Saturday, 11 June 2011

German tests link bean sprouts to deadly E. coli

German tests link bean sprouts to deadly E. coli

Bean sprouts and salad sprouts (file picture) It is believed the bean sprouts were produced in Germany

New data released in Germany strongly suggests that locally produced bean sprouts were, as suspected, the source of the deadly E. coli outbreak.

"It's the bean sprouts," said Reinhard Burger, head of Germany's centre for disease control.

Officials initially blamed the E. coli, which has killed 29 people, on imported cucumbers, then bean sprouts.

In another development, Russia agreed to lift its ban on imports of EU fresh vegetables in return for guarantees.

The Russian ban had compounded a crisis for EU vegetable-growers, with Spanish cucumber producers wrongly blamed for the contamination.

Mr Burger, who heads the Robert Koch Institute, told reporters on Friday that even though no tests of the sprouts from a farm in Lower Saxony had come back positive, the epidemiological investigation of the pattern of the outbreak had produced enough evidence to draw the conclusion.

The institute, he added, was lifting its warning against eating cucumbers, tomatoes and lettuce, but keeping it in place for the sprouts.

Some 3,000 people have been taken ill with the German outbreak of E. coli, which involves a previously unknown strain of the bacterium.

Sufferers may develop haemolytic uraemic syndrome (HUS) where bacteria attack the kidneys and nervous system, giving them fits and often forcing them on to dialysis.

'Hot lead'
A Robert Koch Institute team in protective gear inspect the organic farm in Bienenbuettel, 6 June Robert Koch Institute researchers have been examining the farm in Bienenbuettel

"People who ate sprouts were nine times more likely to have bloody diarrhoea than those who did not," Mr Burger said.

Germany's top disease control official said the origin of the contamination was still believed to be the small organic farm in Lower Saxony which first came under suspicion at the weekend.

"The links are ever clearer - it's a hot lead," he told reporters in Berlin, at a joint news conference with the heads of Germany's federal institute for risk assessment and federal office for consumer protection.

He said it was possible that all tainted sprouts had now either been consumed or thrown away, but he warned the crisis was not yet over.

"There will be new cases coming up," he said.

"Thousands of tests carried out on tomatoes, cucumbers and lettuce have proved negative," he added.

Lower Saxony agriculture minister Gert Lindemann said earlier this week that experts had found no traces of the E. coli bacterium strain at the Bienenbuettel farm but he did not rule it out as the source of the contamination.

In an interview to be published in next week's edition of Focus magazine, Mr Lindemann said some 60 of the people taken ill had eaten sprouts from the farm, which employs about 15 people.

Contamination might have been caused by contaminated seeds or "poor hygiene", he added.

Ban to be lifted

The agreement to lift the Russian ban was announced after talks between top EU officials including the Commission chief, Jose Manuel Barroso, and Russian counterparts in the central Russian city of Nizhny Novgorod.

Health advice

  • Wash fruit and vegetables before eating them
  • Peel or cook fruit and vegetables
  • Wash hands regularly to prevent person-to-person spread of E. coli strain

Source: UK Health Protection Agency

"We are ready to resume the shipments under guarantees of the EU authorities," President Dmitry Medvedev told reporters.

Russia's top food safety officer, Gennady Onishchenko, said Russia would lift its prohibition after receiving food safety guarantees from the European Commission.

Mr Barroso said the EU would send a form for issuing food safety certificates to Russia in the next few days.

According to the Commission, the total value of EU exports of fresh vegetables to Russia is 600m euros (£530m; $870m) a year, a quarter of the total exported.

Spain, France, Germany and Poland are the biggest exporters.

More on This Story

Climate sceptics rally to expose 'myth'


Global warming since 1995 'now significant'

Banksy artwork Phil Jones's comments last year have become a touchstone for climate "sceptics"


Climate warming since 1995 is now statistically significant, according to Phil Jones, the UK scientist targeted in the "ClimateGate" affair.
Last year, he told BBC News that post-1995 warming was not significant - a statement still seen on blogs critical of the idea of man-made climate change.
But another year of data has pushed the trend past the threshold usually used to assess whether trends are "real".
Dr Jones says this shows the importance of using longer records for analysis.

