Whole-genome analysis helps identify source of MRSA outbreak on infant ward.
A superbug outbreak that plagued a special-care neonatal unit in Cambridge, UK, for several months last year was brought to an end by insights gained from genome sequencing. The case, reported today in Lancet Infectious Disease, marks the first time that scientists have sequenced pathogen genomes to actively control an ongoing outbreak.
Sharon Peacock, a clinical microbiologist at the University of Cambridge, and her team became involved in the outbreak after three infants at nearby Rosie Hospital’s 24-cot special-care baby unit tested positive for methicillin-resistant Staphylococcus aureus (MRSA) within a couple days of each other.
Bacteria isolated from the three infants were resistant to a nearly identical spectrum of antibiotics, pointing to a common source, says Peacock. The unit was scrubbed clean, and officials hoped that the outbreak was over. Out of scientific curiosity, though, Peacock's team went on to investigate whether the three cases were linked to a string of MRSA infections at Rosie over the previous six months. Lab tests suggested that at least 8 other children had been infected by MRSA strains with similar antibiotic-resistance profiles in that time. But weeks would go by without an infection, suggesting that the bacteria were not simply spreading from baby to baby in the unit.
Joining the dots. In the hope of connecting the dots, Peacock’s team began sequencing the genomes of MRSA strains from the unit, as well as similar strains collected from adult patients at other hospitals and doctor’s sugeries. They suspected that adult carriers explained the long gaps between infections in the baby unit.
But the latest outbreak wasn’t over. Days after the unit was sterilized, another baby there tested positive for MRSA. Genome sequencing confirmed that the strain matched the other suspected cases. Confronted with an ongoing outbreak, Peacock and the hospital epidemiologists cast their net wider, searching for the outbreak strain among the 154 workers on the baby unit. One tested positive for a matching MRSA strain, despite showing no symptoms.“We thought it was likely that this individual had been involved in bridging the gaps,” Peacock says. “We could take that individual out of circulation and effectively stop the outbreak from continuing.”
Further surveillance turned up additional infections among adults in the community, including parents who had contracted MRSA from their babies. Fourteen patients in total — six infants and eight adults — developed serious infections requiring treatment. The final case, a father who had acquired MRSA from his spouse, occurred a year after the outbreak began. No one died.
Genome sequencing provided clarity that could never have been obtained otherwise, says Julian Parkhill, a microbiologist at the Wellcome Trust Sanger Institute near Cambridge, and a co-author on the Lancet paper. Genome sequencing can reveal the series of small mutations that occur over the course of an outbreak, allowing epidemiologists to create an evolutionary tree and trace the outbreak back to close to its suspected source. The infected employee had probably picked up their MRSA from an infant on the ward, the evolutionary analysis suggests.
Bacteria in the human body thrive in 3D structured communities, so studying pathogens in this type of environment could better show how they interact. Now, scientists are doing just that - with microscopic 3D printed cages.
Scientists from the University of Texas at Austin have used a new 3D printing technology, which allowed them to construct homes for the bacteria at a micro level.
By encasing bacteria in these tiny homes, they were able to study how bacteria found in the human gut and lungs collaborate to develop infections.
A study of their work was published in the journal Proceedings of the National Academy of Sciences.
To construct the cages, which are made of protein, the researchers used a laser and built the cages around bacteria in gelatin. The cages can be almost any shape or size, say the researchers, and they can be moved around other cages that contain other bacteria communities.
In an experiment, they were able to show how a community of bacteria that causes skin infections, Staphylococcus aureus, became more antibiotic-resistant when it was in a cage with a community of another bacteria involved in cystic fibrosis,Pseudomonas aeruginosa.
The researchers say this new method they employed should allow future studies to recreate better conditions - more like the human body - in which bacteria thrive.
PLOS Biology is an open-access, peer-reviewed journal that features works of exceptional significance in all areas of biological science, from molecules to ecosystems, including works at the interface with other disciplines.
After mapping humans' intricate social networks, Nicholas Christakis and colleague James Fowler began investigating how this information could better our lives. Now, he reveals his hot-off-the-press findings: These networks can be used to detect epidemics earlier than ever, from the spread of innovative ideas to risky behaviors to viruses (like H1N1).
According to a team of scientists led by Dr Ross Fitzgerald from the Roslin Institute and the University of Edinburgh, cows may be a source of MRSA CC97 – an epidemic methicillin-resistant strain of Staphylococcus aureus that causes skin and soft tissue infections in humans.
A team of UC Berkeley vision scientists has found that small fragments of keratin protein in the eye play a key role in warding off pathogens. The researchers also put synthetic versions of these keratin fragments to the test against an array of nasty pathogens. These synthetic molecules effectively zapped bacteria that can lead to flesh-eating disease and strep throat (Streptococcus pyogenes), diarrhea (Escherichia coli), staph infections (Staphylococcus aureus) and cystic fibrosis lung infections (Pseudomonas aeruginosa).
These new small proteins in the study were derived from cytokeratin 6A, one of the filament proteins that connect to form a mesh throughout the cytoplasm of epithelial cells. The researchers in Fleiszig’s lab came upon cytokeratin 6A in their efforts to solve the mystery behind the eye’s remarkable resilience to infection. They noticed that the surface of the eye, unlike other surfaces of the body, did not have bacteria living on it, and that corneal tissue could handily wipe out a barrage of pathogens in lab culture experiments.
In the hunt for this mystery compound, the researchers cultured human corneal epithelial cells and exposed them to the P. aeruginosa bacteria. They used mass spectrometry to sort out which peptides were most active in fighting off the bacteria. Cytokeratin 6A-derived peptides emerged the winners, and surprisingly, peptide fragments as short as 10 amino acids were effective. To confirm that they got the right protein, the researchers used gene-silencing techniques to reduce the expression of cytokeratin 6A in the cornea of mice. With a key defense disabled, the amount of bacteria that adhered to the corneas increased fivefold.
Tests showed that cytokeratin 6A-derived fragments could quickly kill bacteria in water and in a saline solution, showing that the salt contained in human tears would not dilute the protein’s effectiveness. Other experiments indicated that cytokeratin 6A fragments prevented the bacteria from attacking epithelial cells, and that the proteins cause bacterial membranes to leak, killing the pathogen within minutes.
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