̽��ֱ�� of Cambridge - Julian Parkhill

System to auto-detect new variants will inform better response to future infectious disease outbreaks

jg533 — Wed, 01 Jan 2025 16:00:35 +0000

̽��ֱ��new approach uses samples from infected humans to allow real-time monitoring of pathogens circulating in human populations, and enable vaccine-evading bugs to be quickly and automatically identified. This could inform the development of vaccines that are more effective in preventing disease.

̽��ֱ��approach can also quickly detect emerging variants with resistance to antibiotics. This could inform the choice of treatment for people who become infected – and try to limit the spread of the disease.

It uses genetic sequencing data to provide information on the genetic changes underlying the emergence of new variants. This is important to help understand why different variants spread differently in human populations.

There are very few systems in place to keep watch for emerging variants of infectious diseases, apart from the established COVID and influenza surveillance programmes. ̽��ֱ��technique is a major advance on the existing approach to these diseases, which has relied on groups of experts to decide when a circulating bacteria or virus has changed enough to be designated a new variant.

By creating ‘family trees’, the new approach identifies new variants automatically based on how much a pathogen has changed genetically, and how easily it spreads in the human population – removing the need to convene experts to do this.

It can be used for a broad range of viruses and bacteria and only a small number of samples, taken from infected people, are needed to reveal the variants circulating in a population. This makes it particularly valuable for resource-poor settings.

̽��ֱ��report was published in the journal Nature.

“Our new method provides a way to show, surprisingly quickly, whether there are new transmissible variants of pathogens circulating in populations – and it can be used for a huge range of bacteria and viruses,” said Dr Noémie Lefrancq, first author of the report, who carried out the work at the ̽��ֱ�� of Cambridge’s Department of Genetics.

Lefrancq, who is now based at ETH Zurich, added: “We can even use it to start predicting how new variants are going to take over, which means decisions can quickly be made about how to respond.”

“Our method provides a completely objective way of spotting new strains of disease-causing bugs, by analysing their genetics and how they’re spreading in the population. This means we can rapidly and effectively spot the emergence of new highly transmissible strains,” said Professor Julian Parkhill, a researcher in the ̽��ֱ�� of Cambridge’s Department of Veterinary Medicine who was involved in the study.

Testing the technique

̽��ֱ��researchers used their new technique to analyse samples of Bordetella pertussis, the bacteria that causes whooping cough. Many countries are currently experiencing their worst whooping cough outbreaks of the last 25 years. It immediately identified 3 new variants circulating in the population that had been previously undetected.

“ ̽��ֱ��novel method proves very timely for the agent of whooping cough, which warrants reinforced surveillance given its current comeback in many countries and the worrying emergence of antimicrobial resistant lineages,” said Professor Sylvain Brisse, Head of the National Reference Center for whooping cough at Institut Pasteur, who provided bioresources and expertise on Bordetella pertussis genomic analyses and epidemiology.

In a second test, they analysed samples of Mycobacterium tuberculosis, the bacteria that causes Tuberculosis. It showed that 2 variants with resistance to antibiotics are spreading.

“ ̽��ֱ��approach will quickly show which variants of a pathogen are most worrying in terms of the potential to make people ill. This means a vaccine can be specifically targeted against these variants, to make it as effective as possible,” said Professor Henrik Salje in the ̽��ֱ�� of Cambridge’s Department of Genetics, senior author of the report.

He added: “If we see a rapid expansion of an antibiotic-resistant variant, then we could change the antibiotic that’s being prescribed to people infected by it, to try and limit the spread of that variant.”

̽��ֱ��researchers say this work is an important piece in the larger jigsaw of any public health response to infectious disease.

A constant threat

Bacteria and viruses that cause disease are constantly evolving to be better and faster at spreading between us. During the COVID pandemic, this led to the emergence of new strains: the original Wuhan strain spread rapidly but was later overtaken by other variants, including Omicron, which evolved from the original and were better at spreading. Underlying this evolution are changes in the genetic make-up of the pathogens.

