Estimates of Deaths Associated with Seasonal Influenza — United States, 1976–2007

Influenza infections are associated with thousands of deaths every year in the United States, with the majority of deaths from seasonal influenza occurring among adults aged ≥65 years (1–4). For several decades, CDC has made annual estimates of influenza-associated deaths, which have been used in influenza research and to develop influenza control and prevention policy. To update previously published estimates of the numbers and rates of influenza-associated deaths during 1976–2003 by adding four influenza seasons through 2006–07, CDC used statistical models with data from death certificate reports. National mortality data for two categories of underlying cause of death codes, pneumonia and influenza causes and respiratory and circulatory causes, were used in regression models to estimate lower and upper bounds for the number of influenza-associated deaths. Estimates by seasonal influenza virus type and subtype were examined to determine any association between virus type and subtype and the number of deaths in a season. This report summarizes the results of these analyses, which found that, during 1976–2007, estimates of annual influenza-associated deaths from respiratory and circulatory causes (including pneumonia and influenza causes) ranged from 3,349 in 1986–87 to 48,614 in 2003–04. The annual rate of influenza-associated death in the United States overall during this period ranged from 1.4 to 16.7 deaths per 100,000 persons. The findings also indicated the wide variation in the estimated number of deaths from season to season was closely related to the particular influenza virus types and subtypes in circulation.

The current study extends estimates of influenza-associated deaths from two previous CDC studies (2,3) by adding data from four more influenza seasons for a total of 31 influenza seasons (1976–2007). Estimates are provided for three age groups (<19 years, 19--64 years, and ≥65 years) and for two categories of underlying cause of death codes: 1) pneumonia and influenza causes and 2) respiratory and circulatory causes. Deaths from pneumonia and influenza causes are highly correlated with the circulation of influenza (1) and can be considered a lower bound for deaths associated with influenza (2,4). However, a diagnosis of influenza virus infection often is not confirmed with sensitive and specific laboratory diagnostics, particularly among older persons, and even when identified is rarely recorded on death certificates (5). Many deaths associated with influenza infections occur from secondary infections such as bacterial pneumonia or complications of chronic conditions such as congestive heart failure and chronic obstructive pulmonary disease (6). Therefore, estimates using underlying respiratory and circulatory mortality data (which include pneumonia and influenza causes) can provide an upper bound for influenza-associated deaths (2,7).

Using methods published previously (2,3), CDC estimated the numbers and rates of influenza-associated deaths by virus type and subtype by using Poisson regression models that incorporated weekly national respiratory viral surveillance data. Weekly influenza test results by virus type and subtype were provided by approximately 80 World Health Organization (WHO) and 70 National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States (8). Prominent influenza type and subtype were defined as at least 20% of all isolates that were tested in that season. Mortality data were obtained from the National Vital Statistics System and reflect the underlying cause of death recorded on death certificates (9). Deaths were categorized using the International Classification of Diseases eighth revision (ICD-8), ninth revision (ICD-9), or 10th revision (ICD-10), as appropriate. Weekly estimates of the U.S. population by age group were used as part of the model to correspond to the weekly viral surveillance estimates. All data for deaths with underlying pneumonia and influenza causes and respiratory and circulatory causes were actual counts based on the death certificate ICD codes. To estimate the proportion of deaths that were influenza associated, the average annual number of deaths estimated by the model was divided by the average annual counts of death with underlying pneumonia and influenza causes and respiratory and circulatory causes.

For deaths with underlying pneumonia and influenza causes during 1976–2007 in the United States, the models estimated an annual overall average of 6,309 (range: 961 in 1986–87 to 14,715 in 2003–04) influenza-associated deaths (Table 1). For these underlying causes, the average annual rate of influenza-associated death was 2.4 deaths per 100,000 (range: 0.4–5.1).

