"Maternal mortality rates peaked in 1918 with 916 per 100,000 births. That means one per 1,000 births. The multiplying factor is enormous. There is not, however, a lot of specific data about pregnancy during that time."

"There is a tremendous amount of wishful thinking that the virus won’t come here. In 1918 the shaping of the cognitive environment varied dramatically from location to location some places elected officials and public officials locked arms on some things. Some tentative evidence shows that social distancing interventions did help. However, Baltimore is a case example of how to do it wron g (e.g., not close the schools). In Baltimore there were fights between elected officials and public health officials. Another example of doing it wrong was Pittsburgh. In Pittsburgh, the Mayor actually told the public to ignore the public health officials."

"I can say that often death notices for doctors and nurses showed up in tiny print in the newspapers. In many places the rates were high; morbidity over 50%. Logic suggests that social distancing measures helped, but I am not convinced that those interventions had an effect that was anything more than random. One can’t really generalize, because morbidity and mortality rates varied so much from community to community."

"Los Angeles introduced interventions during the first few weeks of the epidemic, much earlier than New York, so they did not suffer the types of problems New York experienced. Baltimore newspapers published appeals to the public to minimize the use of telephones, but even at the height of the pandemic the phone system did not fail. Chicago attempted to estimate absenteeism. They estimated absenteeism averaged about 5% over a two-month period, not quite double thnormal average. Absenteeism peeked on October 22. However, the aggregate impact of absenteeism was significantly reduced. Economic impacts were modest, below 5%, when averaged out. A major recession did not ensue. Retail sales did decline in October, but they rebounded in November. New York City transit use, the Dow Jones, and business failures were indiscernible and modest when compared to the volatility of the period. Because of the short duration of the pandemic and human resiliency, it was characterized as a hit-and-run disease that only produced brief slowdowns."

"Cities were more isolated from each other. The pattern of the spread of the virus 1918 was related to troop movements. There has been a considerable amount of work on modeling from Department of Transportation (DOT) looking at connectivity of major urban centers to estimate how infectious diseases would spread now. In recent work looking at real world data, the geographic diffusion process is driven more by work-related travel."

"As bad as a bout of real seasonal influenza is, the H1 strain was far worse. It killed two percent or more of those stricken. In 1918, postmortem examinations helped understand if it was a case of flu. The performance of those autopsies was harrowing. Influenza defiled the lungs with bloody, frothy fluid. Instead of floating, the lungs plummeted to the bottom of water buckets during autopsies. The bronchials were fluid-filled, which explains the air hunger patients experienced. They frequently died from suffocation within 24–48 hours of developing symptoms. Some died later from secondary infections."

"Thomas Wolfe wrote a literary masterpiece about the death of his brother. More fabled is how influenza altered the decision-making abilities of President Woodrow Wilson and his chief aide, Colonel Edward House. Both were in Europe to attend the Paris Peace Conferences—the famed gathering where Wilson hoped to sell his Points and establish a League of Nations. Colonel House, who arrived in Europe just weeks before the Armistice, contracted a severe bout of flu as he was negotiating with the other nations. In late February, as he was recuperating from his serious illness, Colonel House noted that, “When I fell ill in January, I lost the thread of affairs and I am not sure that I have ever gotten fully back.” To make matters worse, when Wilson was in Paris in mid-March, to work with the Big Four in the final stages of a comprehensive peace treaty, he, too, was stricken by influenza. Volumes have been written on how influenza may have altered the terms and negotiations of the Treaty of Versailles as it ravaged the bodies and thoughts of Woodrow Wilson and Edward House, among others. While social historians of medicine warn against focusing too heavily on the illnesses of great men or the landmark cures of great doctors, the fact remains that when a world leader is struck down by influenza, in the midst of a pandemic that is accompanied by other global crises, the microbes’ power can be amplified above and beyond the symptoms it produces or the death it causes."

