Eurosurveillance - Volume 14, Issue 42, 22 October 2009

First infections with the 2009 pandemic H1N1 influenza virus were identified on Réunion Island in July 2009. By the end of July, sustained community transmission of the virus was established. Pandemic H1N1 influenza activity peaked during week 35 (24 to 30 August), five weeks after the beginning of the epidemic and has been declining since week 36. We report preliminary epidemiological characteristics of the pandemic on Réunion Island in 2009 until week 37 ending September 13.

We provide an interim report on pandemic H1N1 influenza activity in South Africa, with a focus on the epidemiology and factors associated with deaths. Following the importation of the virus on 14 July 2009, and the epidemic peak during the week starting 3 August, the incidence in South Africa has declined. A total of 12,331 cases and 91 deaths have been laboratory-confirmed as of 12 October 2009. Age distribution and risk groups were similar to those observed elsewhere. The median age of patients who died (33.5 years) was significantly higher than that of the non-fatal cases (15.0 years, p<0.01). The most common underlying conditions among fatal cases were infection with human immunodeficiency virus (17/32 tested) and pregnancy (25/45 women of reproductive age). Active tuberculosis coinfection was present in seven of 72 fatal cases. These findings should be taken into consideration when planning vaccination strategies for 2010.

Recently, the brunt of the current influenza pandemic has been felt in the southern hemisphere. We report an analysis of the first 34,506 cases of influenza-like illness with severe acute respiratory infection (SARI) notified in Brazil during the epidemiological weeks 16 to 33. The 5,747 confirmed cases of pandemic H1N1 influenza showed two incidence peaks across the age span: one in children up to the age of five years (3.8/100,000) and one in individuals aged 20 to 29 years (4.6/100,000). People over the age of 60 had the lowest incidence (1.1/100,000 inhabitants). The epidemic peaked rapidly. Ninety-four percent of cases were concentrated in two of Brazil’s five geographic regions – the south and southeast, regions that have a more temperate climate and thus colder winters. Case-fatality of pandemic influenza presenting with SARI was 11.2% (95% confidence interval (CI): 10.4%-12.1%). People with a reported comorbidity had approximately twice the risk of those without (relative risk=1.89; 95%CI: 1.64-2.18).

This paper presents a description of Peru’s experience with pandemic H1N1 influenza 2009. It is based on data from four main surveillance systems: a) ongoing sentinel surveillance of influenza-like illness cases with virological surveillance of influenza and other respiratory viruses; b) sentinel surveillance of severe acute respiratory infections and associated deaths; c) surveillance of acute respiratory infections in children under the age of five years and pneumonia in all age groups; and d) case and cluster surveillance. On 9 May 2009, the first confirmed case of pandemic H1N1 influenza in Peru was diagnosed in a Peruvian citizen returning from New York with a respiratory illness. By July, community transmission of influenza had been identified and until 27 September 2009, a total of 8,381 cases were confirmed. The incidence rate per 10,000 persons was 4.4 (in the 0–9 year-olds) and 4.1 (in the 10–19 year-olds). During epidemiological weeks (EW) 26 to 37, a total of 143 fatal cases were notified (a case fatality of 1.71%, based on confirmed cases). The maximum peak in the number of cases was reached in EW 30 with 37 deaths. Currently, the impact of the pandemic in the Peruvian population has not been too severe, and fortunately, healthcare centres have not been overwhelmed. However, the future of this pandemic is uncertain and despite the fact that our country has not been seriously affected, we should be prepared for upcoming pandemic waves.

A range of surveillance systems were used to assess the progression and impact of the first wave of pandemic H1N1 influenza in New South Wales, Australia during the southern hemisphere winter. Surveillance methods included laboratory notifications, near real-time emergency department syndromic surveillance, ambulance despatch surveillance, death certificate surveillance and purpose-built web-based data systems to capture influenza clinic and intensive care unit activity. The epidemic lasted 10 weeks. By 31 August 2009, 1,214 people with pandemic H1N1 influenza infection were hospitalised (17.2 per 100,000 population), 225 were admitted to intensive care (3.2 per 100,000), and 48 died (0.7 per 100,000). Children aged 0-4 years had the highest hospitalisation rates, while adults aged 50-54 had the highest rates of intensive care admission. During the epidemic period, overall presentations to emergency departments were 6% higher than in 2008, while presentations for influenza-like illness were 736% higher. At the peak, confirmed cases of pandemic H1N1 influenza consumed 15% of intensive care capacity. Excess mortality from influenza and pneumonia was lower than in recent influenza seasons. Health services, particularly emergency departments and intensive care units, were substantially affected by the epidemic. Mortality from influenza was comparable with previous seasons.

Victoria was the first Australian state to report widespread transmission of pandemic H1N1 2009 influenza. Notifiable laboratory-confirmed influenza and a general practitioner sentinel surveillance system measuring influenza-like illness (ILI), including laboratory confirmation of influenza as the cause of ILI, were used to assess the pandemic. The pandemic influenza A(H1N1)v virus quickly became the dominant circulating strain and notification rates were highest in children and young adults. Despite a high number of notified cases, comparison of ILI rates suggested the season peaked in late June, was similar in magnitude to 2003 and 2007 and less severe than 1997. The majority of clinical presentations were mild, but one quarter of hospitalised cases required admission to intensive care. Given the low proportion of imported cases in the Victorian pandemic, the rapid increase in cases with no travel history and the low median age of cases notified during the phases of intense surveillance, we suggest there may have been silent importations of pandemic virus into Victoria before the first case was recognised. The usefulness of a general practitioner sentinel surveillance system to provide a comparable assessment of influenza and ILI activity over time was clearly demonstrated, and the need for similar hospital and mortality surveillance systems for influenza in Victoria was highlighted.

Australia was one of the first countries of the southern hemisphere to experience influenza A(H1N1)v with community transmission apparent in Victoria, Australia, by 22 May 2009. With few identified imported cases, the epidemic spread through schools and communities leading to 897 confirmed cases by 3 June 2009. The estimated reproduction ratio up to 31 May 2009 was 2.4 (95% credible interval (CI): 2.1-2.6). Methods designed to account for undetected transmission reduce this estimate to 1.6 (95% CI: 1.5-1.8). Time varying reproduction ratio estimates show a steady decline in observed transmission over the first 14 days of the epidemic. This could be accounted for by ascertainment bias or a true impact of interventions including antiviral prophylaxis, treatment and school closure. Most cases (78%) in the first 19 days in Victoria were under the age of 20 years-old. Estimates suggest that the average youth primary case infected at least two other youths in the early growth phase, which was sufficient to drive the epidemic.

There are few structured data available to assess the risks associated with pandemic influenza A(H1N1)v infection according to ethnic groups. In countries of the Americas and the Pacific where these data are available, the attack rates are higher in indigenous populations, who also appear to be at approximately three to six-fold higher risk of developing severe disease and of dying. These observations may be associated with documented risk factors for severe disease and death associated with pandemic H1N1 influenza infection (especially the generally higher prevalence of diabetes, obesity, asthma, chronic obstructive pulmonary disease and pregnancy in indigenous populations). More speculative factors include those associated with the risk of infection (e.g. family size, crowding and poverty), differences in access to health services and, perhaps, genetic factors. Whatever the causes, this increased vulnerability of indigenous populations justify specific immediate actions in the control of the current pandemic including primary prevention (intensified hygiene promotion, chemoprophylaxis and vaccination) and secondary prevention (improved access to services and early treatment following symptoms onset) of severe pandemic H1N1 influenza infection.