Among persons aged <19 years, an estimated annual average of 97 (range: 41 in 1981--82 to 234 in 1977--78) influenza-associated deaths with underlying pneumonia and influenza causes occurred (Table 1). The average annual rate of influenza-associated deaths for this age group was 0.1 deaths per 100,000 persons (range: 0.1–0.3). Among adults aged 19–64 years, an estimated annual average of 666 (range: 173 in 1981–82 to 1,459 in 2004–05) influenza-associated deaths with underlying pneumonia and influenza causes occurred. The average annual rate of influenza-associated deaths for this age group was 0.4 deaths per 100,000 persons (range: 0.1–0.8). Among adults aged ≥65 years, an estimated annual average of 5,546 (range: 673 in 1978–79 to 13,245 in 2003–04) influenza-associated deaths with underlying pneumonia and influenza causes occurred. The average annual rate of influenza-associated deaths for this age group was 17.0 deaths per 100,000 (range: 2.4–36.7). Deaths among persons aged ≥65 years accounted for 87.9% of the overall estimated average annual influenza-associated deaths with underlying pneumonia and influenza causes.

For deaths with underlying respiratory and circulatory causes (including pneumonia and influenza causes) during 1976–2007, the models estimated an annual U.S. average overall of 23,607 (range: 3,349 in 1986–87 to 48,614 in 2003–04) influenza-associated deaths (Table 2). For these underlying causes, the average annual rate of influenza-associated death was 9.0 deaths per 100,000 (range: 1.4–16.7).

Among persons aged <19 years, an estimated annual average of 124 (range: 57 in 1981--82 to 197 in 1977--78) influenza-associated deaths with underlying respiratory and circulatory causes occurred (Table 2). The average annual rate of influenza-associated deaths for this age group was 0.2 deaths per 100,000 persons (range: 0.1–0.3). Among adults aged 19–64 years, an estimated annual average of 2,385 (range: 504 in 1981–82 to 4,752 in 2003–04) influenza-associated deaths with underlying respiratory and circulatory causes occurred. The average annual rate of influenza-associated deaths for this age group was 1.5 deaths per 100,000 persons (range: 0.4–3.1). Among adults aged ≥65 years, an estimated annual average of 21,098 (range: 2,344 in 1986–87 to 43,727 in 2003–04) influenza-associated deaths with underlying respiratory and circulatory causes occurred. The average annual rate of influenza-associated deaths for this age group was 66.1 deaths per 100,000 (range: 8.0–121.1). Deaths among persons aged ≥65 years accounted for 89.4% of the overall estimated average annual influenza-associated deaths with underlying respiratory and circulatory causes.

For both causes, the average mortality rates for the 22 seasons during which influenza A(H3N2) was a prominent strain were 2.7 times higher than for the nine seasons that it was not. The average annual number of influenza-associated deaths during influenza A(H3N2) prominent seasons was 7,722 for pneumonia and influenza causes and 28,909 for respiratory and circulatory causes, compared with 2,856 deaths for pneumonia and influenza causes and 10,648 deaths for respiratory and circulatory causes in seasons in which it was not.

The distribution of mortality across age groups was similar for the two groups of coded deaths. For pneumonia and influenza causes, the proportions of average deaths overall were 1.5%, 10.6%, and 87.9% for persons aged <19 years, 19--64 years, and ≥65 years, respectively. For respiratory and circulatory causes, the proportions were 0.5%, 10.1%, and 89.4%.

Based on an average annual count of 74,363 for all pneumonia and influenza deaths, and an average annual estimate of 6,309 deaths associated with influenza in this category, 8.5% of all pneumonia and influenza deaths were influenza associated. Based on an annual average count of 1,132,319 for all respiratory and circulatory deaths and an average annual estimate of 23,607 deaths associated with influenza in this category, 2.1% of all respiratory and circulatory deaths were influenza associated.

Reported by

MG Thompson, PhD, DK Shay, MD, H Zhou, MSc, MPH, CB Bridges, MD, PY Cheng, PhD, E Burns, MA, JS Bresee, MD, NJ Cox, PhD, Influenza Div, National Center for Immunization and Respiratory Diseases, CDC.