“Start Quote

It just shows the difficulty of achieving significance with a short time series”
End Quote Phil Jones
By widespread convention, scientists use a minimum threshold of 95% to assess whether a trend is likely to be down to an underlying cause, rather than emerging by chance.
If a trend meets the 95% threshold, it basically means that the odds of it being down to chance are less than one in 20.
Last year's analysis, which went to 2009, did not reach this threshold; but adding data for 2010 takes it over the line.
"The trend over the period 1995-2009 was significant at the 90% level, but wasn't significant at the standard 95% level that people use," Professor Jones told BBC News.
"Basically what's changed is one more year [of data]. That period 1995-2009 was just 15 years - and because of the uncertainty in estimating trends over short periods, an extra year has made that trend significant at the 95% level which is the traditional threshold that statisticians have used for many years.
"It just shows the difficulty of achieving significance with a short time series, and that's why longer series - 20 or 30 years - would be a much better way of estimating trends and getting significance on a consistent basis."
Professor Jones' previous comment, from a BBC interview in Febuary 2010, is routinely quoted - erroneously - as demonstration that the Earth's surface temperature is not rising.
Globally consistent
The dataset that Professor Jones helps to compile - HadCRUT3 - is a joint project between the Climatic Research Unit (CRU) at the University of East Anglia (UEA), where he is based, and the UK Met Office.
Phil Jones Phil Jones is back at the scientific helm of CRU, though relieved of administrative leadership
It is one of the main global temperature records used by bodies such as the Intergovernmental Panel on Climate Change (IPCC).
HadCRUT shows a warming 1995-2010 of 0.19C - consistent with the other major records, which all use slightly different ways of analysing the data in order to compensate for issues such as the dearth of measuring stations in polar regions.
Shortly before the UN climate summit in Copenhagen, Phil Jones found himself at the centre of the affair that came to be known as "ClimateGate", which saw the release of more than 1,000 emails taken from a CRU server.
Critics alleged the emails showed CRU scientists and others attempting to subvert the usual processes of science, and of manipulating data in order to paint an unfounded picture of globally rising temperatures.
Subsequent enquiries found the scientists and their institutions did fall short of best practice in areas such as routine use of professional statisticians and response to Freedom of Information requests, but found no case to answer on the charges of manipulation.
Since then, nothing has emerged through mainstream science to challenge the IPCC's basic picture of a world warming through greenhouse gas emissions.
And a new initiative to construct a global temperature record, based at Stanford University in California whose funders include "climate sceptical" organisations, has reached early conclusions that match established records closely.


Thursday, 9 June 2011

strain of MRSA that appears to spread to humans from cattle

“Scientists in the UK have discovered a new strain of MRSA that appears to spread to humans from cattle and can cause life-threatening illness,” reported The Guardian. It said that a study of dairy herds had found the drug-resistant strain in cows' milk.

MRSA (meticillin-resistant Staphylococcus aureus) is usually detected using a technique called antibiotic-susceptibility testing. Borderline cases of MRSA are confirmed with molecular testing, which detects the presence of a gene that is common to these “superbugs”.

This study looked at strains of MRSA from cattle and humans to see whether they possessed any new genetic features that affect the reliability of these tests.

The study found a new type of gene in many of the cattle samples. This gene makes the bacteria resistant to a range of antibiotics. While the bacteria with this gene showed up in antibiotic-susceptibility testing, molecular testing could not recognise the gene and failed to identify the bacteria as MRSA.

Therefore, if molecular testing is used to detect MRSA or to confirm borderline cases, it will not identify bacteria with the new gene.

The researchers say that only a small proportion of MRSA bacteria possess this gene. However, as it has been detected in MRSA samples from dairy cows, these animals might form a “reservoir of infection”. They warn that close links with farms or contact with dairy cattle could increase the risk of MRSA being transmitted to humans. Further studies are needed to inform tests for diagnosing MRSA.

Experts highlight that the main worry is that bacteria may colonise people who work on farms, and not that people may be at risk from drinking milk. As almost all milk sold in the UK is pasteurised, drinking or eating dairy products is reportedly “not a health concern”.

Where did the story come from?

The study was carried out by researchers from the Department of Veterinary Medicine at the University of Cambridge and other health and academic institutions in Cambridge and the UK.

Funding was provided by the Department for Environment, Food and Rural Affairs, the Higher Education Funding Council for England, the Isaac Newton Trust (University of Cambridge) and the Wellcome Trust.

The study was published in the peer-reviewed medical journalThe Lancet.

The news headlines have oversimplified this complex research and may imply that people are at risk from drinking milk, which is not the case. The main implications of these findings are in the field of laboratory and diagnostic testing.

What kind of research was this?

This laboratory study looked at strains of MRSA from samples taken from cattle and humans. The researchers wanted to see if they possessed any new genetic features that meant that they could not be detected by standard tests for diagnosing MRSA.

The researchers explained that animals are known to act as a “reservoir” for new strains of bacteria, so could be a source of new strains of the superbug MRSA (meticillin-resistant Staphylococcus aureus) in humans. Staphylococcus aureus causes a wide variety of infections in humans, from skin infections to pneumonia and blood poisoning. However, many people carry the bacteria harmlessly on their skin.

MRSA has developed resistance to meticillin and other penicillin antibiotics that would normally kill Staphylococcus aureus. This means that MRSA can cause disease that is harder to treat. It is believed that the Staphylococcus aureus bacteria evolved to develop this resistance by acquiring a certain chromosome element (called SCCmec) which contain a gene called mecA. This gene encodes a protein that binds to penicillin.

The researchers describe how MRSA is usually identified in the laboratory using “antimicrobial susceptibility testing”. In this test, the bacteria are incubated with discs that are impregnated with antibiotics. The zone around the disc where bacterial growth has been prevented is measured. There are standard zones around the disc that confirm the presence of MRSA. If the results are borderline, molecular testing (called PCR testing) is used to detect the mecA gene or penicillin-binding protein in the bacteria.