Pathogens evolve through genetic changes that make them better at spreading. Scientists are particularly worried about genetic changes that allow pathogens to evade our immune system and cause disease despite us being vaccinated against them.

“This work has the potential to become an integral part of infectious disease surveillance systems around the world, and the insights it provides could completely change the way governments respond,” said Salje.

̽��ֱ��research was primarily funded by the European Research Council.

Reference: Lefrancq, N et al: ‘Learning the fitness dynamics of pathogens from phylogenies.’ January 2025, DOI: 10.1038/s41586-024-08309-9

Researchers have come up with a new way to identify more infectious variants of viruses or bacteria that start spreading in humans – including those causing flu, COVID, whooping cough and tuberculosis.

̽��ֱ��approach will quickly show which variants of a pathogen are most worrying in terms of the potential to make people ill. This means a vaccine can be specifically targeted against these variants, to make it as effective as possible.

Henrik Salje

Milan Krasula on Getty

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Licence type:

Attribution

Ability of multi-drug resistant infection to evolve within cystic fibrosis patients highlights need for rapid treatment

cjb250 — Thu, 29 Apr 2021 18:00:25 +0000

Around one in 2,500 children in the UK is born with cystic fibrosis, a hereditary condition that causes the lungs to become clogged up with thick, sticky mucus. ̽��ֱ��condition tends to decrease life expectancy among patients.

In recent years, M. abscessus, a species of multi-drug resistant bacteria, has emerged as a significant global threat to individuals with cystic fibrosis and other lung diseases. It can cause a severe pneumonia leading to accelerated inflammatory damage to the lungs, and may prevent safe lung transplantation. It is also extremely difficult to treat – fewer than one in three cases is treated successfully.

In a study published today in Science, a team led by scientists at the ̽��ֱ�� of Cambridge examined whole genome data for 1,173 clinical M. abscessus samples taken from 526 patients to study how the organism has evolved – and continues to evolve. ̽��ֱ��samples were obtained from cystic fibrosis clinics in the UK, as well as centres in Europe, the USA and Australia.

̽��ֱ��team found two key processes that play an important part in the organism’s evolution. ̽��ֱ��first is known as horizontal gene transfer – a process whereby the bacteria pick up genes or sections of DNA from other bacteria in the environment. Unlike classical evolution, which is a slow, incremental process, horizontal gene transfer can lead to big jumps in the pathogen’s evolution, potentially allowing it to become suddenly much more virulent.

̽��ֱ��second process is within-host evolution. As a consequence of the shape of the lung, multiple versions of the bacteria can evolve in parallel – and the longer the infection exists, the more opportunities they have to evolve, with the fittest variants eventually winning out. Similar phenomena have been seen in the evolution of new SARS-CoV-2 variants in immunocompromised patients.

Professor Andres Floto, joint senior author from the Centre for AI in Medicine (CCAIM) and the Department of Medicine at the ̽��ֱ�� of Cambridge and the Cambridge Centre for Lung Infection at Royal Papworth Hospital, said: “What you end up with is parallel evolution in different parts of an individual’s lung. This offers bacteria the opportunity for multiple rolls of the dice until they find the most successful mutations. ̽��ֱ��net result is a very effective way of generating adaptations to the host and increasing virulence.

“This suggests that you might need to treat the infection as soon as it is identified. At the moment, because the drugs can cause unpleasant side effects and have to be administered over a long period of time – often as long as 18 months – doctors usually wait to see if the bacteria cause illness before treating the infection. But what this does is give the bug plenty of time to evolve repeatedly, potentially making it more difficult to treat.”

Professor Floto and colleagues have previously advocated routine surveillance of cystic fibrosis patients to check for asymptomatic infection. This would involve patients submitting sputum samples three or four times a year to check for the presence of M. abscessus infection. Such surveillance is carried out routinely in many centres in the UK.

Using mathematical models, the team have been able to step backwards through the organism’s evolution in a single individual and recreate its trajectory, looking for key mutations in each organism in each part of the lung. By comparing samples from multiple patients, they were then able to identify the key set of genes that enabled this organism to change into a potentially deadly pathogen.

