10 August 2014
The threat to public health from ever increasing levels of antibiotic resistance amongst bacteria, which cause many devastating human illnesses, is recognised by governmental and nongovernmental organisations around the world.
Combatting this threat will require significant improvement in our understanding of how bacteria develop antibiotic resistance, and how resistance can spread within and between bacterial species. A new study from researchers at the Wellcome Trust Sanger Institute takes an important step towards achieving this goal, for the bacteria Streptococcus pneumoniae.
Many people carry S. pneumoniae in their nose with no ill effects, but for some, particularly the young, elderly and immunocompromised, these bacteria can cause severe infectious diseases such as pneumonia or bacteraemia. Whilst there are effective vaccines to protect against S. pneumoniae, they only cover a subset of all of the disease-causing strains, and so effective antibiotic treatment remains essential for preventing morbidity and mortality associated with these infections.
Increasingly, S. pneumoniae strains are developing resistance to the antibiotics most commonly used to treat them, the beta lactams (which include penicillin). Researchers from the Sanger Institute have used whole genome sequencing to identify changes in the genome of nearly 4000 S. pneumoniae samples. By comparing the genomes of S. pneumoniae samples known to be resistant to beta lactam antibiotics with those that responded to treatment, they identified 50 regions of the genome in which mutations appeared to confer antibiotic resistance. Further study of these regions promises to reveal potentially novel ways in which the bacteria may evade antibiotics and aid detection of antibiotic resistance.
What’s the clinical and public health impact?
Understanding the genome-level determinants of antibiotic resistance in S. pneumoniae and other disease-causing bacteria can help manage infectious disease in two ways:
What’s the challenge to policy makers?
Studies such as these are vital to developing our understanding of how bacteria cause infections and resist treatment. We are entering an era in which genomic information will become routinely used in clinical practice for managing infectious disease. It will therefore be essential that health service leaders support the development of infrastructure and policies to ensure the wealth of genomic and clinical data arising from these studies - and from routine diagnostic and public health microbiology - are captured in centralised and publicly available resources.
By facilitating the discovery of more of the genetic determinants of infectivity, drug resistance and transmission amongst a wider range of pathogens, they could contribute to better clinical and public health care.
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