Before 2003, most cases of MRSA were associated with human transmission and infection, but after this time it was found in livestock. Evidence was also found that some strains may not be restricted to a single species but can cross between humans and farm animals. There is concern that farm animals could act as a reservoir for MRSA and that close human-animal contact could increase the risk of transmission.

What did the research involve?

The researchers took isolates (a pure strain that has been separated from a mixed bacterial culture) of MRSA bacteria from both humans and cows and determined whether antimicrobial susceptibility testing could detect the bacteria.

In 2007, the researchers obtained 24 isolates of bovine MRSA from the Veterinary Laboratories Agency in the UK. These came from a collection of 940 Staphylococcus aureus isolates obtained from the milk of 465 different herds of cows with mastitis, which had been submitted to the agency for testing.

Isolates of human MRSA were obtained from the Health Protection Agency and the Scottish MRSA Reference Laboratory in the UK, and the National MRSA Reference Laboratory in Denmark. The human bacteria had been cultured from blood samples or infected wound swabs.

The researchers carried out antimicrobial susceptibility testing on these bovine and human isolates, and used PCR testing to see whether the mecA gene could be detected.

What were the basic results?

A new mecA gene (called mecALGA251) was discovered in 15 of 24 Staphylococcus aureus isolates from dairy cattle in England. These isolates were from three different strains of MRSA. The new mecALGA251 gene was also identified in 12 of 16 isolates from human samples from Scotland, 15 of 26 isolates from England, and 24 of 32 isolates from Denmark.

Antibiotic-susceptibility testing identified that these isolates were resistant to a wide range of antibiotics. However, PCR testing showed negative results for the mecA gene and penicillin-binding protein. This suggests that if PCR testing is used on its own or to confirm the results of antibiotic-susceptibility testing, it may fail to identify the infection as being due to MRSA.

How did the researchers interpret the results?

The researchers concluded that routine culture and antimicrobial susceptibility testing will identify Staphylococcus aureus bacteria with the new mecA gene as being resistant to meticillin and related antibiotics. However, PCR testing to confirm the results will not detect this gene and will fail to identify the bacteria as MRSA. The researchers concluded that new guidelines for the detection of MRSA should consider including tests for mecALGA251.

Conclusion

MRSA is usually detected by using antibiotic-susceptibility testing. Results are confirmed using molecular testing (PCR), which detects the presence of the mecA gene that is common to these bacteria. This laboratory research tested MRSA obtained from cattle and milk samples, which were stored at veterinary agencies in the UK, and MRSA samples from humans, which were stored at reference laboratories in the UK. In many of the cattle samples tested, the researchers detected a new type of mecA gene. Antibiotic-susceptibility testing showed that MRSA bacteria carrying this gene were resistant to a range of penicillin-related antibiotics, but further PCR testing could not identify these bacteria as MRSA.

The most important finding from this research is that if molecular testing techniques are used to detect or confirm the presence of MRSA, they will not correctly identify the new type of MRSA bacteria.

The researchers noted that only tentative interpretations can be made from these results, and more samples need to be studied. Some points of note include:

  • The strains containing this new gene were only obtained from existing MRSA collections. Researchers will need to carry out the same tests in samples obtained from other populations.
  • It is not known whether disease caused by MRSA with the new mecA gene is any different to that caused by conventional MRSA.
  • According to the researchers, their data suggest that the MRSA infections with the new gene are likely to account for 1 in 100 to 1 in 500 of total MRSA in the UK and Denmark. This is a small proportion of MRSA infections.
  • As this gene has been detected in MRSA samples from dairy cows, it suggests that these animals might form a reservoir of infection. Close links with farms or contact with dairy cattle could increase the risk of this type of MRSA being transmitted to humans. As the study did not look at the spread of resistance from cattle to humans, this will need to be investigated in further research.

The discovery of this previously undetected MRSA, which carries the new mecA gene, is potentially important to public health. Further quality evidence is required from observational and experimental studies to inform tests for diagnosing MRSA.

Experts highlight that the main worry is that bacteria may colonise people who work on farms, and not that people may be at risk from drinking milk. As almost all milk sold in the UK is pasteurised, drinking or eating dairy products is reportedly “not a health concern”.

Links to the headlines

MRSA 'superbug' is found in British milk. The Independent, June 3 2011

New MRSA strain found in British cows' milk. The Daily Telegraph, June 3 2011

New strain of MRSA superbug may have spread from cattle to humans. The Guardian, June 3 2011

New form of MRSA found in cows' milk and human flesh wounds. Daily Mail, June 3 2011

Links to the science

García-Álvarez L, Holden MTG, Lindsay H et al. Meticillin-resistant Staphylococcus aureus with a novel mecA homologue in human and bovine populations in the UK and Denmark: a descriptive study. The Lancet Infectious Diseases, 2011 (published online first)

Further reading

Loeb MB, Main C, Eady A, Walkers-Dilks C. Antimicrobial drugs for treating methicillin-resistant Staphylococcus aureus colonization. Cochrane Database of Systematic Reviews 2003, Issue 4

Hughes C, Smith M, Tunney M. Infection control strategies for preventing the transmission of meticillin-resistant Staphylococcus aureus (MRSA) in nursing homes for older people. Cochrane Database of Systematic Reviews 2008, Issue 1

drugs to treat the brain disorder Creutzfeldt-Jakob Disease (CJD) “have unexpectedly blocked the onset of Alzheimer's disease, the most common cause

A “surprise discovery” has allowed scientists to block Alzheimer's disease, The Independent reported. The newspaper said that researchers developing drugs to treat the brain disorder Creutzfeldt-Jakob Disease (CJD) “have unexpectedly blocked the onset of Alzheimer's disease, the most common cause of dementia”.

