̽��ֱ�� of Cambridge - bacteria

Tiny ‘skyscrapers’ help bacteria convert sunlight into electricity

sc604 — Mon, 07 Mar 2022 16:00:00 +0000

̽��ֱ��researchers, from the ̽��ֱ�� of Cambridge, used 3D printing to create grids of high-rise ‘nano-housing’ where sun-loving bacteria can grow quickly. ̽��ֱ��researchers were then able to extract the bacteria’s waste electrons, left over from photosynthesis, which could be used to power small electronics.

Other research teams have extracted energy from photosynthetic bacteria, but the Cambridge researchers have found that providing them with the right kind of home increases the amount of energy they can extract by over an order of magnitude. ̽��ֱ��approach is competitive against traditional methods of renewable bioenergy generation and has already reached solar conversion efficiencies that can outcompete many current methods of biofuel generation.

Their results, reported in the journal Nature Materials, open new avenues in bioenergy generation and suggest that ‘biohybrid’ sources of solar energy could be an important component in the zero-carbon energy mix.

Current renewable technologies, such as silicon-based solar cells and biofuels, are far superior to fossil fuels in terms of carbon emissions, but they also have limitations, such as a reliance on mining, challenges in recycling, and a reliance on farming and land use, which results in biodiversity loss.

“Our approach is a step towards making even more sustainable renewable energy devices for the future,” said Dr Jenny Zhang from the Yusuf Hamied Department of Chemistry, who led the research.

Zhang and her colleagues from the Department of Biochemistry and the Department of Materials Science and Metallurgy are working to rethink bioenergy into something that is sustainable and scalable.

Photosynthetic bacteria, or cyanobacteria, are the most abundant life from on Earth. For several years, researchers have been attempting to ‘re-wire’ the photosynthesis mechanisms of cyanobacteria in order to extract energy from them.

“There’s been a bottleneck in terms of how much energy you can actually extract from photosynthetic systems, but no one understood where the bottleneck was,” said Zhang. “Most scientists assumed that the bottleneck was on the biological side, in the bacteria, but we’ve found that a substantial bottleneck is actually on the material side.”

In order to grow, cyanobacteria need lots of sunlight – like the surface of a lake in summertime. And in order to extract the energy they produce through photosynthesis, the bacteria need to be attached to electrodes.

̽��ֱ��Cambridge team 3D-printed custom electrodes out of metal oxide nanoparticles that are tailored to work with the cyanobacteria as they perform photosynthesis. ̽��ֱ��electrodes were printed as highly branched, densely packed pillar structures, like a tiny city.

Zhang’s team developed a printing technique that allows control over multiple length scales, making the structures highly customisable, which could benefit a wide range of fields.

“ ̽��ֱ��electrodes have excellent light-handling properties, like a high-rise apartment with lots of windows,” said Zhang. “Cyanobacteria need something they can attach to and form a community with their neighbours. Our electrodes allow for a balance between lots of surface area and lots of light – like a glass skyscraper.”

Once the self-assembling cyanobacteria were in their new ‘wired’ home, the researchers found that they were more efficient than other current bioenergy technologies, such as biofuels. ̽��ֱ��technique increased the amount of energy extracted by over an order of magnitude over other methods for producing bioenergy from photosynthesis.

“I was surprised we were able to achieve the numbers we did – similar numbers have been predicted for many years, but this is the first time that these numbers have been shown experimentally,” said Zhang. “Cyanobacteria are versatile chemical factories. Our approach allows us to tap into their energy conversion pathway at an early point, which helps us understand how they carry out energy conversion so we can use their natural pathways for renewable fuel or chemical generation.”

̽��ֱ��research was supported in part by the Biotechnology and Biological Sciences Research Council, the Cambridge Trust, the Isaac Newton Trust and the European Research Council. Jenny Zhang is BBSRC David Phillips Fellow in the Department of Chemistry, and a Fellow of Corpus Christi College, Cambridge.

Reference:
Xiaolong Chen et al. ‘3D-printed hierarchical pillar array electrodes for high performance semi-artificial photosynthesis.’ Nature Materials (2022). DOI: 10.1038/s41563-022-01205-5

Researchers have made tiny ‘skyscrapers’ for communities of bacteria, helping them to generate electricity from just sunlight and water.

