Herald Wave Research Articles

Racial Disparities in Mortality During the 1918 Influenza Pandemic in United States Cities.

Against a backdrop of extreme racial health inequality, the 1918 influenza pandemic resulted in a striking reduction of non-White to White influenza and pneumonia mortality disparities in United States cities. We provide the most complete account to date of these reduced racial disparities, showing that they were unexpectedly uniform across cities. Linking data from multiple sources, we then examine potential explanations for this finding, including city-level sociodemographic factors such as segregation, implementation of nonpharmaceutical interventions, racial differences in exposure to the milder spring 1918 "herald wave," and racial differences in early-life influenza exposures, resulting in differential immunological vulnerability to the 1918 flu. While we find little evidence for the first three explanations, we offer suggestive evidence that racial variation in childhood exposure to the 1889-1892 influenza pandemic may have shrunk racial disparities in 1918. We also highlight the possibility that differential behavioral responses to the herald wave may have protected non-White urban populations. By providing a comprehensive description and examination of racial inequality in mortality during the 1918 pandemic, we offer a framework for understanding disparities in infectious disease mortality that considers interactions between the natural histories of particular microbial agents and the social histories of those they infect.

Spatial comparison of herald and main waves in London's nineteenth-century cholera epidemics.

Nineteenth-century London experienced four extraordinarily severe summertime cholera epidemics. Three were preceded by less severe non-summer outbreaks. Twenty-first-century research hypothesizes them as herald waves of potentially new cholera strains. This study examined the geographical characteristics of these herald waves and compared them to their subsequent main waves to determine if there was a geographical component to the significant difference in wave severity. Cholera mortality data for London's parishes and registration districts were extracted from contemporaneous records. The data were normalized and scaled. Each epidemic wave was divided into two segments for analysis. A Spearman's rank correlation was used to assess the relationship between a herald and its subsequent main wave. Geospatial analytical tools were used to determine and display each segment's geographic distribution pattern using autocorrelation techniques to determine its central point. Results show that the herald wave of each epidemic shared characteristics similar to its following main wave. Central-point locations were similar and Spearman's rank coefficients showed high degrees of correlation. Autocorrelation results were similar, with one exception reflecting an appalling anomalous cholera outbreak at an institution for children. Because of the demonstrated similarity of each epidemic's herald and main waves, this study did not detect a spatial characteristic that could explain the observed difference in severity between the studied heralds and mains.

Race and 1918 Influenza Pandemic in the United States: A Review of the Literature.

During epidemics, the poorest part of the population usually suffers the most. Alfred Crosby noted that the norm changed during the 1918 influenza pandemic in the US: The black population (which were expected to have higher influenza morbidity and mortality) had lower morbidity and mortality than the white population during the autumn of 1918. Crosby’s explanation for this was that black people were more exposed to a mild spring/summer wave of influenza earlier that same year. In this paper, we review the literature from the pandemic of 1918 to better understand the crossover in the role of race on mortality. The literature has used insurance, military, survey, and routine notification data. Results show that the black population had lower morbidity, and during September, October, and November, lower mortality but higher case fatality than the white population. The results also show that the black population had lower influenza morbidity prior to 1918. The reasons for lower morbidity among the black population both at baseline and during the herald and later waves in 1918 remain unclear. Results may imply that black people had a lower risk of developing the disease given exposure, but when they did get sick, they had a higher risk of dying.

Age-Specific Excess Mortality Patterns During the 1918-1920 Influenza Pandemic in Madrid, Spain.

