Tuesday 6 December 2011

staple crop virus

staple crop virus

UN warns of 'epidemic'


Cassava rootsFarmers may think crops are healthy until harvest; the signs only show on roots

Cassava is one of the world's most important crops providing up to a third of the calorie intake for many people.
UN scientists are warning that a virus attacking the cassava plant is nearing an epidemic in parts of Africa.
The food and agriculture organisation of the UN says the situation is urgent and are calling for an increase in funding for surveillance.
None of the varieties of cassava being distributed to farmers in Africa appears to be resistant to the virus.
Cassava is a global food source of particular importance in Africa as it does well on poor soils with low rainfall.
But like many crops it is threatened by a number of pests and diseases that hinder its production. Viral infections have periodically wiped out the crop in some regions leading to famine.
Now the UN's Food and Agriculture Organization (FAO) says that another virus is threatening the crop in large parts of East Africa.
The scientists say the Cassava Brown Streak Disease (CBSD) is on the verge of becoming an epidemic. It first appeared in Uganda in 2006 but in the past few months has been found in Burundi and the Democratic Republic of Congo for the first time.
According to Mike Robson, a plant production and protection officer with the FAO it's hard to know exactly where the virus is as surveillance systems are poor.
"It is hard to say precisely but we're finding it where we go looking for it "
Robson says that a particular problem with this virus is that farmers may think they have a healthy crop until the harvest, as the symptoms only show on the roots.
"That's a particularly distressing situation where a farmer thinks he has a healthy field of cassava but when they come to uproot it, their expectations of food are not going to be met."
But there are some strategies that can help reduce the impact of the infection, according to Mike Robson.
"The main ways of controlling are to try and control the movement of planting material. Cassava is propagated from cuttings and if you move a cutting that has the infection you're effectively moving it to a new area"
"The other thing that farmers can do if they suspect they have the disease is to harvest early. They will get smaller roots of cassava but they will be less affected by the disease - it shows up late in the production cycle."
The FAO scientists say they are in a race against time with this particular strain of virus. They are calling for a rapid increase in funding to improve surveillance. They also want to improve training for farmers and they want to ban the distribution of infected plants between districts.
Some eight varieties of the crop are under development by the International Institute of Tropical Agriculture which show some level of resistance to CBSD - It is hoped that these varieties could be made widely available within two years.

Friday 2 December 2011

Chicken liver food poisoning


Chicken liver food poisoning link


Wedding receptionChicken liver pate is a popular dish at weddings

R

Over 90% of cases of a common form of food poisoning seen this year were due to people eating undercooked chicken liver pate, often at weddings, infection experts have said.
The Health Protection Agency (HPA) analysed 18 outbreaks of Campylobacter in 2011 across England.
In all, 443 people became unwell and one had to be hospitalised.
The Food Standards Agency (FSA) has reminded caterers to cook poultry livers to prevent infection.
Campylobacter is the most common cause of bacterial food poisoning in Britain - there were estimated to have been more than 600,000 cases in 2010 in England and Wales.
Symptoms include diarrhoea, stomach pains and cramps, fever, and generally feeling unwell. Most people are only ill for a few days.
In 2008 there were just three outbreaks linked to undercooked chicken liver pate, but that rose to nine in 2009 and 14 in 2010.

