ASM 2017 Presentations
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Ian Barr, WHO Collaborating Centre for Reference and Research on Influenza, VIDRL, Doherty Institute, Melbourne, Victoria
The 2016 influenza season in Australia was another moderate-high season overall, similar to 2014 and 2015. Inter-seasonal activity was also increased in some states in 2015-2016 with the main season beginning as usual in mid-June and peaking in early September with many cases still being reported during November . There were some 90,837 NNDSS laboratory confirmed cases of influenza in 2016 compared to 100,542 cases in 2015 (a 9.7% decrease) but this was still the second highest number of cases reported to NNDSS. A moderate to high number of cases were seen in all states, however, NSW had the largest number of cases reported (35,560); while SA had the highest incidence per head of population (487/100,000). In terms of the severity of the season, 2016 was similar to 2015 with similar numbers of hospitalizations, ICU admissions and deaths (92 in 2016 versus 97 in 2015 and 72 in 2014) – see Australian Influenza Reports).
Influenza A(H3N2) was the predominant virus overall in Australia followed by A(H1N1)pdm09 along with a small proportion of B viruses (both B/Victoria and B/Yamagata-lineages circulated). New Zealand had a very low level of influenza in 2016 (below baseline levels which are set at 40 cases/100,000 population) with the majority of the viruses detected there being A(H3N2). The 2016 SH vaccine strains were generally well matched to the circulating strains in Australia and NZ for the A(H1N1)pdm09 and the B viruses and reasonably well matched to the A(H3N2) viruses (in the trivalent vaccine) while the Quadrivalent vaccine also covered the circulating B/Victoria-lineage viruses well. The 2017 SH/Australian influenza vaccine has had the A(H1N1)pdm09 component updated again to a vaccine virus that is more representative of currently circulating A(H1N1)pdm09 viruses. In the current 2016-7 Northern Hemisphere influenza season, both Europe and the USA have had mild-moderate number of influenza cases so far this season with the majority of viruses detected so far being A(H3N2) viruses, similar to those that circulated in Australia in 2016, with very few B viruses being detected. Influenza A(H7N9) cases increased during the 2016-7 winter in Southern China and this 5th wave is the second largest so far. Recent viruses do not appear to have increased human to human transmissibility compared to earlier viruses. A(H5N6) viruses have also infected a small number of humans in China in 2016.
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A debate about the market-leading influenza antiviral medication, oseltamivir, which initially focused on treatment for generally mild illness, has been expanded to question the wisdom of stockpiling for use in future influenza pandemics. Although randomized controlled trial evidence confirms that oseltamivir will reduce symptom duration by 17-25 hours among otherwise healthy adolescents and adults with community-managed disease, no randomized controlled trials have examined the effectiveness of oseltamivir against more serious outcomes. Observational studies, although criticized on methodologic grounds, suggest that oseltamivir given early can reduce the risk for death by half among persons hospitalized with confirmed infection caused by influenza A(H1N1)pdm09 and influenza A(H5N1) viruses. However, available randomized controlled trial data may not be able to capture the effect of oseltamivir use among hospitalized patients with severe disease. We assert that data on outpatients with relatively mild disease should not form the basis for policies on the management of more severe disease.
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The UK is in the 4th season of introducing a universal paediatric influenza vaccination programme with live attenuated influenza vaccine. Results from the first seasons have been encouraging with moderate uptake levels achieved in targeted groups together with early evidence of vaccine effectiveness against the main circulating strains and population impact of vaccinating children of primary school age.
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Kanta Subbarao, Director, WHO Collaborating Centre for Reference and Research on Influenza, VIDRL at the Peter Doherty Institute for Infection and Immunity.
The 2009 H1N1 pandemic caused by a swine-origin influenza virus and human cases of H7N9 and highly pathogenic avian influenza A (H5N1) virus infections are examples of direct transmission of animal influenza viruses to humans that underscore the need for control strategies to prevent an influenza pandemic. Vaccination is the key strategy to prevent severe illness and death from pandemic influenza. Despite long-term experience with vaccines against human influenza viruses, there are several challenges in developing human vaccines against animal influenza viruses. We generated pandemic live attenuated influenza vaccines (pLAIV) with the hemagglutinin (HA) and neuraminidase genes from H5 and H7 viruses and the internal protein genes of the licensed seasonal LAIV. The pLAIVs were promising in preclinical studies but were severely restricted in replication and variably immunogenic in humans. However, subsequent administration of a dose of subunit vaccine (pISV) unmasked long lasting immunity in H5 and H7 pLAIV recipients with a rapid, high titre, high quality antibody response that was broadly cross-reactive across several clades or lineages, even in the absence of detectable antibody responses to primary vaccination. In a series of clinical trials, we have demonstrated that pLAIV are highly effective in priming the immune system to produce robust antibody responses following pISV. Similar findings have been reported with other vaccine platforms including DNA and vectored vaccines. Use of pLAIV to prime and vaccination schedules that combine vaccine platforms warrant consideration in responding to pandemic influenza.
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Pneumococcal disease remains a cause of considerable morbidity and mortality in elderly Australian adults. The national notifications system with its enhanced surveillance provides high quality data on invasive pneumococcal disease (IPD), the severe end of pneumococcal disease spectrum. The Incidence rate of total IPD among non-Indigenous adults ≥ 65 years of age, estimated using notifications, show a 40% decline from 2002 (rate 26 per 100,000, n=637) to 2014 (rate 15 per 100,000, n=514) due largely to the herd effect from pneumococcal conjugate vaccine use in children. In comparison among Indigenous adults the incidence of IPD increased widening the disparity to over six fold. Data on all pneumococcal community acquired pneumonia (CAP) is less robust than for IPD. It is estimated that about 14% of CAP cases among Australian adults is caused by pneumococci. This translates to approximately 6000 cases of pneumococcal CAP hospitalisations among elderly Australians per year.
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Viral respiratory infections cause acute damage and contribute to a long term decline in lung health, particularly in patients with chronic respiratory diseases. The respiratory microbiome is increasingly recognised as a crucial factor in lung health. Viral infections may influence lung health by altering the composition of the respiratory microbiome through several mechanisms. Viruses (IAV], RSV, RV) may upregulate bacterial adhesion molecules (ICAM-1, PAFR, CEACAM-1) on epithelial cells, thus promoting adherence and growth of selective bacteria in the lung microbiome (non-typeable Haemophilus influenza, S. pneumoniae and Pseudomonas aeruginosa) to host cells. Viral infections lead to impaired mucociliary clearance and damaged epithelial cells, which could then facilitate host tissue invasion by pathogenic bacteria (Streptococcus pneumoniae) and thus persistence of pathogens in the lung microbiota. Viruses (e.g. Influenza) can also shape host immune responses during infection through mechanisms such as virus-induced phagocytic dysfunction and activation of anti-inflammatory pathways and thereby increasing the survivability of pathogenic bacteria leading to secondary bacterial infections, outgrowth of opportunistic pathogens or chronic shifts in microbiome composition. Clinically, these mechanisms may be active in patients with chronic respiratory diseases, thus allowing pathogenic bacteria to colonise host tissue and potentially alter the respiratory microbiome and long-term lung health. Conversely, some bacteria such as a Lactobacillus-enriched upper respiratory tract microbiome plays a crucial role in mounting appropriate anti-viral response in individuals, potentially by affecting TLR-3 signaling and inducing expression of anti-inflammatory cytokine by the host, and protecting against viral infections. A detailed study of how major viral pathogens may affect the lung microbiome in healthy individuals and patients with chronic respiratory diseases is warranted to strategise novel therapeutic interventions.
Page published: 7 March 2017