Although much progress has been made to uncover age-specific mortality patterns of the 1918 influenza pandemic in populations around the world, more studies in different populations are needed to make sense of the heterogeneous death impact of this pandemic. We assessed the absolute and relative magnitudes of 3 pandemic waves in the city of Madrid, Spain, between 1918 and 1920, on the basis of age-specific all-cause and respiratory excess death rates. Excess death rates were estimated using a Serfling model with a parametric bootstrapping approach to calibrate baseline death levels with quantified uncertainty. Excess all-cause and pneumonia and influenza mortality rates were estimated for different pandemic waves and age groups. The youngest and oldest persons experienced the highest excess mortality rates, and young adults faced the highest standardized mortality risk. Waves differed in strength; the peak standardized mortality risk occurred during the herald wave in spring 1918, but the highest excess rates occurred during the fall and winter of 1918/1919. Little evidence was found to support a “W”-shaped, age-specific excess mortality curve. Acquired immunity may have tempered a protracted fall wave, but recrudescent waves following the initial 2 outbreaks heightened the total pandemic mortality impact.

A review of the 1918 herald pandemic wave: importance for contemporary pandemic response strategies

Mounting epidemiological evidence supports the occurrence of a mild herald pandemic wave in the spring and summer of 1918 in North America and Europe, several months before the devastating autumn outbreak that killed an estimated 2% of the global population. These epidemiological findings corroborate the anecdotal observations of contemporary clinicians who reported widespread influenza outbreaks in spring and summer 1918, with sporadic occurrence of unusually severe clinical manifestations in young adults. Initially seen as controversial, these findings were eventually confirmed by retrospective identification of influenza specimens collected from U.S. soldiers who died from acute respiratory infections in May–August 1918. Other studies found that having an episode of influenza illness during the spring herald wave was highly protective in the severe autumn wave. Here, we conduct a systematic review of the clinical, epidemiological, and virological evidence supporting the global occurrence of mild herald waves of the 1918 pandemic and place these historic observations in the context of pandemic preparedness. Taken together, historic experience with the 1918 and subsequent pandemics shows that increased severity in second and later pandemic waves may be the rule rather than the exception. Thus, a sustained pandemic response in the first years following a future pandemic is critical; conversely, multiwave pandemic patterns allow for more time to rollout vaccines and antivirals.

Cross protection between the first and second waves of the 1918 influenza pandemic among soldiers of the Canadian Expeditionary Force (CEF) in Ontario

ObjectivesThis research analyses morbidity and mortality during the 1918 influenza pandemic among Ontario soldiers in the Canadian Expeditionary Force (CEF). This paper asks: did exposure to influenza during the first wave confer protection against illness and death during the second wave of the pandemic? MethodsPneumonia and influenza (P&I) cases and deaths among Ontario soldiers were transcribed from the 1918 Admission and Discharge books for the CEF. Following the methods of Barry et al. [10], hospital admission and mortality rates for P&I were compared for new recruits (<1 month service) and seasoned soldiers (>1 month service) in order to assess the possibility of cross protection during successive waves of the pandemic. ResultsThe first wave of the 1918 influenza pandemic occurred between March and May of 1918, with the second wave erupting from September to December. Mortality in the second wave was more severe, with a case fatality rate of 4.7%, which was more than double the rate of 2.3% from March to May. Seasoned soldiers experienced 82.5% protection from illness due to P&I illness in the fall, and 84% protection from death. ConclusionsThe morbidity data for the soldier population of Ontario, data unavailable for civilians, confirms the presence of a herald wave in Ontario. The findings support the hypothesis that exposure to influenza during the first wave of the pandemic had a protective effect during the second more deadly wave in the fall. Regional heterogeneity characterized the pandemic among soldiers in Ontario. Conscription practices may have funnelled vulnerable recruits, such as rural farmers, into training camps after the first wave of the pandemic, but prior to the second wave.

The first wave of the 1918 influenza pandemic among soldiers of the Canadian expeditionary force.

