HOW VIRAL INFECTIONS CAN CAUSE TO BACTERIAL EAR INFECTIONS
EMBARGOED UNTIL: Thursday, September 12, 8:30 AM MDT
(Session 129, Paper B-956)
Odilia Wijburg
The Univ. of Melbourne, Melbourne, , Australia
Email: odilia@unimelb.edu.au
Phone: 61-3-83449919
Ear infections (otitis media) are the number one cause for which children visit a general practitioner for acute illness and the most common reason for antibiotic prescription to children. Recurrent and chronic ear infections can result in permanent hearing loss from a very young age, affecting the child’s well being and learning abilities.
Otitis media is a multifactorial disease often involving more than one infectious microbe. Acute otitis media frequently results from a virus infection of the respiratory tract, and has been associated with a number of human viral infections. Streptococcus pneumoniae (the pneumococcus) is a common bacterium that temporarily lives in the nose of most young children, usually not causing any disease, unless an infection with a virus disturbs the balance between the human host and the pneumococcus. Thus, especially during the winter season when many people are infected with respiratory viruses such as influenza virus, there is an increased spread of bacterial infections, including pneumococcal infections, and increased incidences of pneumococcal disease. In our studies, we have focused on how infection with influenza virus may result in the development of ear infections and pneumonia. We have demonstrated a novel mechanism by which influenza virus facilitates pneumococcal ear infections. We are currently investigating whether our results can be extrapolated to other pneumococcal diseases, such as pneumonia, in which viral infection is a predisposing factor. Our results may be applied to inform the therapeutic use of antiviral drugs and provide predictive information for the future epidemics and pandemics of these communicable diseases.
Who did the work, where, funding, meeting name, city, date of presentation
This work was performed by Kirsty Short (PhD) and Dimitri Diavatopoulos (PhD), under supervision of Patrick Reading (PhD), Lorena Brown (PhD) and Odilia Wijburg (PhD). These studies were performed at the Department of Microbiology and Immunology at The University of Melbourne, Australia, and at Laboratory for Pediatric Infectious Diseases at Radboud University, Nijmegen, The Netherlands. Funding was gratefully received from National Health and Medical Research Council of Australia and the International Symposium on Pneumococci and Pneumococcal Diseases (Robert Austrian Award).
The results of this study will be presented at the ICAAC meeting held in Denver, CO, on 12 September 2013.
Remainder concentrate on work itself, kind of evidence on which conclusions are based, background material to work, what findings could mean to average person
While the association between influenza virus infection and secondary bacterial otitis media has been well documented, the mechanism of virus induced otitis media remains largely unknown. Our studies are based on the use of a clinically relevant, novel experimental model using infant mice as well as studies with human middle ear cells. We have demonstrated for the first time a key role for influenza A virus surface protein hemagglutinin (HA) in facilitating otitis media. Our results suggest that not all influenza A virus strains are able to replicate (grow) in the middle ear, and only those virus strains that do, are able to induce bacterial disease in the middle ear. We demonstrate that this bacterial disease is the result of the inflammatory environment induced by the virus infection: the bacteria seem to thrive in this locally changed environment and interact with the influx of immune cells. We have characterized this inflammatory environment induced by the influenza virus and are studying how the cells of the immune system are involved in this process. Further, we have developed an experimental model to study the spread of pneumococci from infected to non-infected individuals, and demonstrate a critical role for influenza virus through the induction of inflammation in the recipient individual. Thus, we demonstrate that influenza virus infection renders an individual more susceptible to acquiring a pneumococcal infection through changing the local environment in the nose into an environment sustaining inflammation.
The outcome of our studies will hopefully identify potential novel targets for therapy and will have a major impact on clinical research through the discovery of novel mediators of respiratory virus induced pneumococcal disease, including otitis media. Our results also suggest that the prophylactic use of some of the currently used antiviral drugs may not decrease the incidence of secondary bacterial otitis media. Finally, our results provide predictive information about the incidence of pneumococcal disease and spread of pneumococcal infections during future epidemics and pandemics of influenza virus infections.