However, it is not correct to say that researchers have been able to “block” the onset of Alzheimer’s. The study in question carried out laboratory and animal experiments to investigate the binding between two types of protein. One of the proteins investigated (called the amyloid beta protein) builds up in Alzheimer’s disease. An abnormal form of the other protein (called the prion protein) causes CJD. Scientists found that blocking this binding of the proteins stopped the amyloid protein from affecting nerve signals in mouse brain samples and in the brains of live rats.

Alzheimer’s is a complex disease and is caused by the death of nerve cells in certain areas of the brain. What triggers the death of nerve cells in this disease is still not fully understood, and blocking the effects of the amyloid protein in this way may not be sufficient to stop nerve cells dying.

The interesting finding of this study suggests it could be worth testing antibodies that target prion proteins in Alzheimer’s disease. These antibodies have reportedly already been prepared for testing in human diseases such as CJD, which may mean they could tested for Alzheimer’s disease in humans sooner. However, it is likely that more testing of their effects in animals will be needed before human testing is attempted.

Where did the story come from?

The study was carried out by researchers from University College Dublin and other research centres in Ireland and the UK. It was funded by the Science Foundation Ireland, the Health Research Board, a University College Dublin seed funding grant, the UK Medical Research Council and the Department of Health.

The study was published in the peer-reviewed scientific journalNature Communications.

The Independent, The Daily Telegraph and Daily Mirror covered this study. The Independent and Telegraph reported that this research was in rodents, but the Mirror did not. The Independent’s suggestion that scientists have “blocked the onset of Alzheimer's disease” is not correct. They have only shown that a single effect of the amyloid beta protein on nerve cells (neurones) has been prevented, which is not the same as blocking the development of Alzheimer’s disease.

What kind of research was this?

This animal research looked at the interaction between certain proteins involved in the brain conditions Creutzfeldt-Jakob Disease (CJD) and Alzheimer’s disease. These proteins are respectively known as the prion protein and amyloid beta. Both these proteins are present in normal brain tissue, but they are also involved in disease. An abnormal form of prion protein is the cause of CJD, a degenerative brain disorder. In people with Alzheimer’s disease, amyloid beta builds up in the brain and forms abnormal deposits, known as plaques. Amyloid beta is thought to affect the function of nerve cells directly, by influencing the strength of connections between the nerve cells (synapses) and, therefore, affecting memory. The build-up of amyloid beta is also thought to contribute to the death of neurones in the brain, which is the cause of the symptoms of the disease.

Previous research has suggested that amyloid beta might need to bind to the prion protein to have an adverse effect on nerve cell function. The researchers discuss previous research that looked at blocking this binding using antibodies, types of special proteins that the immune system uses to help defend the body. Antibodies have the ability to bind to foreign substances, such as molecules on the surface of bacteria and viruses, allowing the immune system to identify and attack them. The researchers say that in a previous study, an antibody against prion protein was able to prevent it from binding to amyloid beta, reducing its toxic effects on neurones in the laboratory and in a mouse model of Alzheimer’s disease. However, other studies have suggested that not all the adverse effects of amyloid beta seem to need the prion protein to be present.

In this study, the researchers wanted to repeat some of these previous experiments to confirm their findings and to look further at the effects on neurone function of blocking the interaction between amyloid beta and prion protein.

This type of early study helps researchers understand what might be going on in a disease, and suggests potential “targets” for new drugs or treatments. These treatments can then be tested in the laboratory and on animals to try and identify which ones have the most promise for testing in humans. While experimental models in the laboratory and animal models of the disease are useful research tools, they are not exactly the same as human disease, and treatments do not always have the same effect when they are tested in humans.

What did the research involve?

The researchers carried out a wide range of experiments. First, they generated a standardised form of amyloid beta that they could use in their experiments, called amyloid beta-derived diffusible ligand (ADDL). They noted that this preparation is not identical to the brain-derived amyloid beta.

Next, they carried out some tests in brain slices from mice, which were taken from a region of the brain called the hippocampus. This is the area affected in Alzheimer’s disease. They tested the effects of ADDL on neurones in these brain slices. They specifically looked at the effect on a nerve signalling phenomenon known as “long-term potentiation”, which strengthens the connection between neurones and is involved in learning and memory. They then tested whether prion protein needed to be present for ADDL to have an effect within the brain. To do this, they repeated their experiments using brain slices from mice that were genetically engineered to lack prion protein. As well as using their laboratory-generated ADDL, they also repeated these experiments using amyloid beta extracted from the brain of a person with Alzheimer’s disease.