Editorial Note

This report updates estimates of the number of influenza-associated deaths from the 1976–77 through 2006–07 influenza seasons and demonstrates the substantial variability in mortality estimates by year, influenza virus type/subtype, and age group. The estimated rates of influenza-associated hospitalizations and deaths vary substantially from one influenza season to the next, depending, in part, on the characteristics of the circulating influenza virus strains (10). Because of this variability, a single estimate cannot be used to summarize influenza-associated deaths. This report provides estimates for two categories of underlying cause of death codes, pneumonia and influenza causes and respiratory and circulatory causes; if only one category is used to summarize the mortality effects of influenza, the respiratory and circulatory data likely provide the most accurate estimates. During the past three decades, the estimated number of annual influenza-associated deaths from respiratory and circulatory causes ranged from a low of 3,349 to a high of 48,614 deaths.

A previous study (2) presented an average annual estimate of 25,420 influenza-associated respiratory and circulatory deaths during a 23-season period; this study estimated an average of 23,607 annual influenza-associated deaths using the same model but over a 31-year period. The findings in this report are similar to those of previous CDC studies (2,3) and other cross-decade studies that used similar models (4,7).

When describing the severity of seasonal influenza epidemics, examining seasons with the same circulating influenza virus type is useful. For example, during seasons with prominent circulation of influenza A(H3N2) viruses, 2.7 times more deaths occurred than during seasons when A(H3N2) viruses were not prominent. An annual estimate of 36,155 influenza-associated respiratory and circulatory deaths often is quoted from an earlier CDC study (2); however, that average was calculated for the period 1990–1999, when more severe influenza A(H3N2) viruses were prominent for eight of the nine seasons.

Variations in influenza-associated mortality by age group also should be noted. As reported in this and other studies (2,3), approximately 90% of influenza-associated deaths occur among adults aged ≥65 years. An estimated annual average of 124 persons aged <19 years and 2,385 aged 19--64 years die from influenza-associated respiratory or circulatory causes. Future research that considers years-of-life-lost is needed to better communicate the mortality burden of influenza in these younger populations. Future research also is needed to estimate and communicate the risk for influenza-associated mortality among different demographic and health risk groups.

The findings in this report are subject to at least four limitations. First, the models do not account for cocirculating pathogens such as respiratory syncytial virus (RSV). Future research should replicate and extend models that distinguish between deaths associated with influenza versus RSV (2). Second, estimates over time might not be comparable because the influenza virus surveillance data used to model mortality rely on national influenza testing practices, which have changed over the past decade (8). Future research should consider how trends in testing practices can be included in these models and cross-season estimates of influenza-associated mortality. Third, increases in the U.S. population aged ≥65 years during the study period could have contributed to a general increase in influenza-associated mortality. Age-adjusting future estimates or estimating deaths in smaller age categories among older adults could address this issue. Finally, because the estimates made in this report rely on national death certificate data and these data currently are available only through 2007, preliminary estimates of 2009 influenza A(H1N1)-associated deaths are not directly comparable with these results.*

Debate will continue regarding the most appropriate statistical models and cause of death categories to use in estimating the number of influenza-associated deaths (1,7). This study’s provision of estimates for more narrow (pneumonia and influenza causes) and more broad (respiratory and circulatory causes) categories continues the strategy of comparing and contrasting results from different models as advocated by CDC (1–3) and others (7).

Influenza infections are associated with substantial medical costs, hospitalizations, lost productivity, and thousands of deaths every year in the United States. Annual influenza vaccination is the best way to reduce the risk for complications from influenza infections and is now recommended for all persons aged ≥6 months in the United States. Prompt treatment with influenza antiviral medications can reduce the risk for severe illness and death among persons at increased risk for influenza or who are hospitalized with suspected or confirmed influenza.

References

1. Thompson WW, Moore MR, Weintraub E, et al. Estimating influenza-associated deaths in the United States. Am J Pub Health 2009;99:S225–30.


2. Thompson WW, Shay DK, Weintraub E, et al. Mortality associated with influenza and respiratory syncytial virus in the United States. JAMA 2003;289:179–86.


3. Thompson WW, Weintraub E, Dhankhar P, et al. Estimates of US influenza-associated deaths made using four different methods. Influenza Other Respi Viruses 2009;3:37–49.


