favorable to bacterial growth.”

What the sources say

• ?Not checked — no full text of the sourcecites [80] Stevens J Blixt O Glaser L Glycan microarray analysis of the hemagglutinins from modern and pandemic influenza viruses reveals different receptor specificities J Mol Biol 2006 355 1143 55 16343533 source

In the paper

“we searched major bibliographic sources [e.g., 11–17] for papers in all languages and tables of contents of major journals in English, German, and French; in addition, we searched all of the papers we identified for additional citations.”

What the sources say

• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [11] Billings JS Fletcher R Garrison FH Index Medicus 18 Series II Washington, DC Government Printing Office 1903–1920
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [12] Library of the Surgeon General’s Office, United States Army Index-catalogue of the Library of the Surgeon-General’s Office, United States Army. Authors and Subjects 10 Series III Washington, DC US Government Printing Office 1918–1932
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [13] Vaughan WT Influenza: an epidemiological study. Monograph series no. 1 Baltimore, Maryland American Journal of Hygiene 1921
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [14] Jordan EO Epidemic influenza: a survey Chicago, Illinois American Medical Association 1927
• ?Not checked — no full text of the sourcecites [15] Thomson D Thomson R Annals of the Pickett-Thomson Research Laboratory Volume X. Influenza (Part II) With special reference to the complications and sequellæ, bacteriology of influenzal pneumonia, pathology, epidemiological data, prevention and treatment London Baillière, Tindall & Cox 1934 source
• ?Not checked — no full text of the sourcecites [16] Phillips H Killingray D The Spanish Influenza Pandemic of 1918–19. New Perspectives London Routledge 2003 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [17] Byerly CR Fever of War: the influenza epidemic in the U. S. Army during World War I New York New York University Press 2005

In the paper

“A priori, we stratified data by military and civilian populations (see Discussion), and by the quality of lung tissue culture results, considering to be of “higher quality” the 68 autopsy series with lung tissue culture results that reported, for all autopsies, both the presence and absence of negative culture results and the bacterial components of mixed culture results.”

In the paper

“If, as some fear, a future pandemic is caused by a derivative of the current highly pathogenic avian H5N1 virus, lessons from previous pandemics may not be strictly applicable.”

In the paper

“Because few autopsy reports and, to our knowledge, no autopsy series addressed conditions other than predominantly pulmonary complications, nonpulmonary causes of death are not considered here.”

In the paper

“These might include the use of antibiotics and antiviral agents, the rate of influenza vaccination and bacterial vaccination, and demographic and social factors.”

In the paper

“The viral etiology of and timing of the next influenza pandemic cannot be predicted [87].”

What the sources say

• ?Not checked — no full text of the sourcecites [87] Taubenberger JK Morens DM Fauci AS The next influenza pandemic: can it be predicted? JAMA 2007 297 2025 27 17488968 PMC2504708 source