These adaptations can occur very quickly, but the team found that their ability to transmit between patients was constrained: paradoxically, those mutations that allowed the organism to become a more successful pathogen within the patient also reduced its ability to survive on external surfaces and in the air – the key mechanisms by which it is thought to transmit between people.

Potentially one of the most important genetic changes witnessed by the team was one that contributed towards M. abscessus becoming resistant to nitric oxide, a compound naturally produced by the human immune system. ̽��ֱ��team will shortly begin a clinical trial aimed at boosting nitric oxide in patients’ lung by using inhaled acidified nitrite, which they hope would become a novel treatment for the devastating infection.

̽��ֱ��researchers say their findings highlight the need to treat patients with Mycobacterium abscessus infection immediately, counter to current medical practice.

Examining the DNA taken from patient samples is also important in helping understand routes of transmission. Such techniques are used routinely in Cambridge hospitals to map the spread of infections such as MRSA and C. difficile – and more recently, SARS-CoV-2. Insights into the spread of M. abscessus helped inform the design of the new Royal Papworth Hospital building, opened in 2019, which has a state-of-the-art ventilation system to prevent transmission. ̽��ֱ��team recently published a study showing that this ventilation system was highly effective at reducing the amount of bacteria in the air.

Professor Julian Parkhill, joint senior author from the Department of Veterinary Medicine at the ̽��ֱ�� of Cambridge, added: “M. abscessus can be a very challenging infection to treat and can be very dangerous to people living with cystic fibrosis, but we hope insights from our research will help us reduce the risk of transmission, stop the bug evolving further, and potentially prevent the emergence of new pathogenic variants.”

̽��ֱ��team have used their research to develop insights into the evolution of M. tuberculosis – the pathogen that causes TB about 5,000 years ago. In a similar way to M. abscessus, M. tuberculosis likely started life as an environmental organism, acquired genes by horizontal transfer that made particular clones more virulent, and then evolved through multiple rounds of within-host evolution. While M. abscessus is currently stopped at this evolutionary point, M. tuberculosis evolved further to be able to jump directly from one person to another.

Dr Lucy Allen, Director of Research at the Cystic Fibrosis Trust, said: “This exciting research brings real hope of better ways to treat lung infections that are resistant to other drugs. Our co-funded Innovation Hub with the ̽��ֱ�� of Cambridge really shows the power of bringing together world-leading expertise to tackle a health priority identified by people with cystic fibrosis. We’re expecting to see further impressive results in the future coming from our joint partnership.”

̽��ֱ��study was funded by the Wellcome Trust, Cystic Fibrosis Trust, NIHR Cambridge Biomedical Research Centre and Fondation Botnar.

Reference
Bryant, JM et al. Stepwise pathogenic evolution of Mycobacterium abscessus. Science; 30 Apr 2021

Scientists have been able to track how a multi-drug resistant organism is able to evolve and spread widely among cystic fibrosis patients – showing that it can evolve rapidly within an individual during chronic infection.

We hope insights from our research will help us reduce the risk of transmission, stop the bug evolving further, and potentially prevent the emergence of new pathogenic variants

Julian Parkhill

Jon Sneddon

Patient with cystic fibrosis

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Study highlights ‘unbridled globetrotting’ of the strangles pathogen in horses

jg533 — Tue, 09 Mar 2021 09:32:59 +0000

̽��ֱ��results, published today in the journal Microbial Genomics, provide evidence of the important role played by the movement of horses in spreading this disease, providing new opportunities for interventions that will prevent future outbreaks.

Strangles, caused by the bacteria Streptococcus equi, is the most frequently diagnosed infectious disease of horses, with 600 outbreaks estimated to occur in the United Kingdom each year.

Streptococcus equi invades the lymph nodes of head and neck of horses, causing them to swell and form abscesses that can, in around 2% of cases, literally strangle the horse to death. Some of the horses that recover from strangles remain persistently infected. These apparently healthy animals shed bacteria into the environment and spread the disease to other horses that they come into contact with.