They then further investigated how the prion protein and amyloid beta interact. They did this to identify key parts of the proteins that allow interaction to occur, so they could target these with antibodies to see if this would stop the interaction. They then tested a range of antibodies against different parts of the prion protein to see whether this would stop it binding to amyloid beta.

Once they identified antibodies that blocked this binding, they looked at whether they could stop the effects of amyloid beta on long-term potentiation in mouse brain slices. Finally, they tested the effects of one of these antibodies in living rats. Again, they looked at the effects on long-term potentiation, which normally occurs in response to stimulating the rat’s brain with high-frequency electrical stimulation. They injected the rats’ brains with amyloid beta extracted from a human brain with Alzheimer’s and looked at the effect on long-term potentiation. They then tested whether pre-injecting the brains with the antibody before injecting amyloid beta blocked it from having an effect.

What were the basic results?

The researchers found that both amyloid beta preparations (one made in the lab and the other extracted post mortem from the brain of a person with Alzheimer’s disease) inhibited long-term potentiation in the brain slices from normal mice, but not from genetically engineered mice lacking prion protein. This showed that the prion protein needed to be present for amyloid beta to have this effect.

The researchers found that two anti-prion antibodies, called ICSM-18 and ICSM-35, that have been tested in human prion disease could block the binding of amyloid beta and prion protein in the laboratory. These antibodies were also able to stop amyloid beta from having an effect on long-term potentiation in mouse brain slices. ICSM-18 was also shown to stop the effect of amyloid beta on long-term potentiation in live rats.

How did the researchers interpret the results?

The researchers concluded that their findings confirm that prion protein binds to amyloid protein and facilitates amyloid’s damaging effects on the function of nerve cells.

They say that the two main antibodies they tested, ICSM-18 and ICSM-35, could block the effects of amyloid beta on neurone signalling (long-term potentiation). This confirms that these antibodies are candidates for testing as potential treatments for Alzheimer’s disease, either on their own or in combination.

Conclusion

This animal research supports the theory that the prion protein plays a role in the effects that the amyloid beta protein has on neurones. It also suggests that using antibodies can prevent at least one effect of amyloid protein on the nerve cells.

It is important to note that the study looked at only one effect of amyloid beta on nerve cells: the effect on one aspect of neurone signalling called long-term potentiation, which is involved in learning and memory. Alzheimer’s is a complex disease and is largely caused by the death of neurones in certain areas of the brain. What causes the death of neurones in this disease is still not fully understood. Blocking the effects of amyloid beta on long-term potentiation may not be sufficient to stop neurones dying and, therefore, to affect disease progression.

The interesting finding of this study suggests that antibodies that target the prion protein could be tested for their effects in Alzheimer’s disease. These antibodies have reportedly already been extensively tested in mice and prepared for use in human testing for prion diseases, such as CJD. This means that they may be able to be tested in human Alzheimer’s disease sooner than if these steps had not been taken. However, it is likely that more testing in animals will be needed before human testing is attempted.

Links to the headlines

Surprise discovery allows scientists to block Alzheimer's. The Independent, June 8 2011

CJD drugs could help Alzheimer's patients. The Daily Telegraph, June 8 2011

Mad cow drugs could help beat Alzheimer's. Daily Mail, June 8 2011

Links to the science

Freir DB, Nicoll AJ, Klyubin I et al. Interaction between prion protein and toxic amyloid β assemblies can be therapeutically targeted at multiple sites. Nature Communications, June 7 2011

'Chemical cosh' dementia drug prescriptions concern

'Chemical cosh' dementia drug prescriptions concern


Elderly woman There are around 750,000 people living with dementia in the UK

Related Stories

More than 50 health and social care organisations are calling for fresh action to cut the prescription of "chemical cosh" drugs.

Around 180,000 people with dementia are thought to be prescribed antipsychotic drugs in the UK.

But 80% of those prescriptions are said by critics to be inappropriate.

Long-term use of the drugs can make dementia symptoms worse, reduce the ability to talk and walk and increase the risk of stroke and even death.

The Dementia Action Alliance - which includes the Alzheimer's Society, Age UK and the Department of Health - want all prescriptions for antipsychotics to be reviewed by the end of March 2012.

To help patients and carers, the Alliance has published a booklet giving information and advice about how to make sure antipsychotics are not prescribed inappropriately.

Powerful sedative

Antipsychotics have a powerful sedative effect and are often used when dementia patients become aggressive, agitated or distressed.

Start Quote

It is unacceptable that 1,800 people with dementia die prematurely every year as a result of antipsychotic medication”

End Quote Paul Burstow MP Care Services Minister

They are most commonly given to dementia sufferers in care homes and hospitals.

Guidelines say they should only be used as a last resort and over a short period of time, but the evidence suggests that in some cases they are being prescribed for years.

A study published in January 2009 showed the medication nearly doubled the risk of death for many dementia patients when taken over a prolonged period.