Our approach is a step towards making even more sustainable renewable energy devices for the future

Jenny Zhang

Gabriella Bocchetti

3D-printed custom electrodes

̽��ֱ��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

Identification of viruses and bacteria could be sped up through computational methods

sc604 — Mon, 30 Mar 2020 19:00:00 +0000

̽��ֱ��researchers, led by the ̽��ֱ�� of Edinburgh, with colleagues from Cambridge, London, Slovenia and China, used a combination of theoretical and experimental methods to develop a strategy to detect the DNA of infectious diseases. ̽��ֱ��results are reported in the Proceedings of the National Academy of Sciences.

̽��ֱ��current coronavirus pandemic highlights the need for fast and accurate detection of infectious diseases. Importantly, viral infections like coronavirus and bacterial infections like those associated with antimicrobial resistance (AMR) need to be distinguished. This is usually done by using a complementary sequence that binds selectively to the genome of interest. Normally, this is done by targeting a single, long DNA sequence that is unique to the pathogen.

However, the researchers believe that much higher selectivities can be achieved by simultaneously targeting many shorter sequences that occur with a higher frequency in the pathogen of interest than in the DNA of other organisms that may be present in the patient samples.

"This approach exploits a phenomenon called ‘multivalency’, and the extensive numerical calculations, based on real bacterial and viral DNA sequences show that this approach should significantly outperform current approaches," said co-author Professor Erika Eiser from Cambridge’s Cavendish Laboratory. "Even though the individual shorter sequences bind more weakly to the target DNA than a single, longer sequences, the strength of the multivalent binding increases much faster than linearly with the number of short sequences."

In other words, instead of designing molecular probes that bind strongly to one place on the target DNA, researchers should, counterintuitively, design probes that bind weakly all over the target DNA. Making such relatively short probe sequences is, at present, a standard procedure and the sequences can be ordered online.

̽��ֱ��experimental part of the project started with experiments in Cambridge, showing that the method can work in principle on a mixture of viral DNA and colloids coated with short complementary strands. Then the simulations took over to predict what combination of probe sequences would give the highest selectivity.

This part of the project has so far only been tested in computer models. ̽��ֱ��next step is to carry out experiments on real mixtures of viral and bacterial DNA.

"Experiments are needed to test how well this works in practice – but it is exciting work, given the urgent need for fast, reliable disease detection methods, especially those that can be applied in countries with a weak health infrastructure," said Professor Rosalind Allen from the ̽��ֱ�� of Edinburgh, who led the research.

This work was performed before the COVID-19 pandemic. However, the current emergency illustrates the need for robust and highly selective methods to quickly identify specific viruses – particularly in ‘low-tech’ environments.

̽��ֱ��research was funded in part by the Royal Society and the European Research Council.

Reference:
Tine Curk et al. ‘Computational design of probes to detect bacterial genomes by multivalent binding.’ PNAS (2020). DOI: 10.1073/pnas.1918274117

Adapted from a ̽��ֱ�� of Edinburgh press release.

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A new multinational study has shown how the process of distinguishing viruses and bacteria could be accelerated through the use of computational methods.

Yes

In living colour: Brightly-coloured bacteria could be used to 'grow' paints and coatings

sc604 — Tue, 20 Feb 2018 09:06:20 +0000

̽��ֱ��study is a collaboration between the ̽��ֱ�� of Cambridge and Dutch company Hoekmine BV and shows how genetics can change the colour, and appearance, of certain types of bacteria. ̽��ֱ��results open up the possibility of harvesting these bacteria for the large-scale manufacturing of nanostructured materials: biodegradable, non-toxic paints could be 'grown' and not made, for example.

Flavobacterium is a type of bacteria that packs together in colonies that produce striking metallic colours, which come not from pigments, but from their internal structure, which reflects light at certain wavelengths. Scientists are still puzzled as to how these intricate structures are genetically engineered by nature, however.