4. Simonsen L, Reichert TA, Viboud C, Blackwelder WC, Taylor RJ, Miller MA. Impact of influenza vaccination on seasonal mortality in the US elderly population. Arch Intern Med 2005;165:265–72.


5. Wiselka M. Influenza: diagnosis, management, and prophylaxis. BMJ 1994;308:1341–5.


6. Schanzer DL, Langley JM, Tam TW. Co-morbidities associated with influenza-attributed mortality, 1994–2000, Canada. Vaccine 2008;26:4697–703.


7. Newall AT, Viboud C, Wood JG. Influenza-attributable mortality in Australians aged more than 50 years: a comparison of different modelling approaches. Epidemiol Infect 2010;138:836–42.


8. Brammer L, Budd A, Cox N. Seasonal and pandemic influenza surveillance considerations for constructing multicomponent systems. Influenza Other Respi Viruses 2009:3,51–8.


9. CDC. Mortality data, multiple cause detail, 1972–2007. Public use data tapes contents and documentation package. Hyattsville, MD: US Department of Health and Human Services, CDC, National Center for Health Statistics; 2007.


10. Russell CA, Jones TC, Barr IG, et al. Influenza vaccine strain selection and recent studies on the global migration of seasonal influenza viruses. Vaccine 2008;26(Suppl 4):D31–4.

Pandemic (H1N1) 2009

출처 : The Medical Journal of Australia, 30 November 2009
http://www.mja.com.au/public/issues/192_02_180110/cha10960_fm.html

eMJA Rapid Online Publication – 30 November 2009

In early April 2009, a novel influenza A virus was identified in Mexico and Southern California.1 The subsequent rapid international spread and sustained community transmission in the Americas, Europe, New Zealand and Australia resulted in the World Health Organization escalating the pandemic influenza response to Phase 6 on 11 June 2009.2

The Australian Health Management Plan for Pandemic Influenza, which includes the ALERT, DELAY, CONTAIN, SUSTAIN, CONTROL and RECOVER phases of response,3 was predicated on pandemic influenza causing high morbidity and mortality. However, pandemic (H1N1) 2009 influenza appeared to be causing milder disease. Cases of severe disease and deaths have been reported,4 in particular, pregnant women could have severe disease.5,6 A modified strategy, the “PROTECT” phase, was thus enacted on 17 June 2009.7 It focused on identifying and treating infection in people with moderate to severe disease and those with certain risk factors (pregnancy and underlying chronic diseases), controlling outbreaks in institutions, and monitoring hospitalisation.8

The PROTECT phase coincided with the start of the influenza season in Sydney, and the surge in hospital admissions of patients with pandemic (H1N1) 2009 influenza coincided with the expected surge in seasonal influenza. This situation allowed us to compare patient characteristics, clinical features and outcomes of infection with pandemic (H1N1) 2009 influenza and seasonal influenza. Part of this work was presented at the 14th Congress of the Asian Pacific Society of Respirology in Seoul, Korea, 14–18 November 2009 (Poster no. APSR 2009-594).

Methods

We reviewed the medical records of all adult patients (aged 18 years and over) with a laboratory-confirmed diagnosis of influenza who were admitted to Liverpool Hospital, Sydney, from 17 June (the beginning of the PROTECT Phase) to 31 July 2009.

During this period, nose and/or throat swabs were collected from all patients admitted with an influenza-like illness. Following total nucleic acid extraction using the MagNA Pure System (Roche Diagnostics Australia, Sydney, NSW) influenza was confirmed by polymerase chain reaction using the Influenza 4 Easy-Plex assay kit (AusDiagnostics, Sydney, NSW). Subsequent typing was performed on all influenza A-positive isolates on the stored extract (− 80°C) using the Influenza 6 Easy-Plex assay kit (AusDiagnostics, Sydney, NSW).