Chemical cosh

Jeremy Hughes, Chief Executive of the Alzheimer's Society, said it was unacceptable that people with dementia were having their health and quality of life put at risk because of antipsychotics:

"It is essential we bring an end to this chemical cosh and empower people with dementia and carers with the information they need to ensure they are not prescribed these drugs inappropriately. This call to action can do just that.

Michelle Freaser says two years on antipsychotics had "horrendous" side effects on her father Michael Rainford

"It's not just about reducing antipsychotics but also about improving quality care. This means developing alternative treatments and finding better ways to manage pain and other medical conditions."

Following an independent report for the government in November 2009 that found the drugs killed around 1,800 patients a year, ministers announced plans to cut prescribing rates by two-thirds within three years.

But new figures from the NHS Information Centre suggest prescription may have dropped by less than 20% over the past two years.

When in opposition, Paul Burstow, now Care Services Minister, campaigned to cut the use of the 'chemical cosh'.

"It is unacceptable that 1,800 people with dementia die prematurely every year as a result of antipsychotic medication. That is why I'm backing this campaign," he said.

"Reducing the use of antipsychotic medication is one of the Coalition Government's four key priorities for dementia. With the right support, people can live well with dementia and continue to do the things they enjoy for years after diagnosis."

Alternative therapies

The campaign is also being supported by Dr Clare Gerada, Chair of Royal College of General Practitioners.

"Dealing with very agitated or aggressive patients can be distressing, and it can be difficult knowing what to do for the best of the patient, but antipsychotics should in most cases only be used as a last resort, and for the short term.

"Antipsychotics have potential to do real harm to patients, including an increased risk of stroke. There are viable alternatives - including behavioural therapies - that we should encourage wherever possible to ensure the care our patients receive is appropriate, in their best interests and does not cause them harm."

Rebecca Wood, Chief Executive of Alzheimer's Research UK, the UK's leading dementia research charity, said:

"Action to reduce the prescription of these drugs and develop alternative treatments has lacked urgency.

"This campaign should renew that urgency and drive home the need to invest in more research so that safer, more effective treatments can be found."

Martin Green of the English Community Care Association, a body that represents care homes, said: "ECCA really welcomes the commitment by the Department of Health to reduce anti-psychotic prescribing and we want to see all sections of the system - primary care, acute hospitals, pharmacists and care homes - working in partnership to reduce inappropriate anti-psychotic prescribing".

Are you affected by this story? Does one of your family members have dementia and use chemical cosh drugs? Or perhaps they have stopped using them? If you are willing to be interviewed by the BBC about this subject please fill in the form below

Monday, 6 June 2011

mrsa

Scientists in the UK have discovered a new strain of MRSA that appears to spread to humans from cattle and can cause life-threatening illness,” reported The Guardian. It said that a study of dairy herds had found the drug-resistant strain in cows' milk.
MRSA (meticillin-resistant Staphylococcus aureus) is usually detected using a technique called antibiotic-susceptibility testing. Borderline cases of MRSA are confirmed with molecular testing, which detects the presence of a gene that is common to these “superbugs”.
This study looked at strains of MRSA from cattle and humans to see whether they possessed any new genetic features that affect the reliability of these tests.
The study found a new type of gene in many of the cattle samples. This gene makes the bacteria resistant to a range of antibiotics. While the bacteria with this gene showed up in antibiotic-susceptibility testing, molecular testing could not recognise the gene and failed to identify the bacteria as MRSA.
Therefore, if molecular testing is used to detect MRSA or to confirm borderline cases, it will not identify bacteria with the new gene.
The researchers say that only a small proportion of MRSA bacteria possess this gene. However, as it has been detected in MRSA samples from dairy cows, these animals might form a “reservoir of infection”. They warn that close links with farms or contact with dairy cattle could increase the risk of MRSA being transmitted to humans. Further studies are needed to inform tests for diagnosing MRSA.
Experts highlight that the main worry is that bacteria may colonise people who work on farms, and not that people may be at risk from drinking milk. As almost all milk sold in the UK is pasteurised, drinking or eating dairy products is reportedly “not a health concern”.

Where did the story come from?
The study was carried out by researchers from the Department of Veterinary Medicine at the University of Cambridge and other health and academic institutions in Cambridge and the UK.
Funding was provided by the Department for Environment, Food and Rural Affairs, the Higher Education Funding Council for England, the Isaac Newton Trust (University of Cambridge) and the Wellcome Trust.
The study was published in the peer-reviewed medical journal The Lancet.
The news headlines have oversimplified this complex research and may imply that people are at risk from drinking milk, which is not the case. The main implications of these findings are in the field of laboratory and diagnostic testing.