"It is crucial to map the genes responsible for the structural colouration for further understanding of how nanostructures are engineered in nature," said first author Villads Egede Johansen, from Cambridge's Department of Chemistry. "This is the first systematic study of the genes underpinning structural colours -- not only in bacteria but in any living system."

̽��ֱ��researchers compared the genetic information to optical properties and anatomy of wild-type and mutated bacterial colonies to understand how genes regulate the colour of the colony.

By genetically mutating the bacteria, the researchers changed their dimensions or their ability to move, which altered the geometry of the colonies. By changing the geometry, they changed the colour: they changed the original metallic green colour of the colony in the entire visible range from blue to red. They were also able to create duller colouration or make the colour disappear entirely.

"We mapped several genes with previously unknown functions and we correlated them to the colonies' self-organisational capacity and their colouration," said senior author Dr Colin Ingham, CEO of Hoekmine BV.

"From an applied perspective, this bacterial system allows us to achieve tuneable living photonic structures that can be reproduced in abundance, avoiding traditional nanofabrication methods," said co-senior author Dr Silvia Vignolini from the Cambridge's Department of Chemistry. "We see a potential in the use of such bacterial colonies as photonic pigments that can be readily optimised for changing colouration under external stimuli and that can interface with other living tissues, thereby adapting to variable environments. ̽��ֱ��future is open for biodegradable paints on our cars and walls -- simply by growing exactly the colour and appearance we want!"

Reference:
Villads Egede Johansen et al. 'Livingcolors: Genetic manipulation of structural color in bacterial colonies.' PNAS (2018). DOI: 10.1073/pnas.1716214115

Researchers have unlocked the genetic code behind some of the brightest and most vibrant colours in nature. ̽��ֱ��paper, published in the journal PNAS, is the first study of the genetics of structural colour - as seen in butterfly wings and peacock feathers - and paves the way for genetic research in a variety of structurally coloured organisms.

This is the first systematic study of the genes underpinning structural colours -- not only in bacteria but in any living system.

Villads Egede Johansen

Dr Colin Ingham (Hoekmine BV)

Colony of the Flavobacterium IR1

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

Yes

Postgraduate Pioneers 2017 #1

ta385 — Tue, 17 Oct 2017 10:00:00 +0000

First in the series is Himansha Singh, a Pharmacologist from India whose research aims to help tackle antimicrobial resistance.

My research sets out to

Today, we can survive an organ transplant but then die because of a bacterial infection. ̽��ֱ��rise of antimicrobial resistance (AMR) and ‘superbugs’, along with the lack of antibiotic development in the last decades, is a major concern for global healthcare. Whilst there are several mechanisms responsible for AMR, our research group is examining multidrug efflux pumps or transporters that expel drugs rendering bacteria resistant to a broad range of antibiotics.

While we know some things about the architecture of bacteria, we don’t fully understand how they conduct transportation of antibiotics. If we could understand their operating system, we could develop compounds, which might help switching off the system and stop them from rejecting antibiotics. In particular, my project is looking into a very interesting E.coli ATP-binding cassette (ABC) transporter MsbA. We are working towards characterising how this protein uses energy to operate dynamic changes in its structure to facilitate drug transport.

My Motivation

During my master's degree, I worked with AstraZeneca and my neighbouring lab was working on transporters in drug development. Their work caught my attention. I also visited India that summer and my hometown, Gwalior, in Madhya Pradesh, was suffering a severe outbreak of tuberculosis and typhoid. These experiences exposed me to the seriousness of antibiotic resistance. Transporters play a huge role in this and after reading up on the topic, I looked for a relevant PhD project and was delighted to be accepted into Dr Hendrik W. van Veen's lab to work on various transporters, both in humans and bacteria.

Day-to-day

I am based in the Department of Pharmacology, which is in the city center – it’s a great location. I work in a team of ten and my average day in the lab is spent working on culturing liters of bacterial cells to extract MsbA and reconstitute it in artificial lipid membranes. I then test MsbA activity under different energy conditions and drugs, or test different inhibitors.

My best days

That has to be when we first noticed that the ATP dependent transporter MsbA could also work without ATP. ATP is an energy currency of cells and ABC transporters, such as MsbA, utilize it as their main source of power for drug transport. But we showed that MsbA is also dependent on another form of energy source, an electrochemical gradient. In fact, MsbA cannot function without the involvement of both of these power sources. That brought a paradigm shift in our understanding of translocation by MsbA, which may lead us to new ways to tackle bacteria.