Using standard diagnostic testing, the Streptococcus equi strains look almost identical. But by carefully examining the DNA of the bacteria, the team were able to track different variants as they spread across the world.

̽��ֱ��research used the new online Pathogenwatch resource, developed at the Wellcome Sanger Institute, to visualise and share genome data to track the course of infections.

“Piecing the puzzle together, we showed that cases in Argentina, the United Kingdom and the United Arab Emirates were closely linked. Along with other examples, we provide evidence that the global trade and movement of horses is helping to spread the disease,” said Professor Matthew Holden of the ̽��ֱ�� of St Andrews, who was involved in the study.

"This study shows once again the power of genomic data to uncover the fine detail of pathogen transmission locally and globally,” said Professor Julian Parkhill in the ̽��ֱ�� of Cambridge’s Department of Veterinary Medicine, who was involved in the study.

He added: “Using whole genome sequences we can track the movement of pathogens with very high precision, showing how and where to intervene to prevent the disease spreading."

Strangles was first described in Medieval times and, with the exception of Iceland, affects horses in all corners of the world. ̽��ֱ��freedom from this disease enjoyed by Iceland is by virtue of a ban on the import of horses, which has been in place for over 1,000 years.

“This has been an incredible team effort, which was only possible through the collaboration of leading researchers from twenty-nine different scientific institutes in eighteen countries” said Dr Andrew Waller of Intervacc AB.

Horses are transported all over the world as they move to new premises or attend competitions and events. New cases of Strangles can be prevented by treating carriers before they pass on the bacteria.

Reference

Mitchell, C. et al. 'Globetrotting strangles: the unbridled national and international transmission of Streptococcus equi between horses.' Microbial Genomics, March 2021.

Collaborating Institutes

Argentina: Clinica Equina, Buenos Aires

Australia: ̽��ֱ�� of Melbourne

Belgium: Ghent ̽��ֱ��, Merelbeke

France: LABÉO Frank Duncombe, Caen

Germany: Labor Dr. Böse GmbH, Harsum

Ireland: Irish Equine Centre, Naas; ̽��ֱ�� College Dublin

Israel: Kimron Veterinary Institute, Bet Dagan

Italy: ̽��ֱ�� of Camerino

Japan: Japan Racing Association, Tochigi

Poland: Institute of Veterinary Medicine, Warsaw ̽��ֱ�� of Life Sciences - SGGW

New Zealand: Massey ̽��ֱ��, Palmerston North; ̽��ֱ�� of Waikato, Hamilton

Saudi Arabia: Al Khalediah Equine Hospital, Riyadh

Spain: Exopol, Zaragoza; Universidad Complutense, Madrid

Sweden: Department of Biomedical Science and Veterinary Public Health, Swedish ̽��ֱ�� of Agricultural Sciences, Uppsala; Intervacc AB, Stockholm

̽��ֱ��Netherlands: Royal GD, Deventer

United Arab Emirates: Central Veterinary Research Laboratory, Dubai; Emirates Racing Authority, Dubai

United Kingdom: Animal Health Trust, Newmarket; Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Medicine, ̽��ֱ�� of Oxford; Centre for Genomic Pathogen Surveillance, Wellcome Trust Sanger Institute, Cambridge; Redwings Horse Sanctuary; ̽��ֱ�� of Cambridge; ̽��ֱ�� of St Andrews

United States of America: Gluck Equine Research Center, Lexington; Weatherford Equine Medical Centre, Texas

Adapted from a press release by Intervacc.

In the largest ever study of its kind into an equine pathogen, scientists in 18 countries used the latest DNA sequencing techniques to track the bacteria responsible for a disease called 'strangles’ in horses around the world.

Using whole genome sequences we can track the movement of pathogens with very high precision, showing how and where to intervene to prevent the disease spreading.