What kind of research was this?
This laboratory study looked at strains of MRSA from samples taken from cattle and humans. The researchers wanted to see if they possessed any new genetic features that meant that they could not be detected by standard tests for diagnosing MRSA.
The researchers explained that animals are known to act as a “reservoir” for new strains of bacteria, so could be a source of new strains of the superbug MRSA (meticillin-resistant Staphylococcus aureus) in humans. Staphylococcus aureus causes a wide variety of infections in humans, from skin infections to pneumonia and blood poisoning. However, many people carry the bacteria harmlessly on their skin.
MRSA has developed resistance to meticillin and other penicillin antibiotics that would normally kill Staphylococcus aureus. This means that MRSA can cause disease that is harder to treat. It is believed that the Staphylococcus aureus bacteria evolved to develop this resistance by acquiring a certain chromosome element (called SCCmec) which contain a gene called mecA. This gene encodes a protein that binds to penicillin.
The researchers describe how MRSA is usually identified in the laboratory using “antimicrobial susceptibility testing”. In this test, the bacteria are incubated with discs that are impregnated with antibiotics. The zone around the disc where bacterial growth has been prevented is measured. There are standard zones around the disc that confirm the presence of MRSA. If the results are borderline, molecular testing (called PCR testing) is used to detect the mecA gene or penicillin-binding protein in the bacteria.
Before 2003, most cases of MRSA were associated with human transmission and infection, but after this time it was found in livestock. Evidence was also found that some strains may not be restricted to a single species but can cross between humans and farm animals. There is concern that farm animals could act as a reservoir for MRSA and that close human-animal contact could increase the risk of transmission.

What did the research involve?
The researchers took isolates (a pure strain that has been separated from a mixed bacterial culture) of MRSA bacteria from both humans and cows and determined whether antimicrobial susceptibility testing could detect the bacteria.
In 2007, the researchers obtained 24 isolates of bovine MRSA from the Veterinary Laboratories Agency in the UK. These came from a collection of 940 Staphylococcus aureus isolates obtained from the milk of 465 different herds of cows with mastitis, which had been submitted to the agency for testing.
Isolates of human MRSA were obtained from the Health Protection Agency and the Scottish MRSA Reference Laboratory in the UK, and the National MRSA Reference Laboratory in Denmark. The human bacteria had been cultured from blood samples or infected wound swabs.
The researchers carried out antimicrobial susceptibility testing on these bovine and human isolates, and used PCR testing to see whether the mecA gene could be detected.

What were the basic results?
A new mecA gene (called mecALGA251) was discovered in 15 of 24 Staphylococcus aureus isolates from dairy cattle in England. These isolates were from three different strains of MRSA. The new mecALGA251 gene was also identified in 12 of 16 isolates from human samples from Scotland, 15 of 26 isolates from England, and 24 of 32 isolates from Denmark.
Antibiotic-susceptibility testing identified that these isolates were resistant to a wide range of antibiotics. However, PCR testing showed negative results for the mecA gene and penicillin-binding protein. This suggests that if PCR testing is used on its own or to confirm the results of antibiotic-susceptibility testing, it may fail to identify the infection as being due to MRSA.

How did the researchers interpret the results?
The researchers concluded that routine culture and antimicrobial susceptibility testing will identify Staphylococcus aureus bacteria with the new mecA gene as being resistant to meticillin and related antibiotics. However, PCR testing to confirm the results will not detect this gene and will fail to identify the bacteria as MRSA. The researchers concluded that new guidelines for the detection of MRSA should consider including tests for mecALGA251.

Conclusion
MRSA is usually detected by using antibiotic-susceptibility testing. Results are confirmed using molecular testing (PCR), which detects the presence of the mecA gene that is common to these bacteria. This laboratory research tested MRSA obtained from cattle and milk samples, which were stored at veterinary agencies in the UK, and MRSA samples from humans, which were stored at reference laboratories in the UK. In many of the cattle samples tested, the researchers detected a new type of mecA gene. Antibiotic-susceptibility testing showed that MRSA bacteria carrying this gene were resistant to a range of penicillin-related antibiotics, but further PCR testing could not identify these bacteria as MRSA.
The most important finding from this research is that if molecular testing techniques are used to detect or confirm the presence of MRSA, they will not correctly identify the new type of MRSA bacteria.
The researchers noted that only tentative interpretations can be made from these results, and more samples need to be studied. Some points of note include:
The strains containing this new gene were only obtained from existing MRSA collections. Researchers will need to carry out the same tests in samples obtained from other populations.
It is not known whether disease caused by MRSA with the new mecA gene is any different to that caused by conventional MRSA.
According to the researchers, their data suggest that the MRSA infections with the new gene are likely to account for 1 in 100 to 1 in 500 of total MRSA in the UK and Denmark. This is a small proportion of MRSA infections.
As this gene has been detected in MRSA samples from dairy cows, it suggests that these animals might form a reservoir of infection. Close links with farms or contact with dairy cattle could increase the risk of this type of MRSA being transmitted to humans. As the study did not look at the spread of resistance from cattle to humans, this will need to be investigated in further research.
The discovery of this previously undetected MRSA, which carries the new mecA gene, is potentially important to public health. Further quality evidence is required from observational and experimental studies to inform tests for diagnosing MRSA.
Experts highlight that the main worry is that bacteria may colonise people who work on farms, and not that people may be at risk from drinking milk. As almost all milk sold in the UK is pasteurised, drinking or eating dairy products is reportedly “not a health concern”.
Links to the headlines
MRSA 'superbug' is found in British milk. The Independent, June 3 2011
New MRSA strain found in British cows' milk. The Daily Telegraph, June 3 2011
New strain of MRSA superbug may have spread from cattle to humans. The Guardian, June 3 2011
New form of MRSA found in cows' milk and human flesh wounds. Daily Mail, June 3 2011
Links to the science
García-Álvarez L, Holden MTG, Lindsay H et al. Meticillin-resistant Staphylococcus aureus with a novel mecA homologue in human and bovine populations in the UK and Denmark: a descriptive study. The Lancet Infectious Diseases, 2011 (published online first)
Further reading