I hope my work will lead to

Apart from being a multidrug transporter, MsbA is an essential membrane protein that transports phospholipids in E.coli to form its cell membrane; so inhibiting this pump is clinically important to develop or establish foundations for a new class of antibiotics against E.coli. We can only design inhibitors if we know the fundamental basis of their transport mechanism and I hope my PhD research will provide some insight into this. We believe that our findings will be of great interest to the wider scientific community.

It had to be Cambridge because

My supervisor, Dr. Hendrik W. van Veen has played a crucial role in developing my enthusiasm for scientific research. And Cambridge has provided a tight-knit, supportive and stimulating intellectual environment which has shaped my career and understanding of academia in really important ways. Other than benefiting from the world-class research facilities in my lab and department, I’ve been able to immerse myself in Cambridge’s rich culture and exciting critical atmosphere. ̽��ֱ��collegiate system also ensures a thriving social life and this paved the way for me to develop interests in various other disciplines over formal dinners and drinks in our college bars.

In 2017, Himansha Singh was one of twelve PhD students to win an award from the Cambridge Society for the Application of Research.

With our Postgraduate Open Day fast approaching (3 Nov), we introduce five PhD students who are already making waves at Cambridge.

I have benefited from world-class research facilities and immersed myself in Cambridge’s rich culture.

Himansha Singh

Himansha Singh, Dept of Pharmacology

Postgraduate Open Day

For more information about the ̽��ֱ��'s Postgraduate Open Day on 3rd November 2017 and to book to attend, please click here.

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

Yes

̽��ֱ��bug hunters and the microbiome

lw355 — Wed, 21 Jun 2017 11:00:54 +0000

Their microbial quarry gives Dr Trevor Lawley and Professor Gordon Dougan an interesting take on the world and human interaction. When we meet at the Wellcome Trust Sanger Institute, where they both lead research groups, we shake hands. For me, it’s a social norm; for them, it’s a chance to swap bugs.

“When we shook hands, you probably got some of my spores and I got some of yours. It’s a form of kinship that we are just starting to understand,” says Lawley. “When we think about spreading bugs, we often focus on pathogens and disease. ̽��ֱ��truth is, pathogens are a tiny proportion of the whole community of diverse microorganisms that are on and within us and there’s probably an element of spreading health through this microbiome.”

̽��ֱ��microorganisms live on our skin, up our noses and – in particularly large numbers – in our gut. ̽��ֱ��average human intestine harbours some 100 trillion bacteria from 1,000 species. They have around three million genes and make up 3% of our body weight. “We’re coated with microorganisms – bacteria, viruses, fungi – they outnumber human cells by at least three to one, so we’re more microbial than eukaryotic,” he explains.

So what are they all doing there? Although much remains a mystery, we know that changes in the microbiome appear to be linked with health and disease. They produce vitamins we cannot make ourselves and break down food to extract essential nutrients; and they help our immune systems develop and defend us against harmful bugs.

It seems that as well as being a community, our microbiome is also like an organ or tissue. “Some 30–40% of metabolites in our blood come from microbes in the intestine, so lots of our physiology and wellbeing is probably driven by factors in the gut that we don’t fully appreciate,” says Dougan, who holds a Chair in Cambridge’s Department of Medicine. “But we’re starting to realise that several human diseases are caused by pathological imbalances in these microbial communities, and that genetics, diet, antibiotics and infections can create these imbalances.”

̽��ֱ��idea that our microbiome contributes to our health is not new. In 1908, the Russian microbiologist Ilya Mechnikov won a Nobel Prize for his discovery of phagocytes. He also sought to nurture his microbiota by consuming copious quantities of fermented milk, having noticed the longevity of yoghurt-loving Bulgarians.