This article evaluates the evidence for the presence of the first, mild wave of the 1918 influenza pandemic among soldiers in the Canadian Expeditionary Force (CEF). Death records for soldiers in the CEF who died in Canada in 1917 and 1918 were extracted from the Commonwealth War Graves Commission and record-linked to the Canada War Graves Registers, Circumstances of Casualty database. Monthly mortality rates from pneumonia and influenza (P&I) were compared with mortality rates from all other causes for 1917 and 1918, and by region for 1918. The herald wave of influenza was present among CEF soldiers in 1918. P&I mortality was significantly higher in March and April 1918 than during the same period in 1917. P&I mortality rates varied across the country and were significantly higher among soldiers who died in the Maritime region of Canada. In March, Maritime P&I mortality was significantly higher than its counterpart in the West; in April it was significantly higher than P&I mortality in both the Central and Western regions. The CEF findings suggest that local, geographic heterogeneity characterized the first wave of the 1918 influenza pandemic in Canada and illustrate the ways in which well-established, historical patterns of cross-border social contact with the United States, coupled with the special conditions created by warfare, disproportionately funnelled influenza into particular regions. Identification of the mild first wave among soldiers in the CEF calls for more research on the civilian experience of both waves of influenza in Canada.

Emergence of a new lineage of dengue virus type 2 identified in travelers entering Western Australia from Indonesia, 2010-2012.

Dengue virus (DENV) transmission is ubiquitous throughout the tropics. More than 70% of the current global dengue disease burden is borne by people who live in the Asia-Pacific region. We sequenced the E gene of DENV isolated from travellers entering Western Australia between 2010–2012, most of whom visited Indonesia, and identified a diverse array of DENV1-4, including multiple co-circulating viral lineages. Most viruses were closely related to lineages known to have circulated in Indonesia for some time, indicating that this geographic region serves as a major hub for dengue genetic diversity. Most notably, we identified a new lineage of DENV-2 (Cosmopolitan genotype) that emerged in Bali in 2011–2012. The spread of this lineage should clearly be monitored. Surveillance of symptomatic returned travellers provides important and timely information on circulating DENV serotypes and genotypes, and can reveal the herald wave of dengue and other emerging infectious diseases.

The influence of changing host immunity on 1918–19 pandemic dynamics

The sociological and biological factors which gave rise to the three pandemic waves of Spanish influenza in England during 1918–19 are still poorly understood. Symptom reporting data available for a limited set of locations in England indicates that reinfection in multiple waves occurred, suggesting a role for loss of infection-acquired immunity. Here we explore the role that changes in host immunity, driven by a combination of within-host factors and viral evolution, may play in explaining weekly mortality data and wave-by-wave symptomatic attack-rates available for a subset of English cities. Our results indicate that changes in the phenotype of the pandemic virus are likely required to explain the closely spaced waves of infection, but distinguishing between the detailed contributions of viral evolution and changing adaptive immune responses to transmission rates is difficult given the dearth of sero-epidemiological and virological data available even for more contemporary pandemics. We find that a dynamical model in which pre-pandemic protection in older “influenza-experienced” cohorts is lost rapidly prior to the second wave provides the best fit to the mortality and symptom reporting data. Best fitting parameter estimates for such a model indicate that post-infection protection lasted of order months, while other statistical analyses indicate that population-age was inversely correlated with overall mortality during the herald wave. Our results suggest that severe secondary waves of pandemic influenza may be triggered by viral escape from pre-pandemic immunity, and thus that understanding the role of heterosubtypic or cross-protective immune responses to pandemic influenza may be key to controlling the severity of future influenza pandemics.

A deterministic model for influenza infection with multiple strains and antigenic drift

We describe a multiple strain Susceptible Infected Recovered deterministic model for the spread of an influenza subtype within a population. The model incorporates appearance of new strains due to antigenic drift, and partial immunity to reinfection with related circulating strains. It also includes optional seasonal forcing of the transmission rate of the virus, which allows for comparison between temperate zones and the tropics. Our model is capable of reproducing observed qualitative patterns such as the overall annual outbreaks in the temperate region, a reduced magnitude and an increased frequency of outbreaks in the tropics, and the herald wave phenomenon. Our approach to modelling antigenic drift is novel and further modifications of this model may help improve the understanding of complex influenza dynamics.