Julian Parkhill

Nicky on Pixabay

Horse

Yes

Licence type:

Attribution

New innovation hub aims to take a 'moon shot' at cystic fibrosis

cjb250 — Wed, 18 Apr 2018 14:01:05 +0000

John Winn’s office at Microsoft Research looks like that of any typical academic: on one wall is a whiteboard graffitied with impenetrable equations and mathematical scribblings, on the opposite wall books and files line shelves, and on his desk are photos of his family.

His desk, however, is somewhat different: it can rise or fall, depending on whether he wants to work standing or sitting – and underneath is a treadmill for walking and working at the same time. “There have been times when I’ve been deep in thought and almost fallen off it,” he jokes.

Winn has cystic fibrosis (CF) and keeping fit is an important part of managing his condition: the stronger his lung function, the better equipped he is to fight the potentially life-threatening infections that plague people living with the condition.

CF occurs when an individual inherits two copies of a single genetic variant, one from each parent. ̽��ֱ��disease causes a build-up of thick, sticky mucous in the lungs, intestines and organs, and those affected by the condition are particularly susceptible to lung infections leading to progressive inflammatory lung damage. Although life expectancy for people with CF has almost doubled in recent decades, it is still significantly below average.

Winn is a machine learning specialist and is using his expertise to fight the condition that affects his everyday life. Together with Professor Andres Floto from the Department of Medicine at Cambridge, he is turning data from the daily lives of people with cystic fibrosis into potentially life-saving information.

As part of this study, funded by the Cystic Fibrosis Trust and Royal Papworth Hospital, participants have been submitting data – everything from heart rate and lung function through to self-reported wellbeing – via an app that also monitors their activity levels. Machine learning then sifts through the data, looking for patterns and – it’s hoped – building a model that can predict when a patient’s health is about to deteriorate and advise them to seek medical help.

“ ̽��ֱ��overarching principle is about giving people control over their own health data and making it work for them,” says Winn. “There’s some informal feedback that just participating in the study and taking these readings has already improved health outcomes for some individuals: for example, it’s helped with adherence with taking their medications as they noticed that if they missed taking certain medicines, their readings got worse.”

̽��ֱ��project is just one strand of a major new Cystic Fibrosis Innovation Hub based on the Cambridge Biomedical Campus and run by Floto. ̽��ֱ��Hub is supported through a £5 million commitment from the Cystic Fibrosis Trust and matching funds from the ̽��ֱ�� of Cambridge. It will strengthen existing collaborations across the ̽��ֱ�� and with the Wellcome Trust Sanger Institute, as well as build new collaborative research networks with CF centres around the UK. ̽��ֱ��Trust’s Chief Executive, David Ramsden, said it will “provide in CF research across the country”.

Floto agrees with this sentiment: “We have an opportunity to uplift UK CF research in general by providing knowhow, training and reagents in a number of areas including genomics, bioinformatics, stem cells and clinical trials technology.”

A major part of the Hub’s activities will be around developing new drugs that target chronic inflammation in CF, in collaboration with the pharmaceutical company GSK as part of the GSK/Cambridge Strategic Partnership, as well as new antibiotic therapy for the main causes of lung infection in the condition.

Finding new drugs against these bacteria is becoming increasingly urgent – Floto and Professor Julian Parkhill at Sanger recently showed that Mycobacterium abscessus, the pathogen behind one of the most serious infections, is becoming increasingly multi-drug resistant and spreading globally. This is one reason why people with CF are advised not to meet each other.

“Clearly the techniques that we develop – and the drug-like molecules that come out of it – will have more general applicability to patients with other multi-drug resistant infections,” Floto says. This will be welcome news to England’s Chief Medical Officer, Professor Dame Sally Davies, who has warned of a future where “any one of us could go into hospital in 20 years for minor surgery and die because of an ordinary infection that can’t be treated by antibiotics.”

̽��ֱ��timing of all this is particularly good: Papworth Hospital, whose Adult Cystic Fibrosis Centre has gained a national and international reputation for its treatment of patients and its contribution to research, is due to move to the Biomedical Campus later in 2018. ̽��ֱ��CF wards will feature state-of-the-art air flow systems, designed with Floto’s work on the spread of multi-drug resistant CF pathogens in mind.