Since then, the microbiome has been implicated in many areas of health and disease. “Evidence is accumulating that our microbiota can protect us against infection and inflammatory diseases of the bowel, influence factors such as obesity, and that bad microbiota, such as Clostridium difficile, can damage us,” Dougan explains. C. diff is a key part of this story. First described in the 1930s, C. diff lives in the gut of around 3% of healthy adults and, kept in check by a healthy microbiota, it does no damage. When antibiotics disrupt the microbiota, however, C. diff can be life threatening, especially among frail, elderly adults in hospitals and care homes.

In such circumstances what works best is not more antibiotics, but reintroducing gut bugs from healthy volunteers via faecal transplants. While not the most marketable of treatments, its astonishing success led Lawley and Dougan to believe that the microbiome could be an important therapeutic target.

“When I started training in Gordon’s lab ten years ago, we realised that faecal transplants could cure 90% of people with C. diff who had failed standard antibiotic treatment,” says Lawley. “That’s when we started to think that if we could identify the good bugs, we could make a medicine.”

Unfortunately, identifying the good bugs is harder than it sounds and for many years researchers lacked the necessary tools to culture them, characterise them and chart their modes of action.

Three recent advances changed all that. Genomics has helped us understand the microbiome as a whole. In 2003, scientists at Stanford ̽��ֱ�� sequenced the gut microbiome (the collective genomes of all resident microorganisms) of healthy human volunteers for the first time, and 2008 saw the establishment of the Human Microbiome Project (a United States National Institutes of Health initiative). Then, germ-free mice provided researchers with a model system to test their ideas. Finally, Lawley discovered a way of growing gut bacteria in the lab – something that for decades was thought impossible.

“One of the things we had to overcome – a dogma as well as a technical barrier – was to culture the unculturable,” he says. “Now, we are culturing at scale and sequencing. This means we have access to the bugs to follow up and work out what they do, and then even to make a medicine from.”

Buoyed by their success, the Sanger Institute last year spun out a new company – Microbiotica – to exploit their unique capabilities in microbiome science, particularly in culture collection, genome database and animal models, to develop new medicines.

“We’re collecting samples of poo from around the world – from Vietnam and India to Nigeria and Kenya – to build a globally representative collection of microbiome bacteria. No-one else has such a large and diverse collection,” Dougan says. “It will allow us to mine these isolates – and their genomes – for new antibiotics and design new bacterial-based therapies.”

As well as finding a more palatable alternative to faecal transplants for C. diff infections, Lawley and Dougan have their sights set on using bugs as drugs in other areas. There is strong evidence that both inflammatory bowel disease (which affects around 0.5% of the population) and irritable bowel syndrome (which affects 15–20%) result from a damaged microbiome, so these conditions are prime candidates.

Lawley and Dougan are also working with Imperial College London to study links between the lung microbiome and chronic obstructive pulmonary disease and asthma, as well as the microbiome differences of babies born by C-section versus vaginal delivery. They are also working with American collaborators on the bladder, where the hallmark of a healthy microbiome is very different to that of the gut.

“In the gut, the signature of health is diverse microbes. In the vagina and the bladder, it’s the opposite – simplified is healthy. Once they become diverse, there’s something wrong,” explains Lawley, who is also Chief Scientific Officer at Microbiotica.

̽��ֱ��researchers are also working on some cancers for which modern immunotherapies are successful against the disease but cannot be used in some patients because they damage the microbiome so badly. “We’re involved in MelResist, a multi-university collaboration on new therapies for melanoma. Long-term survival in melanoma patients treated with antibody therapies is now a remarkable 50%,” says Lawley. “But if they have two different antibodies, they can develop life-threatening diarrhoea and colitis and have to stop treatment – we think there’s a microbiome element there.”

It’s a far cry from Bulgarian yoghurt, and while there’s much science yet to be done, and many regulatory challenges to bring an entirely new kind of medicine to market, it’s a challenge they relish. “We want to innovate and encourage links and partnerships with other organisations,” Dougan concludes. “It’s a whole new science – but we’re confident that we can deliver new medicines.”

Inset images: Trevor Lawley (left) and Gordon Dougan; credit: Wellcome Trust Sanger Institute.

Read more about research on future therapeutics in Research Horizons magazine.