"In 1918, the childhood mortality rate for children under five-years-old was one in five. Every household knew of a child who died at a very young age, often of a contagious disease or dehydration issues. Back then, the care of the ill was almost exclusively at home. Today, death has been taken out of the household. Very few people have seen someone die today. In 1918, it was probably 90%. Death issues need to be talked about. For example, what should we do if public gatherings for funerals are cancelled? How will that affect people? There are social effects of quarantine, although now we have some resources to mitigate the effects. Public health departments (municipal, state, and federal) are all funded very differently. Post 9-11, bioterrorism preparedness efforts have been good for public health, because they are not mutually exclusive problems. Whether man-made or ecological, the strategies we need to use to address these problems are not that different."

"There are two great tragedies: The death of a child, or the death of a young child’s parent. Society saw a lot of both in 1918. There were many orphans in 1918. Several states put together orphan trains for adoption stops, which led to the establishment of the Child Welfare Department."

"The 1918 influenza pandemic offers the worst-case planning scenario for public health officials because it resulted in unparalleled numbers of deaths. The virus, an A(H1N1) subtype, may have infected half the world’s population and caused at least 50 million deaths, according to estimates; 675,000 deaths are thought to have occurred in the United States. The source of the 1918 H1N1 virus is unknown; avian and swine origins have been proposed. Although 3 later pandemics, in 1957, 1968, and 2009, resulted in much lower estimated rates of morbidity and death, the threat of a 1918-like severity pandemic remains, because reports of human infections with novel influenza A viruses (generally of avian or swine origin) that pose pandemic potential have increased in recent years. In particular, Asian lineage avian influenza A (H7N9) viruses caused 1,557 reported human infections and at least 605 deaths during 5 epidemics in China during 2013–2017. Now, 100 years after the 1918 pandemic, is an important time to recall the significant impact of the pandemic and to reflect on the current state of readiness to respond to the next influenza pandemic."

"In addition to differences in case fatality risk estimates due to the differences in case definition (denominator), the definition of the numerator is also an important issue. Almost all of the studies in our review based the numerator on deaths among patients with laboratory-confirmed influenza infection. In contrast, most estimates of the population impact of seasonal influenza epidemics have been based on estimation of the number of excess deaths associated with influenza (i.e. estimated deaths), with the greatest annual impact in the elderly — despite influenza virus infections rarely being confirmed in this age group. The use of excess deaths rather than laboratory-confirmed deaths in the numerator of the infection fatality risk would theoretically be justified because the denominator includes all infections and not only those with a positive laboratory result. For a similar reason, deaths of patients with laboratory-confirmed infection might be a more appropriate numerator for the case fatality risk based on symptomatic case denominators."

"In preparation for the next influenza pandemic, it is essential to reach a consensus on how to define and measure the seriousness of infection (an important indicator of the severity of the pandemic), and whether the analysis can be based entirely on estimates of age-specific risk of death among cases. The consistent estimates of the infection fatality risk at around 1 to 10 deaths per 100,000 infections identified in our review may represent the seriousness of H1N1pdm09 in developed countries where data were available. Similar estimates for seasonal influenza viruses, however, are not available for comparison, and neither are estimates from less developed countries in which the seriousness profile would likely be higher."

"In April 2009 the World Health Organization declared a formal “public health emergency of international concern,” marking the start of an international public health response to the first influenza pandemic of the 21st Century. One of the immediate priorities was to quantify the transmissibility of the new pandemic influenza A (H1N1pdm09) virus (denoted H1N1pdm09 hereafter) and the seriousness of infection with this virus, because these two epidemiologic measures in combination determine the severity of the pandemic in the absence of control measures. Whereas a number of transmissibility estimates, based on the reproduction number R, were published with broad agreement from the early stages of the pandemic, there was far greater difficulty in estimating the seriousness of infections. In the report of the World Health Organization’s Review Committee on the functioning of the 2005 International Health Regulations in relation to H1N1pdm09, Fineberg et al. identified “the absence of a consistent, measurable and understandable depiction of severity of the pandemic” as one of the major shortcomings of the international public health response."