Demographic and clinical details were extracted from the clinical notes and electronic information system. These details included age, sex, place of residence, and presence of comorbid conditions or risk factors for possible severe illness (eg, obesity, diabetes, pregnancy and immunosuppression). The date of onset of presenting influenza-like illness symptoms (coryza, fever, cough, breathlessness, chest pain, sore throat, lethargy, myalgia, vomiting, diarrhoea and abdominal pain), clinical signs and laboratory results (including haematological, biochemical, serological, microbiological and arterial blood gas results with patients breathing room air) were also extracted. The clinical course, management directed by the attending physicians, and outcomes at discharge were similarly recorded.

Chest x-rays were reviewed and classified according to the type, pattern and extent of any abnormalities. The principal respiratory diagnosis was made after review of the complete record, with pneumonia defined as the presence of consistent radiological abnormalities and clinical signs.

Health-care-associated influenza was defined as onset of symptoms more than 4 days after admission, to correspond with the upper limit of influenza virus incubation.9

Statistical analysis

Continuous and categorical data were analysed with Microsoft Office Excel 2007 (Microsoft Corporation, Redmond, Wash, USA) and SPSS student version 16.0 (SPSS Inc, Chicago, Ill, USA) using two-sample t tests, Fisher’s Exact test, or adjusted or unadjusted χ2 tests, as appropriate.

The study was approved by the Sydney South West Area Health Service, Human Research Ethics Committee (Project No. QA2009/047).

Results

Sixty-five patients were admitted to Liverpool Hospital with a laboratory-confirmed diagnosis of influenza between 17 June and 31 July 2009. One of these patients had been admitted for ischaemic gut, and was excluded from the analysis because the patient did not have a concurrent influenza-like illness. Of the remaining 64 patients, 48 tested positive for pandemic (H1N1) 2009 influenza and the remaining 16 tested positive for seasonal influenza A (11 for subtype H3 and five for untypeable non-pandemic [H1N1] 2009 influenza). The epidemic curve showed that the peak of the outbreak occurred around 8 July (Box 1). Five of the 64 cases of influenza (all pandemic [H1N1] 2009) were health-care associated.

Box 2 shows demographic characteristics and presenting features and outcomes for patients admitted with pandemic (H1N1) 2009 and seasonal influenza. Patients with pandemic (H1N1) 2009 influenza were significantly younger than those presenting with seasonal influenza (mean age, 45 years v 64 years; P < 0.01). Patients with seasonal influenza were more commonly immunosuppressed than patients with pandemic (H1N1) 2009 (P < 0.05). Although a relationship with pregnancy (patients in their postpartum period or pregnant) was more common in the pandemic (H1N1) 2009 group (eight patients v one patient with seasonal influenza), this difference did not reach statistical significance (Box 2).

Thirteen patients were admitted to the intensive care unit (ICU) — three with seasonal and 10 with pandemic (H1N1) 2009 influenza. The clinical course and hospitalisation of these patients is illustrated in Box 3. Of the three patients remaining in ICU, two died (patient 13 and patient 6 in Box 3 on 8 August and 12 August, respectively), with the remaining patient discharged alive from hospital on 23 September 2009.

Box 2 shows that the mean duration of symptoms before presentation was 4 days, with fever, cough and dyspnoea being the most common symptoms in both groups. Similarly, there was no difference in the clinical signs between the two groups, with a diagnosis of pneumonia occurring in similar proportions of patients with seasonal and pandemic (H1N1) 2009 influenza.

Laboratory results showed no difference between the two groups in mean total white blood cell count, nadir lymphocyte count, C-reactive protein concentration, and mean partial pressure of arterial oxygen (patients breathing room air) at presentation. Forty-six patients had blood cultures and 12 had sputum cultures performed. Three patients had bacterial co-infections with Streptococcus pneumoniae and Haemophilus influenzae confirmed by blood culture, and methicillin-sensitive Staphylococcus aureus was isolated from one sputum culture.

Chest x-rays were taken of 59 of the 64 patients, and abnormalities were detected in 31 patients. Abnormal radiological features ranged from localised infiltrates to bilateral airspace consolidation (Box 4). Four patients had radiological abnormalities attributable to chronic lung conditions without evidence of concurrent pneumonia.