Trevor Lawley and Gordon Dougan are bug hunters, albeit not the conventional kind. ̽��ֱ��bugs they collect are invisible to the naked eye. And even though we’re teeming with them, researchers are only beginning to discover how they keep us healthy – and how we could use these bugs as drugs.

When we think about spreading bugs, we often focus on pathogens and disease. ̽��ֱ��truth is, there’s probably an element of spreading health through this microbiome.

Trevor Lawley

Jonathan Settle

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

Yes

Bacteria in the world’s oceans produce millions of tonnes of hydrocarbons each year

sc604 — Mon, 05 Oct 2015 19:00:00 +0000

An international team of researchers, led by the ̽��ֱ�� of Cambridge, has estimated the amount of hydrocarbons – the primary ingredient in crude oil – that are produced by a massive population of photosynthetic marine microbes, called cyanobacteria. These organisms in turn support another population of bacteria that ‘feed’ on these compounds.

In the study, conducted in collaboration with researchers from the ̽��ֱ�� of Warwick and MIT, and published today (5 October) in the journal Proceedings of the National Academy of Sciences of the USA, the scientists measured the amount of hydrocarbons in a range of laboratory-grown cyanobacteria and used the data to estimate the amount produced in the oceans.

Although each individual cell contains minuscule quantities of hydrocarbons, the researchers estimated that the amount produced by two of the most abundant cyanobacteria in the world – Prochlorococcus and Synechococcus – is more than two million tonnes in the ocean at any one time. This indicates that these two groups alone produce between 300 and 800 million tonnes of hydrocarbons per year, yet the concentration at any time in unpolluted areas of the oceans is tiny, thanks to other bacteria that break down the hydrocarbons as they are produced.

“Hydrocarbons are ubiquitous in the oceans, even in areas with minimal crude oil pollution, but what hadn’t been recognised until now is the likely quantity produced continually by living oceanic organisms,” said Professor Christopher Howe from Cambridge’s Department of Biochemistry, the paper’s senior author. “Based on our laboratory studies, we believe that at least two groups of cyanobacteria are responsible for the production of massive amounts of hydrocarbons, and this supports other bacteria that break down the hydrocarbons as they are produced.”

̽��ֱ��scientists argue that the cyanobacteria are key players in an important biogeochemical cycle, which they refer to as the short-term hydrocarbon cycle. ̽��ֱ��study suggests that the amount of hydrocarbons produced by cyanobacteria dwarfs the amount of crude oil released into the seas by natural seepage or accidental oil spills.

However, the hydrocarbons produced by cyanobacteria are continually broken down by other bacteria, keeping the overall concentrations low. When an event such as an oil spill occurs, hydrocarbon-degrading bacteria are known to spring into action, with their numbers rapidly expanding, fuelled by the sudden local increase in their primary source of energy.

̽��ֱ��researchers caution that their results do not in any way diminish the enormous harm caused by oil spills. Although some microorganisms are known to break down hydrocarbons in oil spills, they cannot repair the damage done to marine life, seabirds and coastal ecosystems.

“Oil spills cause widespread damage, but some parts of the marine environment recover faster than others,” said Dr David Lea-Smith, a postdoctoral researcher in the Department of Biochemistry, and the paper’s lead author. “This cycle is like an insurance policy – the hydrocarbon-producing and hydrocarbon-degrading bacteria exist in equilibrium with each other, and the latter multiply if and when an oil spill happens. However, these bacteria cannot reverse the damage to ecosystems which oil spills cause.”

̽��ֱ��researchers stress the need to test if their findings are supported by direct measurements on cyanobacteria growing in the oceans. They are also interested in the possibility of harnessing the hydrocarbon production potential of cyanobacteria industrially as a possible source of fuel in the future, although such work is at a very early stage.

Reference:
Lea-Smith, D. et. al. “Contribution of cyanobacterial alkane production to the ocean hydrocarbon cycle.” PNAS (2015). DOI: 10.1073/pnas.1507274112

Scientists have calculated that millions of tonnes of hydrocarbons are produced annually by photosynthetic bacteria in the world’s oceans.