This close proximity between the patients and the researchers will help Floto test the new treatments he is pioneering. He is particularly excited about the potential for new cellular therapies he’s developing with Professor Ludovic Vallier at the Department of Surgery. Floto describes these as their “moon shot”. These would involve taking cells from a CF patient, re-programming them – correcting the genetic defect along the way – and then re-injecting them into patients. “This could provide a way to regenerate damaged lungs,” he says.

Floto knows his plans for the Hub are ambitious, but given that it’s almost 30 years since the gene that causes CF was discovered and there is still no cure for the disease, believes it’s time to take this shot at the moon.

Floto’s collaborators in the CF Innovation Hub include Chris Abell (Chemistry), Sir Tom Blundell (Biochemistry), Julian Parkhill and Ludovic Vallier.

Almost 30 years on from the discovery of the genetic defect that causes cystic fibrosis, treatment options are still limited and growing antibiotic resistance presents a grave threat. Now, a team of researchers from across Cambridge, in a major new centre supported by the Cystic Fibrosis Trust, hopes to turn fortunes around.

We have an opportunity to uplift UK cystic fibrosis research in general by providing knowhow, training and reagents in a number of areas including genomics, bioinformatics, stem cells and clinical trials technology

Andres Floto

Cambridge Biomedical Campus

A no-strings-attached scientific relationship

Professor Claire Bryant, like Floto, works on an inflammatory lung disease as part of the GSK/Cambridge Strategic Partnership. In her case, she’s looking at chronic obstructive pulmonary disease (COPD).

COPD is a condition caused by smoking, pollution and severe asthma. Bryant is looking in particular at how COPD makes the lungs ‘stickier’ to bacteria, increasing the risk of infections.

She holds two grants under the GSK/Cambridge Strategic Partnership, which aims to develop the next wave of ‘game-changing’ medicines by bringing academic and industrial expertise together to tackle often intractable disease. Based at Cambridge’s Department of Veterinary Medicine, Bryant currently has a three-day-a-week sabbatical at GSK’s headquarters in Stevenage. As such, it’s arguable whether anyone embodies the partnership more than she does.

̽��ֱ��three-year sabbatical provides Bryant with three postdocs, two PhD students and budget, with access to GSK resources, but with “no strings attached”. ̽��ֱ��only proviso is that if she works with a GSK reagent, they have first rights on what she does with this. Crucially, she says, it gives her “the space to think”.

Bryant is embedded in GSK’s Respiratory Drug Discovery Unit and attends its lab meeting every week. “I’ve met really smart, clever scientists at GSK, with different skills to those of us in academia,” she says. “I get to see all aspects of what happens at GSK, everything from how a target is identified to how drugs are developed to target it, through to taking these drugs to clinical trials. I see the whole spectrum.”

It is, though, a mutually beneficial programme, she stresses. Bryant brings her knowledge of innate immunity and her experience of multi-disciplinary collaborations, particularly in imaging. “It’s effectively like being a consultant,” she says. “I want them to get as much out of me as I do out of them.”

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

Yes

Multi-drug resistant infection spreading globally among cystic fibrosis patients

cjb250 — Thu, 10 Nov 2016 19:00:00 +0000

̽��ֱ��study, led by the ̽��ֱ�� of Cambridge and the Wellcome Trust Sanger Institute, also suggests that conventional cleaning will not be sufficient to eliminate the pathogen, which can be transmitted through contaminated surfaces or in the air.

Mycobacterium abscessus, a species of multidrug resistant mycobacteria, has recently emerged as a significant global threat to individuals with cystic fibrosis and other lung diseases. It can cause a severe pneumonia leading to accelerated inflammatory damage to the lungs, and may prevent safe lung transplantation. It is also extremely difficult to treat – fewer than one in three cases is treated successfully.

It was previously thought that patients acquired the infection from the environment and that transmission between patients never occurred. ̽��ֱ��research team had previously studied one specialist CF centre in the UK and identified genetic and epidemiological evidence suggesting person-to-person transmission of M. abscessus but it was unclear whether this was a one off incident.