Fifty-three hospitalised patients were treated with a neuraminidase inhibitor and antibiotics. Corticosteroids were significantly more likely to be prescribed in the seasonal influenza group compared with the pandemic (H1N1) 2009 group (P < 0.05; Box 2). However, all corticosteroid use was deemed to be for treatment of an underlying respiratory illness rather than influenza. Treatment response did not differ significantly between the two groups, and the overall mean time to defervescence was 2.6 days (range, 0–10 days) and mean number of days in hospital was 8 days (range, 0–61 days). Overall, there were five deaths (four in the pandemic (H1N1) 2009 group and one in the seasonal influenza group). Two deaths occurred in the ICU (see above).

Discussion

A major strength of our study was that the epidemics of seasonal and pandemic (H1N1) 2009 influenza occurred concurrently, which allowed us to make a direct comparison. Our data show that there was no difference between the two groups except that patients admitted with pandemic (H1N1) 2009 influenza tended to be younger and less immunocompromised. The clinical, radiological and laboratory features at presentation were similar in both patient groups, as were the clinical course, management and outcomes. Our findings show that, for hospitalised patients, the clinical manifestations and severity of pandemic (H1N1) 2009 and seasonal influenza were similar. This suggests that the number of admissions to our hospital and ICU reflected the higher burden of disease in the community rather than a greater virulence of the novel pandemic influenza virus.

Significant morbidity and mortality from influenza in pregnant women during previous pandemics has been reported.10,11 For seasonal influenza, the highest morbidity for pregnant women occurred in the third trimester.12 There have been several reports that pregnant women are at increased risk of severe complications from pandemic (H1N1) 2009 influenza.5,6 However, we were unable to demonstrate a difference in clinical severity between the seasonal and the pandemic viruses. The reliability of our estimate is limited by the small sample size, and a definitive answer to this question requires a multicentre study.

The clinical and epidemiological characteristics of 18 people hospitalised with pneumonia caused by pandemic (H1N1) 2009 influenza in Mexico City have been reported.13 The age, presence of comorbid conditions, presenting symptoms, laboratory findings and clinical features were similar to those in our group. However, in the Mexican series the higher proportion of abnormalities on chest x-ray (all patients), the number of patients with severe disease requiring invasive ventilation (12), and the mortality rate (39%) differ from our series (mortality rate, 8%). This could reflect differing admission criteria and smaller numbers.

In conclusion, our study shows that the clinical disease caused by the novel pandemic (H1N1) 2009 influenza virus in humans is comparable to that caused by the current circulating seasonal influenza strains in Sydney. The number of patients with severe disease reflects the disease burden in the community resulting from the pandemic. Pregnant women are at risk of severe infection from influenza, but whether pandemic (H1N1) 2009 influenza is particularly virulent in pregnant women and those in their postpartum period requires further study. It remains unclear whether antiviral drugs alter the clinical course of severe influenza infection.

1 Admissions to Liverpool Hospital of 64 adults with confirmed seasonal and pandemic (H1N1) 2009 influenza during the “PROTECT” phase of the epidemic*

* The peak of both epidemics occurred around 8 July 2009.

2 Demographic, clinical and laboratory features of the 64 patients admitted to Liverpool hospital with seasonal and pandemic (H1N1) 2009 influenza, 17 June to 31 July 2009