This cycle is like an insurance policy – the hydrocarbon-producing and hydrocarbon-degrading bacteria exist in equilibrium with each other

David Lea-Smith

Image courtesy SeaWiFS Project

Global chlorophyll

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

Yes

Food poisoning: the bacteria lurking in your chicken

amb206 — Wed, 17 Jun 2015 12:52:44 +0000

Scroll to the end of the article to listen to the podcast.

Poultry is an important source of protein; almost half the meat we eat in the UK is chicken. And the popularity of chicken is rising: it’s convenient, tasty and cheap. On average we eat around 190g per person per week. Poultry, however, harbours a hidden problem. Around two-thirds of raw chicken sold by British retailers is infected with bacteria called Campylobacter.

Campylobacter is ubiquitous in the environment. All chicken flocks, large or small, factory-farmed or free range, are susceptible to infection. ̽��ֱ��bacteria have the ability to survive the production chain from farm to fork.

Adequate cooking, however, kills the bacteria and makes chicken safe to eat. Consumers are advised not to wash chicken before cooking and to follow basic hygiene rules when handling raw chicken.

If Campylobacter is ingested by humans, it can lead to diarrhoea. Four out of five cases of food poisoning in the UK can be traced to poultry; sickness from Campylobacter costs the economy an estimated £900 million each year. Recovery can take a week or more, and infection with the bacteria is also associated with serious complications – including reactive arthritis and Guillain-Barré Syndrome.

These facts are the driving force behind research being undertaken by microbiologists Dr Andrew Grant, Professor Duncan Maskell and their groups at the Department of Veterinary Medicine. “Campylobacter is the leading source of bacterial gastroenteritis, affecting half a million people and killing an estimated 100 people each year in the UK,” says Grant. “This is why it’s a major target for research efforts.”

Poultry is big business. Production units supplying the major supermarkets can house 50,000 birds or more. Even when stringent biosecurity measures are taken, incursions occur when barriers are broken. “It takes just a couple of bacteria, or perhaps even one, entering a unit for a flock of thousands of birds to be infected in less than a week,” says Grant. “ ̽��ֱ��chicken gut is the ideal vessel for Campylobacter to flourish. Transmission is guaranteed by a continual process of consumption and excretion known as coprophagy.”

There are no vaccines – either for poultry or humans – to protect against Campylobacter. ̽��ֱ��ubiquity and resilience of Campylobacter jejuni (the strain that colonises poultry and causes most gastroenteritis in humans) have prompted a government-led push to reduce the level of infection by developing ways in which to contain, and ultimately eliminate, its presence in the nation’s most popular meat.

“We need to look at the problem both on an industry-wide scale and on a microbial scale. ̽��ֱ��first approach involves working hand-in-hand with producers and processors and the second working in the lab to understand the structure and behaviour of Campylobacter,” says Grant.

“Working with the industry, we’re building a picture of the highly dynamic process of transmission from one bird to another and also at the ways in which Campylobacter is spread during slaughtering and processing. In the lab we’re looking at how we can manipulate Campylobacter so that it can’t spread – essentially we’re trying to identify and target its Achilles heel.”

One avenue being explored is the identification of the Campylobacter genes required for chicken colonisation, which could make good targets for therapeutic intervention. Another approach is to disarm Campylobacter by altering its characteristic shape from spiral to rod-shaped. Once rod shaped it loses its ability to colonise chickens and cause disease in humans.

Scientists working on Campylobacter face formidable challenges. Highly successful in the environments where it thrives best, the bug is difficult to culture in the lab where scientists need to work with live bacteria.

In the food production and retailing sectors, a reluctance to take ownership of the problem has led to lack of investment in measures to address an issue that each sector sees as the other’s problem. ̽��ֱ��profit margins made by farmers are tiny – as low as one or two pence per bird produced. ̽��ֱ��onus therefore is seen to lie with processors and retailers to invest in intervention and control strategies.

There is a mounting sense of urgency in the drive to eliminate Campylobacter from the nation’s food chain. Incidents of Campylobacter food poisoning are continuing to rise. Around 75,000 cases per year are ‘culture confirmed’ and, due to under-reporting, the true total is estimated to be equivalent to at least 460,000, and possibly 750,000, cases.