The 1918–19 Influenza Pandemic in Boyacá, Colombia

To quantify age-specific excess-mortality rates and transmissibility patterns for the 1918-20 influenza pandemic in Boyacá, Colombia, we reviewed archival mortality records. We identified a severe pandemic wave during October 1918-January1919 associated with 40 excess deaths per 10,000 population. The age profile for excess deaths was W shaped; highest mortality rates were among infants (<5 y of age), followed by elderly persons (>60 y) and young adults (25-29 y). Mean reproduction number was estimated at 1.4-1.7, assuming 3- or 4-day generation intervals. Boyacá, unlike cities in Europe, the United States, or Mexico, experienced neither a herald pandemic wave of deaths early in 1918 nor a recrudescent wave in 1920. In agreement with reports from Mexico, our study found no death-sparing effect for elderly persons in Colombia. We found regional disparities in prior immunity and timing of introduction of the 1918 pandemic virus across populations.

Influenza activity in Saint Joseph, Missouri 1910-1923: Evidence for an early wave of the 1918 pandemic.

While the 1918/1919 H1N1 influenza pandemic is widely recognized as a “worst-case scenario” for the emergence of a new influenza strain, relatively little is known about the origin of the responsible virus and its pattern of spread. Most studies of this virus in the United States rely on temporally and spatially aggregated data. Location-specific studies of the impact of the 1918 pandemic strain in the United States have been confined primarily to large cities on the East Coast or West Coast. In this study, data on pneumonia and influenza fatalities from 1910-1923 have been extracted from death certificates for Saint Joseph, Missouri, a typical mid-sized city in the central United States. An increase in pneumonia and influenza mortality was noted starting in the 1915/1916 influenza season. Initially, increased mortality was observed in infants and the elderly. In February 1918, an age-shift typical of pandemic strains of virus was seen, as the burden of mortality shifted to young adults, a characteristic of the 1918 pandemic virus. These results provide one of the first confirmations of the existence of a “herald wave” of influenza activity in the United States prior to the recognized start of the H1N1 pandemic in Spring 1918. This study is one of very few that measures the impact of 1918/1919 influenza in a particular location in the central United States.

Herald waves of cholera in nineteenth century London.

Deaths from cholera in London, UK, were recorded weekly from 1824 to 1901. Three features of the time series stand out: (i) cholera deaths were strongly seasonal, with peak mortality almost always in the summer, (ii) the only non-summer outbreaks occurred in the spring of 1832, the autumn of 1848 and the winter of 1853, and (iii) extraordinarily severe summer outbreaks occurred in 1832, 1849, 1854 and 1866 (the four 'great' cholera years). The non-summer outbreaks of 1832, 1848 and 1853 appear to have been herald waves of newly invading cholera strains. In addition, a simple mathematical model confirms that a non-summer introduction of a new cholera strain can result in an initial herald wave, followed by a severe outbreak the following summer. Through the analysis of the genomes of nineteenth-century specimens, it may be possible to identify the strains that caused these herald waves and the well-known cholera epidemics that followed.

Mortality Patterns Associated with the 1918 Influenza Pandemic in Mexico: Evidence for a Spring Herald Wave and Lack of Preexisting Immunity in Older Populations

Although the mortality burden of the devastating 1918 influenza pandemic has been carefully quantified in the United States, Japan, and European countries, little is known about the pandemic experience elsewhere. Here, we compiled extensive archival records to quantify the pandemic mortality patterns in 2 Mexican cities, Mexico City and Toluca. We applied seasonal excess mortality models to age-specific respiratory mortality rates for 1915-1920 and quantified the reproduction number from daily data. We identified 3 pandemic waves in Mexico City in spring 1918, autumn 1918, and winter 1920, which were characterized by unusual excess mortality among people 25-44 years old. Toluca experienced 2-fold higher excess mortality rates than Mexico City but did not experience a substantial third wave. All age groups, including that of people 65 years old, experienced excess mortality during 1918-1920. Reproduction number estimates were <2.5, assuming a 3-d generation interval. Mexico experienced a herald pandemic wave with elevated young adult mortality in spring 1918, similar to the United States and Europe. In contrast to the United States and Europe, there was no mortality sparing among Mexican seniors 65 years old, highlighting potential geographical differences in preexisting immunity to the 1918 virus. We discuss the relevance of our findings to the 2009 pandemic mortality patterns.