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Loeb MB, Main C, Eady A, Walkers-Dilks C. Antimicrobial drugs for treating methicillin-resistant Staphylococcus aureus colonization. Cochrane Database of Systematic Reviews 2003, Issue 4
Hughes C, Smith M, Tunney M. Infection control strategies for preventing the transmission of meticillin-resistant Staphylococcus aureus (MRSA) in nursing homes for older people. Cochrane Database of Systematic Reviews 2008, Issue 1

Friday, 29 April 2011

Screen may spot autism

Screen may spot autism in one-year-olds

baby check The screen could be added to the list of health checks normally carried out a the one-year screen
Asking parents a few simple questions about their baby during routine one-year well-baby checks can help spot early autism, say US experts.
The condition, which affects how the child relates to other people, is usually only spotted some years later.
But enquiring about a child's use of eye contact, sounds, words and gestures can flag up early on if more detailed screening is needed, a study shows.
The findings in over 10,000 infants are published in the Journal of Pediatrics.
Of the 10,479 one-year-olds seen, 184 failed the initial check-up and were referred for further evaluation by the team at the University of California, San Diego School of Medicine.
To date, 32 have received a provisional or final diagnosis of autism spectrum disorder and another 101 have been found to have other conditions that involve developmental delay.
These rates, say the authors, are typical of what you might expect to see in a population of this size, suggesting that the screening could work.
Lead researcher Karen Pierce said: "Given lack of universal screening of infants for such disorders at 12 months, this programme could be adopted by any paediatric office, at virtually no cost, to aid in the identification of children with developmental delays.
"Importantly, parents will be able to get help for their children at a much earlier age than before."
Autism is a spectrum condition, which means that, while all people with autism share certain difficulties, their condition will affect them in different ways.
Early diagnosis
Some people with autism are able to live relatively independent lives but others may have accompanying learning disabilities and need a lifetime of specialist support.
The sooner the condition is diagnosed, the quicker they can access the care available.
Carol Povey, Director of the National Autistic Society's Centre for autism, said: "We welcome research which could help autism be diagnosed earlier.
"Whilst a formal diagnosis requires a comprehensive clinical assessment, screening checks at key developmental stages can help professionals identify children who may be showing signs of autism."



    Friday, 8 April 2011

    Monkeys 'harbour malaria threat'

    Monkeys 'harbour malaria threat'

    Monkeys A type of malaria could move from monkeys to humans, say scientists

    Related Stories

    Scientists are warning that a species of malaria could switch from targeting monkeys to humans.

    Macaques in south east Asia are a vast source of Plasmodium knowlesi which can spread to people, they write in PLoS Pathogens.

    They believe that growing human populations and increased deforestation in the region could lead to the parasite switching host.

    But those changes could also reduce the spread of the disease.

    Around one million people die each year as a result of malaria.

    It is caused by parasites and is spread by mosquitoes when they drink blood.

    'Huge reservoir'

    P. knowlesi is known as the fifth malarial parasite in humans.

    It mostly exists in monkeys, however, there have been human cases and it has been shown in the laboratory to be able to spread from human to human.

    Start Quote

    With increasing human populations and deforestion we may get a shift to humans”

    End Quote Professor Balbir Singh University Malaysia Sarawak

    In south east Asia, the macaques are the second most common primate after humans.

    Blood tests on 108 wild macaques showed that more than three quarters were infected with the malaria parasite.

    Professor Balbir Singh, from the Malaria Research Centre at Universiti Malaysia Sarawak, told the BBC: "they are a huge reservoir of Plasmodium knowlesi."

    Genetic analysis showed that P. knowlesi had existed in monkeys since before humans settled in south east Asia. The researchers said humans were being infected from the 'reservoir', rather than the disease spreading between humans.

    Prof Singh raised concerns about what could happen in the future: "We don't know how mosquito behaviour will change.

    "With increasing human populations and deforestation we may get a shift to humans. The number of malaria cases is coming down so there is also decreased immunity. Or would deforestation reduce numbers? It could go either way."

    Dr Hilary Ranson, from the Liverpool School of Tropical Medicine, said: "It seems a very reasonable thing to speculate.

    "Deforestation or any perturbation of the ecosystem frequently leads to humans being exposed to an expanded range of biting insects and the pathogens they transmit, yellow fever is a good example of this."

    She said if humans catch the parastite more often then P knowlesi may evolve to target humans.

    "To me the important message is that disruption of the environment exposes people to a range of known and potentially unknown pathogens transmitted by blood feeding insects that do not typically feed on humans" she added.

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