Patient features	Seasonal influenza	H1N1 2009 influenza
No. of patients	16	48
Mean age (years)	64	45*
No. female	13	30
Comorbid conditions
None	6	21
Chronic obstructive pulmonary disease	4	9
Obesity	2	9
Diabetes	1	15
Immunocompromised	7	8*
Pregnancy related	1†	8‡
Community acquired	16	43
Health-care associated	0	5
Symptoms
Fever	15	46
Cough	15	34
Dyspnoea	8	33
Lethargy	7	21
Myalgia	4	10
Sore throat	2	11
Vomiting and/or diarrhoea	5	23
Mean days from symptom onset to presentation (range)	4 (0–10)	4 (0–15)
Observations at presentation
Febrile (temperature > 37.5°C)	10	38
Tachycardia (> 100 beats per min)	8	29
Hypotensive (blood pressure < 90 mmHg systolic or < 60 mmHg diastolic)	5	7
Tachypnoea (> 16 breaths per min)	15	44
Hypoxia (peripheral blood oxygen saturation < 95%)	9	29
Laboratory results
Mean white blood cell count (cells × 109/L[range])	8.86 (0.1–20.7)	8.87 (1.1–27.6)
Nadir lymphocyte count (cells × 109/L[range])	0.68 (0–1.5)	0.66 (0.1–1.9)
Mean C-reactive protein concentration (mg/L[range])	134 (9–580)	104 (6–630)
Mean Pao2 with patient breathing room air (mmHg [kPa])	61 (8.1)	72 (9.6)
Chest x-ray findings
Normal	9	19
Abnormal	6	25
No chest x-ray	1	4
Diagnosis of pneumonia	6	21
Pneumonia severity index (range)	135 (100–158)	92 (30–160)
Non-pneumonic diagnosis	10	27
Treatment
Oseltamivir or zanamivir	13	40
Antibiotics	15	43
Corticosteroids	10	13
Intensive care unit admission	3	10
Non-invasive or invasive ventilation	2	10
Extracorporeal membrane oxygenation	0	2
Mean days to defervescence (range)	2.6 (0–10)	3.2 (0–14)
Mean days in hospital (range)	7 (1–18)	8 (0–61)
Overall deaths	1	4§
Pao2 = partial pressure of oxygen in arterial blood. * P < 0.05. † Patient in the second trimester of pregnancy. ‡ Of the eight patients, three were in the postpartum period, with two in the first, two in the second and one in the third trimester of pregnancy. § Of the five deaths, three occurred during the study period; the remaining two occurred on 8 and 12 August 2009.

3 Clinical courses of 13 patients admitted to Liverpool Intensive Care Unit (ICU) with pandemic (H1N1) 2009 influenza and seasonal influenza, 17 June to 31 July 2009*

* As of 31 July 2009, three patients remained in the ICU, with two of these being treated with extracorporeal membrane oxygenation.

4 Chest x-rays showing typical abnormalities found in patients hospitalised with influenza, 17 June to 31 July 2009

Patient with pandemic (H1N1) 2009 influenza showing airspace opacity in the left upper and left lower lobes and medial right upper zone.

Patient with pandemic (H1N1) 2009 influenza showing bilateral interstitial and airspace opacity.

Patient with seasonal influenza showing bilateral airspace opacity.

Acknowledgements

We thank the medical and nursing staff of Liverpool Hospital, who assisted with the clinical care of patients affected by influenza, and the scientific staff of Sydney South West Pathology Service — Liverpool, who performed the diagnostic testing on the patients. We also thank Professor Guy Marks for his comments on our manuscript.

Competing interests

None identified.

Author detailsYa-Shu Chang, MB ChB, Respiratory Registrar1Sebastiaan J van Hal, MB ChB, FRACP, FRCPA, Infectious Diseases Physician2Peter M Spencer, MB BS, Respiratory Registrar1Iain B Gosbell, MD, FRACP, FRCPA, Foundation Professor of Microbiology and Infectious Diseases,3 and Infectious Diseases Physician2Peter W Collett, MB BS, PhD, FRACP, Respiratory Physician1

1 Department of Respiratory Medicine, Liverpool Hospital, Sydney, NSW.

2 Department of Microbiology and Infectious Diseases, Sydney South West Pathology Service, Sydney, NSW.

3 Microbiology and Infectious Diseases Unit, School of Medicine, University of Western Sydney, Sydney, NSW.

Correspondence: i.gosbellATuws.edu.au

References

1. Ginsberg M, Hopkins J, Maroufi A, et al. Swine influenza A (H1N1) infection in two children — southern California, March–April 2009. MMWR Morb Mortal Wkly Rep 2009; 58: 400-402.
   
2. World Health Organization. Pandemic (H1N1) 2009. http://www.who.int/csr/disease/swineflu/en/index.html (accessed 6 Aug 2009).
   