Rapid clinical diagnosis of Legionnaires' disease during the “herald wave” of the swine influenza (H1N1) pandemic: The Legionnaires' disease triad

BackgroundIn adults hospitalized with atypical community-acquired pneumonia (CAP), Legionnaires' disease is not uncommon. Legionnaire's disease can be differentiated from typical CAPs and from other atypical CAPs based on its characteristic pattern of extrapulmonary organ involvement. The first clinically useful diagnostic weighted point score system for the clinical diagnosis of Legionnaires' disease was developed by the Infectious Disease Division at Winthrop-University Hospital in the 1980s. It has proven to be diagnostically accurate and useful for more than two decades, but was time-consuming. Because Legionella spp. diagnostic tests are time-dependent and problematic, a need was perceived for a rapid, simple way to render a clinical, syndromic diagnosis of Legionnaires' disease pending Legionella test results. During the “herald wave” of the swine influenza (H1N1) pandemic in the New York area, our hospital, like others, was inundated with patients who presented to the Emergency Department with influenza-like illnesses (ILIs) for H1N1 testing/evaluation. Most patients with ILIs did not have swine influenza. Hospitalized patients with ILIs who tested positive with rapid influenza diagnostic tests (RIDTs) were placed on influenza precautions and treated with oseltamivir. Unfortunately, approximately 30% of adult patients admitted with an ILI had negative RIDTs. Because the definitive laboratory diagnosis of H1N1 pneumonia by reverse transcription-polymerase chain reaction(RT-PCR), testing was restricted by health departments, resulted in clinical and infection control dilemmas in determining which RIDT-negative patients did, in fact, have H1N1 pneumonia.ObjectiveAccordingly, a diagnostic weighted point score system was developed for H1N1 pneumonia patients, based on RT-PCR positivity by the Infectious Disease Division at Winthrop-University Hospital. This diagnostic point score system for hospitalized adults with negative RIDTs was time-consuming. As the pandemic progressed, a simplified diagnostic swine influenza (H1N1) triad was developed for the rapid clinical diagnosis of probable H1N1 pneumonia, which also differentiated it from its mimics as well as from bacterial pneumonia, eg, Legionnaires' disease. During the “herald wave” of the H1N1 pandemic, we noticed an unexplained increase in Legionnaires' disease CAPs. Because clinical resources were stressed to the maximum during the pandemic, it was critically important to rapidly identify patients rapidly with Legionnaire's disease who did not require influenza precautions or oseltamivir, but who did require anti-Legionella antimicrobial therapy.MethodsBased on the Winthrop-University Hospital Infectious Disease Division's diagnostic weighted point score system for Legionnaires' disease (modified), key indicators were identified and became the basis for the diagnostic Legionnaires' disease triad. The diagnostic Legionnaires' disease triad was used to make a clinical diagnosis of Legionnaires' disease until the results of Legionella diagnostic tests were reported. The diagnostic Legionnaires' disease triad diagnosed Legionnaires' disease in hospitalized adults with CAPs with extrapulmonary findings (atypical CAP) and relative bradycardia, accompanied by any three (ie, a triad) of the following: otherwise unexplained relative lymphopenia, early/mildly elevated serum transaminases (SGOT/SGPT), highly increased ferritin levels (≥2 × n), or hypophosphatemia. The diagnostic Legionnaires' disease triad provides clinicians with a rapid way to clinically diagnose Legionnaires' disease, pending Legionella test results.ResultsThe accuracy of the diagnostic Legionnaires' disease triad was confirmed in our 9 cases of Legionnaires' disease by subsequent Legionella diagnostic testing.ConclusionsThe diagnostic Legionnaires' disease triad is particularly useful in situations where a rapid clinical syndromic diagnosis is needed, ie, during an H1N1 pandemic.