Now, by sequencing the whole genomes of over 1,000 isolates of mycobacteria from 517 individuals attending CF specialist centres in Europe, the US and Australia, researchers have demonstrated that the majority of CF patients have acquired transmissible forms of M. abscessus that have spread globally. Further analysis suggests that the infection may be transmitted within hospitals via contaminated surfaces and through airborne transmission. This presents a potentially serious challenge to infection control practices in hospitals.

Using a combination of cell-based and mouse models, the researchers showed that the recently-evolved mycobacteria were more virulent, likely to cause more serious disease in patients.

“This mycobacterium can cause very serious infections that are extremely challenging to treat, requiring combination treatment with multiple antibiotics for 18 months or longer,” says Professor Andres Floto from the Department of Medicine, ̽��ֱ�� of Cambridge, and the Cambridge Centre for Lung Infection at Papworth Hospital NHS Foundation Trust. “ ̽��ֱ��bug initially seems to have entered the patient population from the environment, but we think it has recently evolved to become capable of jumping from patient to patient, getting more virulent as it does so.”

Professor Julian Parkhill from the Wellcome Trust Sanger Institute at Hinxton, Cambridgeshire, adds: “Our research should provide a degree of hope: now that we know the extent of the problem and are beginning to understand how the infection spreads, we can start to respond. Our work has already helped inform infection control policies and provides the means to monitor the effectiveness of these.”

̽��ֱ��Adult Cystic Fibrosis Centre at Papworth Hospital, Cambridgeshire, has led the development and implementation of new infection control policies to reduce the risk of transmission, now adopted across the UK and elsewhere. This study has also influenced the design of a new CF unit, due to open within the New Papworth Hospital on the Cambridge Biomedical Campus in 2018, which will incorporate a state-of-the-art air handling system.

One question that the researchers will now aim to answer is how the pathogen manages to spread globally. Their current study has shown that not only can it spread between individuals within specialist centres, but it has also been able to spread from continent to continent. ̽��ֱ��mechanism for this is unclear, but the researchers speculate that healthy individuals may be unwittingly carrying the mycobacteria between countries.

̽��ֱ��sequencing data has also revealed potential new drug targets, and the team is now focused on working with other groups at the ̽��ֱ�� of Cambridge and Colorado State ̽��ֱ�� to develop these further.

Dr Janet Allen, Director of Strategic Innovation at the CF Trust, said: “This paper highlights the risks posed through transmission of multi-drug resistant organisms between people with cystic fibrosis. ̽��ֱ��team in Cambridge are a world authority in this area. This work demonstrates the global threat of this infection, the risks of cross-infection within and between CF centres, and the need for improved surveillance. This study exemplifies the enormous impact of CF Trust-funded Strategic Research Centres, which were designed to generate world-class research with the very highest impact. Without the support of the CF community, this landmark study would not have been possible.”

Around one in 2,500 children in the UK is born with cystic fibrosis, a hereditary condition that causes the lungs to become clogged up with thick, sticky mucus. ̽��ֱ��condition tends to decrease life expectancy among patients.

̽��ֱ��research was funded by the Wellcome Trust and the UK Cystic Fibrosis Trust.

Reference
Bryant, JM et al. Emergence and spread of a human transmissible multidrug-resistant nontuberculous mycobacterium. Science; 11 Nov 2016; DOI: 10.1126/science.aaf8156

A multi-drug resistant infection that can cause life-threatening illness in people with cystic fibrosis (CF) and can spread from patient to patient has spread globally and is becoming increasingly virulent, according to new research published today in the journal Science.

Our research should provide a degree of hope: now that we know the extent of the problem and are beginning to understand how the infection spreads, we can start to respond

Julian Parkhill

Hey Paul Studios

Blue and Brown Anatomical Lung Wall Decor. Hand Embroidery Applique by Hey Paul Studios

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

Yes

Licence type:

Attribution