Start Quote

It's really important that chefs cook livers thoroughly to kill any bacteria, even if recipes call for them to be seared and left pink in the middle.”
Bob MartinFood Standards Agency
Poultry livers carry a particularly high risk of Campylobacter as the bacteria can be present throughout the liver, not just the surface as is the case for other poultry meat, and may remain a source of infection if they are not cooked sufficiently.
Of the 18 outbreaks, 14 occurred in catering venues, and 13 of these were linked to chicken or duck liver pate.
Seven were linked to wedding receptions at hotels, banqueting venues or public houses and six were associated with catering at other functions such as hotels, clubs and restaurants.
The HPA found that livers used to make the parfait or pate were undercooked allowing the liver to remain pink in the centre.
It said caterers can reduce the risk of their people becoming infected by ensuring that Campylobacter is killed through proper cooking and by avoiding cross-contamination to other foods.
'Inadequate cooking'
Dr Christine Little, an expert in gastrointestinal infections at the HPA, said: "The increase in outbreaks which are due to the consumption of chicken liver pate has been steadily increasing over the last few years.
"Not only is this dish popular in food recipe magazines, it is being served in a variety of different catering venues.
"Illness occurs because the livers are only cooked until they are pink, and inadequate cooking will not be sufficient to kill the bacteria.
"Both the public and the catering industry need to be aware that undercooking this product can result in food poisoning."
She said anyone planning a wedding, or other special event, should be aware of the risks if they were having chicken liver pate to prevent people becoming unwell.
The FSA issued updated advice to caterers on the safe handling and cooking of livers twice in 2010, but Campylobacter outbreaks associated with the consumption of chicken liver pate have continued to occur.
Bob Martin, head of foodborne disease strategy at the FSA, said: "Unfortunately, levels of Campylobacter in most raw chicken are high, so it's really important that chefs cook livers thoroughly to kill any bacteria, even if recipes call for them to be seared and left pink in the middle.
"The only way of ensuring the pate or parfait will be safe to serve to your guests or customers is by cooking the livers the whole way through.
"Caterers should also follow good general hygiene practices when cooking and handling poultry livers, to avoid cross contamination with Campylobacter."

Wednesday 30 November 2011

e.coli- Extended Spectrum Beta Lactamase e. coli 'not from Singleton Hospital



Singleton Hospital's maternity unitSingleton Hospital's maternity unit is still open for full-term births


A mother suspected to have contracted an E. coli strain at a maternity unit where two premature babies have died did not pick up the bug at the hospital, say health chiefs.
Her case was initially one of two investigated at Singleton Hospital's maternity and neonatal unit.
Tests now show the mother was carrying a different ESBL E. coli sub-type.
The other case was a premature baby who died after contracting the strain at the unit.
Abertawe Bro Morgannwg (ABM) University Health Board, which runs the hospital, said a second baby who died at the unit had contracted ESBL E. coli elsewhere.
ABM announced on Friday a third baby had tested positive but showed no symptoms.
Tests are under way to see if that baby has the same sub-type as the cross-infection, or whether it is unconnected.

What is ESBL E. coli?

  • ESBL E. coli is not the same as the E. coli O157 which causes food poisoning
  • ESBL stands for Extended Spectrum Beta Lactamase
  • ESBL E. coli is most often found in the gastrointestinal tract but may cause urinary tract infections
  • ESBL E. coli is resistant to commonly-used antibiotics such as penicillin, but can be treated
  • In most people ESBL E. coli does not cause harm but in vulnerable individuals it can cause serious infections
  • Source: ABM health board
ABM said in a statement: "While these tests are under way, as a continuing precaution, the neonatal unit is restricted to routine admission for babies over 36 weeks' gestation only.
"We are also taking additional precautions, including restricting visitors to the maternity unit and continuing to ask visitors to wash their hands and use hand hygiene gel."
Two other people in the maternity unit were also found to have been infected, but contracted it outside the hospital.
Officials have stressed that ESBL E. coli is not the same as E. coli O157 which causes food poisoning.
They say a very small proportion of people carry ESBL E. coli harmlessly in their body.
ABM added: "Our investigations into the cross infection have not yet identified how the ESBL E. coli was transmitted, but we continue to do all we can to determine the cause.
"However, in other similar instances of this kind elsewhere in the UK the cause of transmission was never identified."

no to eye drug Lucentis for diabetes


Watchdog NICE says no to eye drug Lucentis for diabetes                       


eyeThe drug is injected into the patient's eye
A drug that could save the sight of people with diabetes will not be made available on the NHS in England and Wales, an advisory body has concluded.
The National Institute for Health and Clinical Excellence (NICE) says ranibizumab, sold under the brand name Lucentis, is too expensive to use in people with diabetic macular oedema.
Charities say they will continue to campaign for the drug to be used.
At least 50,000 people in the UK are affected by this eye condition.
Sight saver
Macular oedema occurs when fluid leaks from the small blood vessels in the eye.
The fluid collects in the central part of the retina at the back of the eye, called the macular area, which can lead to severe visual impairment.