Legionnaires' disease mimicking swine influenza (H1N1) pneumonia during the “herald wave” of the pandemic

BackgroundNew York area hospitals were hit hard by the swine influenza (H1N1) pandemic in spring and summer 2009. During a pandemic, the initial cases may be difficult to recognize, but subsequent clinical diagnoses were relatively straightforward, given the high volume of cases and their typical clinical presentation. Swine influenza pneumonia presents as an influenza-like illness (ILI) with dry cough, fever >102°F and myalgias. A variety of other viral pneumonias, eg, cytomegalovirus, human parainfluenza virus 3 (HPIV 3), and adenovirus, as well as bacterial community-acquired pneumonias (CAPs) that may present with some of the clinical and laboratory features of H1N1 pneumonia. Most adults admitted to hospitals with ILIs during the pandemic had, in fact, definite or probable H1N1 pneumonia. The Infectious Disease Division at Winthrop-University Hospital developed a diagnostic weighted point score to identify probable H1N1 cases in hospitalized adults with rapid negative influenza diagnostic tests (RIDTs).MethodsWe present a case of an elderly male who presented with an ILI and negative RIDTs during the H1N1 pandemic. He was admitted with a diagnosis of possible H1N1, and placed on influenza precautions and oseltamivir. Although the patient had features consistent with H1N1 pneumonia, Legionnaires' disease was included in the differential diagnosis because of his elevated serum ferritin levels. A Legionella urinary antigen test was positive for Legionella pneumophila (serogroups 01-06).ResultsThe peak seasonal incidence of sporadic Legionnaires' disease occurs in the summer and fall. Even in the midst of a pandemic, clinicians should be on the alert for other infectious diseases that may mimic H1N1 pneumonia. In our experience, the best way to differentiate H1N1 from ILIs or other bacterial CAPs is through the Winthrop-University Hospital Infectious Disease Division's diagnostic weighted point score system for H1N1 pneumonia or its rapid simplified version, ie, the diagnostic swine influenza triad. Legionnaires' disease is the atypical CAP pathogen most likely to mimic H1N1 pneumonia.ConclusionsBased on this and other nine cases at our institution during the “herald wave” of pandemic, we conclude that Legionnaires' disease may mimic swine influenza (H1N1) pneumonia.

Nosocomial swine influenza (H1N1) pneumonia: lessons learned from an illustrative case

In the spring of 2009, our institution found itself at the epicentre of the "herald wave" of the swine influenza (H1N1) pandemic in New York. We were inundated with hundreds of patients exhibiting influenza-like illnesses (ILIs), presenting for rapid influenza A testing. During this pandemic, an infant with newly diagnosed acute lymphatic leukaemia (ALL) was admitted for induction chemotherapy. After being in hospital for a week, she developed high fever and shortness of breath, although her chest X-ray was clear. She was admitted to the paediatric intensive care unit (PICU) for mechanical ventilation. As we were in the midst of the pandemic, diagnosis of H1N1 pneumonia was considered and reverse transcription-polymerase chain reaction for H1N1 was positive. Contact investigation revealed that none of her family members/visitors had been in recent/close contact with anyone with ILI/H1N1. The investigation also revealed that paediatric healthcare staff, in contact with H1N1 patients, had rotated into PICU to care for the patient. Although no specific individual could be identified, it seems likely that H1N1 was transmitted to the patient by a healthcare worker who worked both in the paediatric ward and the PICU. This is the first known case of nosocomial paediatric transmission of H1N1 pneumonia.

Rapid clinical diagnosis in fatal swine influenza (H1N1) pneumonia in an adult with negative rapid influenza diagnostic tests (RIDTs): Diagnostic swine influenza triad