3. Australian Government Department of Health and Ageing. Australian health management plan for pandemic influenza. 2008. http://www.flupandemic.gov.au/internet/panflu/publishing.nsf/Content/ahmppi-1 (accessed 6 Aug 2009).
   
4. Kaufman MA, Duke GJ, McGain F, et al. Life-threatening respiratory failure from H1N1 influenza 09 (human swine influenza). Med J Aust 2009; 191: 154-156.
   
5. Fonseca V, Davis M, Wing R, et al. Novel influenza A (H1N1) virus infections in three pregnant women — United States, April–May 2009. MMWR Morb Mortal Wkly Rep 2009; 58: 497-500.
   
6. Jamieson DJ, Honein MA, Rasmussen SA, et al. H1N1 2009 influenza virus infection during pregnancy in the USA. Lancet 2009; 374: 451-458.
   
7. Australian Government Department of Health and Ageing. H1N1 Influenza 09 latest news. New pandemic phase PROTECT. 17 June 2009. http://www.health.gov.au/internet/healthemergency/publishing.nsf/Content/news-170609 (accessed Nov 2009).
   
8. New South Wales Department of Health. Emergency. Pandemic influenza A (H1N1) 2009. Questions and answers. Common questions and answers regarding H1N1 Influenza 09. http://www.emergency.health.nsw.gov.au/swineflu/consumers/qa.asp (accessed 6 Aug 2009).
   
9. Centers for Disease Control and Prevention. Influenza. In: Heymann DL, editor. Control of communicable diseases manual. Washington, DC: American Public Health Association, 2008: 315-331.
   
10. Harris JW. Influenza occurring in pregnant women. JAMA 1919; 72: 978-980.
    
11. Freeman DW, Barno A. Deaths from Asian influenza associated with pregnancy. Am J Obstet Gynecol 1959; 78: 1172-1175.
    
12. Neuzil KM, Reed GW, Mitchel EF, et al. Impact of influenza on acute cardiopulmonary hospitalizations in pregnant women. Am J Epidemiol 1998; 148: 1094-1102.
    
13. Perez-Padilla R, de la Rosa-Zamboni D, Ponce de Leon S, et al. Pneumonia and respiratory failure from swine-origin influenza A (H1N1) in Mexico. N Engl J Med 2009; 361: 680-689. Epub 2009 Jun 29.

(Received 13 Aug 2009, accepted 9 Nov 2009)
=============================

Swine flu `is no worse than seasonal strains’

source : http://www.theaustralian.com.au/news/health-science/swine-flu-is-no-worse-than-seasonal-strains/story-e6frg8y6-1225805509987?from=public_rss

THE dominant expert view that swine flu is much more dangerous than seasonal strains is under attack from Australian research, which has found little to no difference in patients infected by the two types.

In results that could undermine uptake of the swine flu vaccine, researchers tracked the progress of all patients admitted to a major Sydney hospital during the recent epidemic, finding the course of the illness was “comparable to those of the current circulating seasonal influenza in Sydney”. The findings threaten to debunk the firming medical orthodoxy that swine flu hits patients much harder than the strains that circulate every winter, particularly children and pregnant women.

The results have already been criticised by some infectious diseases experts, who say the findings are based on very small numbers and do, in fact, point to a greater danger from swine flu.

The study’s authors, from Sydney’s Liverpool Hospital, the Sydney South West Pathology Service and the University of Western Sydney, said their results showed that high numbers of hospital admissions for swine flu reflected the rapid spread of the disease, not any increased virulence of the H1N1 virus.

“Our findings show that, for hospitalised patients, the clinical manifestations and severity of pandemic (H1N1) 2009 and seasonal influenza were similar,” they wrote in the study published online yesterday by the Medical Journal of Australia.

Even among pregnant women — a group that was said to have been particularly at risk of severe complications in the recent epidemic — the authors said they were “unable to demonstrate a difference in clinical severity” compared with pregnant women with annual flu strains. For the research, the authors tracked all 64 adults who were admitted to Liverpool Hospital with influenza from June 17 until July 31.