The last line of antibiotic defence against some serious infections is under threat, say experts who have identified a gene that enables resistance to spread between bacteria in China.
The gene, called mcr-1, allows a range of common bacteria, including E coli, to become resistant to the last fully functional class of antibiotics, the polymyxins. This gene, they say, is widespread in bugs called Enterobacteriaceae carried by both pigs and people in south China and is likely to spread worldwide.
The gene is easily transferred from one strain of bacteria to another.Enterobacteriaceae are capable of causing a range of diseases, from pneumonia to serious blood infections. Some of the strains of Enterobacteriaceae with the gene have epidemic potential, say experts in the Lancet Infectious Diseases journal.
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The journal article can be found in:
The Lancet Infectious Diseases
Emergence of plasmid-mediated colistin resistance mechanism MCR-1 in animals and human beings in China: a microbiological and molecular biological study
Yi-Yun Liu et al, 2015
The MenAfriVa, introduced into Africa in 2010, has been a huge success: the caseload of Meningitis A has plummeted to zero in 16 countries that organized mass vaccination campaigns. However, health experts now worry that this one-off success will not, at least in some countries, be followed by the introduction of MenAfriVac into routine schedules of infant vaccination. A study just published in Clinical Infectious Diseases by Andromachi Karachaliou of Cambridge University and her colleagues shows what this could lead to: Ms Karachaliou’s computer model predicts that the epidemics will return with a vengeance in about 15 years if MenAfriVac does not become a routine childhood jab, as the World Health Organisation (WHO) recommends it should.
Read the full story in The Economist online…
A new study published in Cell Host & Microbe found that treating MRSA with certain first-line antibiotics can make MRSA infections worse.
The research team at Cedars-Sinai Medical Center in California found that in laboratory mice, treatment with antibiotics called beta-lactams – which are similar to methicillin – caused the MRSA bacteria to build inflammatory cell walls that damage tissues. Beta-lactam antibiotics kill normal staph by neutralizing their enzymes that make cell walls.
However, the researchers found that one of these enzymes – called PBP2A – is not neutralized by the antibiotics. Furthermore, PBP2A actually enables the superbug to continue building its cell wall.
They also found that the cell wall’s structure is different from normal staph, which allows the superbug to proliferate. Co-senior author David Underhill, PhD, further explains:
“This altered cell wall induces a powerful inflammatory response. In mice infected with MRSA, induction of PBP2A with methicillin led to more inflammation and pathology.”
The researchers say their take-home message from all of this is that, after introducing the antibiotics to the MRSA-infected mice, they became even sicker.
Still, the researchers warn that because their findings are based on studies involving laboratory mice, their results need to be carefully assessed in humans.
Read the full article on Medical News Today.
The journal article can be found in:
Cell Host & Microbe, Volume 18, Issue 5, 11 November 2015, Pages 604-612
Sabrina Müller, Andrea J. Wolf, Iliyan D. Iliev, Bethany L. Berg, David M. Underhill, George Y. Liu
Poorly Cross-Linked Peptidoglycan in MRSA Due to mecA Induction Activates the Inflammasome and Exacerbates Immunopathology
Taking a Christmas vacation to New York? Be sure to take your kids to see The Secret World Inside You, an exhibition of the human microbiome at the American Museum of Natural History.
You can read the full story about the exhibition on the New York Times website.