“Campylobacter found in raw chicken sold to consumers is generally on the surface of the birds, which means that adequate cooking quickly destroys the bacteria. But we now think that it might be entering chickens’ muscle tissue and internal organs,” says Grant.

“Infection by Campylobacter is considered to be the most prevalent cause of bacterial diarrhoeal disease worldwide. Compared to many other pathogens we know comparatively little about the bacteria and there are still many more questions than answers. There is a need for alternative strategies to reduce Campylobacter in chickens and Campylobacter-induced disease burden in humans.”

Next in the Cambridge Animal Alphabet: D is for a creature that prowls the Museum of Archaeology and Anthropology, confronts students in the Department of Anglo-Saxon, Norse and Celtic, and was a fertile symbol for medieval poets.

Inset images: Raw chicken in a pot (eltpics); Campylobacter jejuni (Andrew Grant).

The Cambridge Animal Alphabet series celebrates Cambridge's connections with animals through literature, art, science and society. Here, C is for Chicken – a popular source of protein that carries a hidden hazard in the form of Campylobacter.

In the lab we’re looking at how we can manipulate Campylobacter so that it can’t spread – we’re trying to identify and target its Achilles heel

Andrew Grant

U.S Department of Agriculture

Broiler chickens

̽��ֱ��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

Cambridge partners with India to fight multidrug resistant TB

Anonymous — Fri, 13 Feb 2015 16:30:42 +0000

̽��ֱ��Cambridge-Chennai Centre Partnership on Antimicrobial Resistant Tuberculosis will bring together a multidisciplinary team of international researchers, and will be led by Professor Sharon Peacock and Dr Soumya Swaminathan. ̽��ֱ��team, including Professors Lalita Ramakrishnan, Ken Smith, Tom Blundell and Andres Floto, will focus on developing new diagnostic tools and treatments to address the sharp rise in cases of multidrug resistant tuberculosis (TB).

This will include research into:

the use of emerging sequence-based diagnostics to improve the accuracy of individual patient treatment for drug resistant TB
predicting the impact of genetic mutations on drug resistance based on modelling of bacterial genome data
the development of an in-depth understanding of bacterial genes associated with so-called ‘drug-tolerance’, where the drug’s ability to kill the bacteria gradually weakens
novel approaches to treatment of TB based on enhancing the body’s immune system to enable it to fight infection.

̽��ֱ��partnership will generate a rich and lasting clinical and genomic dataset for studying TB, and the transfer of scientific training and technology will foster future international collaborative projects.

“I am delighted that Cambridge has been given the opportunity to work on a disease of global importance through the development of this partnership,” said Professor Sharon Peacock. “Chennai was the site for many of the early MRC-funded TB treatment trials, and the chance to explore new therapies and diagnostics to improve patient outcome through the use of state-of-the-art technologies represents an exciting opportunity.”

̽��ֱ��funding is part of a landmark collaboration between the MRC and the Government of India DBT. Nearly £3.5million will be invested by the UK, through the MRC and the Newton Fund, a new initiative intended to strengthen research and innovation partnerships between the UK and emerging knowledge economies, with matched funding provided by DBT.

Prof K. VijayRaghavan, Secretary, Department of Biotechnology added: “ ̽��ֱ��Department of Biotechnology, Government of India is delighted to partner with the MRC in creating research centres which will address vexing challenges in medicine through quality science and collaboration. India is committed to working with the best in the world, for India and for the world. We are acutely aware that the fruits of our partnership can mean better lives for the most- needy everywhere and are committed to make the collaboration succeed.”

̽��ֱ�� ̽��ֱ�� of Cambridge has been awarded £2 million from the UK Medical Research Council and the Government of India’s Department for Biotechnology to develop a partnership with the National Institute for Research in Tuberculosis (NIRT) in Chennai.

I am delighted that Cambridge has been given the opportunity to work on a disease of global importance through the development of this partnership

Sharon Peacock

CDC/ Melissa Brower

This illustration depicts a three-dimensional (3D) computer-generated image of a cluster of rod-shaped drug-resistant Mycobacterium tuberculosis bacteria, the pathogen responsible for causing the disease tuberculosis (TB). ̽��ֱ��artistic recreation was base

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