BackgroundThe “herald wave” of the H1N1 pandemic spread from Mexico to the United States in spring 2009. Initially, the epicenter of H1N1 in the United States was in the New York area. Our hospital, like others, was inundated with large numbers of patients who presented at the Emergency Department (ED) with influenza-like illnesses (ILIs) for swine influenza testing and evaluation.MethodsThe Winthrop-University Hospital ED used rapid influenza (QuickVue A/B) tests to screen for H1N1 infection. Patients who were rapid influenza A test-positive were also reverse transcription-polymerase chain reaction (RT-PCR) positive for H1N1. In our ED, 30% of patients with ILIs and possible H1N1 pneumonia had negative rapid influenza A screening tests. Because H1N1 RT-PCR testing was restricted, there was no laboratory test to confirm or rule out H1N1. Other rapid influenza diagnostic tests (RIDTs), e.g., the respiratory fluorescent antibody (FA) viral panel test, were used to identify H1N1 patients with negative RIDTs.ResultsUnfortunately, there was not a good correlation between RIDT results and RT-PCR results. There was a critical need to develop a clinical syndromic approach for diagnosing hospitalized adults with probable H1N1 pneumonia with negative RIDTs. Early in the pandemic, the Winthrop-University Hospital Infectious Disease Division developed a diagnostic weighted point score system to diagnose H1N1 pneumonia clinically in RIDT-negative adults. The point score system worked well, but was time-consuming. As the “herald wave” of the pandemic progressed, our ED staff needed a rapid, simplified method to diagnose probable H1N1 pneumonia in hospitalized adults with negative RIDTs. A rapid and simplified diagnosis was based on the diagnostic weighted point score system, which we simplified into a triad of key, nonspecific laboratory indicators. In adults hospitalized with an ILI, a fever >102°F with severe myalgias, and a chest x-ray without focal segmental/lobar infiltrates, the presence of three indicators, i.e., otherwise unexplained relative lymphopenia, elevated serum transaminases, and an elevated creatinine phosphokinase, constituted the diagnostic swine influenza triad. The Infectious Disease Division's diagnostic swine flu triad was used effectively as the pandemic progressed, and was not only useful in correctly diagnosing probable H1N1 pneumonia in hospitalized adults with negative RIDTs, but was also in ruling out mimics of swine influenza, e.g., exacerbations of chronic bronchitis, asthma, or congestive heart failure, as well as bacterial community-acquired pneumonias (CAPs), e.g., legionnaire's disease.ConclusionClinicians can use the Winthrop-University Hospital Infectious Disease Division's Diagnostic swine influenza triad to make a rapid clinical diagnosis of probable H1N1 pneumonia in hospitalized adult patients with negative RIDTs.

Qualitative analysis of the level of cross-protection between epidemic waves of the 1918–1919 influenza pandemic

The 1918–1919 influenza pandemic was composed of multiple waves within a period of nine months in several regions of the world. Increasing our understanding of the mechanisms responsible for this multi-wave profile has important public health implications. We model the transmission dynamics of two strains of influenza interacting via cross-immunity to simulate two temporal waves of influenza and explore the impact of the basic reproduction number, as a measure of transmissibility associated to each influenza strain, cross-immunity and the timing of the onset of the second influenza epidemic on the pandemic profile. We use time series of case notifications during the 1918 influenza pandemic in Geneva, Switzerland, for illustration. We calibrate our mathematical model to the initial wave of infection to estimate the basic reproduction number of the first wave and the corresponding timing of onset of the second influenza variant. We use this information to explore the impact of cross-immunity levels on the dynamics of the second wave of influenza. Our results for the 1918 pandemic in Geneva, Switzerland, indicate that a second wave can occur whenever R 0 1 < 1.5 or when cross-immunity levels are less than 0.58 for our estimated R 0 2 of 2.4. We also explore qualitatively profiles of two-wave pandemics and compare them with real temporal profiles of the 1918 influenza pandemic in other regions of the world including several Scandinavian cities, New York City, England and Wales, and Sydney, Australia. Pandemic profiles are classified into three broad categories namely “right-handed”, “left-handed”, and “M-shape”. Our results indicate that avoiding a second influenza epidemic is plausible given sufficient levels of cross-protection are attained via natural infection during an early (herald) wave of infection or vaccination campaigns prior to a second wave. Furthermore, interventions aimed at mitigating the first pandemic wave may be counterproductive by increasing the chances of a second wave of infection that could potentially be more virulent than the first.

Understanding Influenza Backward

Understanding Influenza Backward