"A unique epidemiological feature of the 1918 influenza virus, related to its origin, was infection of both humans and swine. Influenza was first recognized as a clinical entity in swine in the United States in autumn 1918, concurrent with the spread of the pandemic in humans, having apparently been transmitted from humans to pigs. This host switch split the virus off into two independent viral lineages, one human and the other porcine. After 1918, the epizootic disease became widespread among herds of swine in the U.S. midwest. Epizootic viruses appeared annually thereafter, leading to Shope’s 1930 isolation of the first influenza virus, A/swine/Iowa/30, 3 years before the first human isolation of a descendant of the parent 1918 virus, A/WS/33. The two 1918 viral H1N1 lineages, one human and the other porcine, evolved and antigenically drifted at different rates until 2009. In the 2009 pandemic, the human-adapted H1N1 descendant was replaced by a different H1N1 virus that was also a 1918 viral descendant, ironically one that had been circulating enzootically in pigs. The original 1918 classical swine lineage still circulates enzootically today."

"An instructive example of our inability to predict pandemic emergence, or to precisely characterize pandemic viral genetic evolutionary pathways, is that of the 2009 swine influenza pandemic caused by the H1N1pdm virus. This virus appeared in an era of unprecedented human and animal influenza viral surveillance and the near real-time deposition of thousands of influenza virus genome sequences into public databases. The first recognized human cases caused by the 2009 pandemic H1N1pdm virus occurred in Mexico. However, multiple co-circulating genotypes of related swine influenza A viruses, resulting from multiple complex reassortments of various swine influenza A virus lineages (including those similar to the 1918 pandemic H1N1 virus from which the ancestral 2009 swine virus lineage had been derived in 1918), were identified not only in swine populations in central Mexico but also in Asia. Clearly, most, if not all, of the major pre-emergence genetic events of 2009 had happened at some time, and in some unknown place, that escaped detection. Even if the future pandemic virus had been identified in swine populations in the months and years before 2009, it would likely not have been recognized as a virus with pandemic potential. This is because viral phenotypic properties associated with human adaptation and transmissibility cannot yet be predicted from genetic sequences. The implications are sobering: Identifying pre-pandemic viruses by increased viral surveillance in mammals and birds may be difficult or impossible. There is reason to believe that every influenza virus pandemic and panzootic/epizootic event (the animal counterparts to pandemics and epidemics in humans) may be fundamentally different from every other. Although these pandemic (or panzootic/epizootic) viruses-to-be already exist in nature, or evolve and adapt in humans or other mammals, there is a growing realization that each seems to achieve its host switch success through different cooperative polygenic adaptive mutations that, in unique combination, are able to support pandemic or panzootic spread."

"I would tell members of my family -- and I have -- I wouldn't go anywhere in confined places now....It's not (just) going to Mexico, it's you're in a confined aircraft when one person sneezes it goes all the way through the aircraft."

"To a patient whose lungs are temporarily compromised, short-term ventilator support is often the difference between life and death. Unfortunately, if a future pandemic leaves millions of Americans temporarily unable to breath -- vastly exceeding the number of mechanical ventilation machines or the trained staff needed to operate them -- our hospitals will be forced to decide which patients to help breathe and which to let die."

"I mean, by the fall of 2009, when Joe Biden was vice president the swine flu had infected 60 million Americans, and if it had had the same fatality rate as the coronavirus does, we would have lost more than two million American lives."

"There is very substantial heterogeneity in published estimates of case fatality risk for H1N1pdm09, ranging from <1 to >10,000 per 100,000 infections. Large differences were associated with the choice of case definition (denominator). Because influenza virus infections are typically mild and self-limiting, and a substantial proportion of infections are subclinical and do not require medical attention, it is challenging to enumerate all symptomatic cases or infections. In 2009, some of the earliest available information on fatality risk was provided by estimates based primarily on confirmed cases. However, because most H1N1pdm09 infections were not laboratory-confirmed, the estimates based on confirmed cases were up to 500 times higher than those based on symptomatic cases or infections. The consequent uncertainty about the case fatality risk — and hence about the severity of H1N1pdm09 — was problematic for risk assessment and risk communication during the period when many decisions about control and mitigation measures were being made."