Straight lines may appear wavy and people can have blurred central vision or sensitivity to light.Sight can become so impaired that the person can no longer read, work or drive.Laser treatment has been the standard treatment for diabetic macular oedema on the NHS, but this only stops vision from deteriorating further.
An injection of Lucentis in the eye, however, can improve vision.
NICE already recommends Lucentis to the NHS for a different eye condition called wet age-related macular degeneration.
Diabetic macular oedemaAn eye examination can reveal the problem
Four UK charities - Diabetes UK, the Juvenile Diabetes Research Foundation, the Macular Disease Society and the Royal National Institute of Blind People (RNIB) - are urging government to rapidly agree a Patient Access Scheme with the manufacturer of Lucentis, Novartis, in order to bring down the cost of the drug to the NHS for treating diabetic macular oedema.
Currently, the drug costs £742.17 per injection.
Steve Winyard from the RNIB said: "We now hope that a patient access scheme can be agreed swiftly, so that patients with diabetic macular oedema are not left to needlessly lose their sight."
A spokeswoman for Novartis said the company would continue to work with NICE and the Department of Health to "ensure appropriate patients are able to receive this very important treatment, which in clinical trials has been shown to double the likelihood of gaining vision and reduce the chance of losing vision by up to three-fold compared to laser treatment".
Novartis believes that NICE did not consult sufficiently with clinical and patient experts on the data it submitted to the appraisal committee.
But Sir Andrew Dillon, Chief Executive at NICE, said the manufacturer significantly underestimated the cost of treatment.
  • Cancer drug hope for eye disorder 11 JUNE 2010HEALTH
  • Father wins fight for sight drug 29 APRIL 2009SHROPSHIRE

Tuesday 29 November 2011

Timothy syndrome


Timothy syndrome                   mengele-westof


From Wikipedia, the free encyclopedia
Timothy syndrome
Classification and external resources
OMIM601005
DiseasesDB34006
Timothy syndrome is a rare autosomal dominant disorder characterized by physical malformations, as well as neurological and developmental defects, including heart QT-prolongation, heart arrhythmias, structural heart defects, syndactyly (webbing of fingers and toes) and autism spectrum disorders.
Timothy syndrome often ends in early childhood death.

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[edit]Signs and symptoms

The most striking sign of Timothy syndrome is the co-occurrence of both syndactyly (~0.03% of births) and long QT syndrome (1% per year) in a single patient. Other common symptoms of Timothy syndrome are cardiac arrhythmia (94%), heart malformations (59%), autism or an autism spectrum disorder (80% who survive long enough for evaluation). Facial dysmorphologies such as flattened noses also occur in approximately half of patients. Children with this disorder have small teeth which, due to poor enamel coating, are prone to dental cavities and often require removal. The average age of death due to complications of these symptoms is 2.5 years.[1][2][3]
Atypical Timothy syndrome has largely the same symptoms as the classical form. Differences in the atypical form are the lack of syndactyly, the presence of musculoskeletal problems (particularly hyperflexible joints), and atrial fibrillation. Patients with atypical Timothy syndrome also have more facial deformities, including protruding foreheads and tongues. Finally, one patient with atypical Timothy syndrome had a body development discrepancy wherein her upper body was normally developed (that of a 6-year-old) while her lower half resembled a 2- or 3-year-old.[4]
Children with Timothy syndrome tend to be born via caesarean section due to fetal distress.[1][2]

[edit]Diagnosis

Syndactyly and other deformities are typically observed and diagnosed at birth. Long QT syndrome sometimes presents itself as a complication due to surgery to correct syndactyly. Other times, children collapse spontaneously while playing. In all cases it is confirmed with ECG measurements. Sequencing of the CACNA1C gene further confirms the diagnosis.

[edit]Pathophysiology


Timothy syndrome has an autosomal dominant pattern of inheritance.
There are two recognized types of Timothy syndrome, classical (type-1) and atypical (type-2). They are both caused by mutations in CACNA1C, the gene encoding the calcium channel Cav1.2 α subunit. Timothy syndrome mutations in CACNA1C cause delayed channel closing and, thus, increased cellular excitability.
Both classical and atypical Timothy syndromes are caused by mutations in CACNA1C. These mutations are in exon 8 (atypical form) and exon 8a (classical form), an alternatively spliced exon. Exon 8a is highly expressed in the heart, brain, gastrointestinal system, lungs, immune system and smooth muscle. Exon 8 is also expressed in these regions and its level is approximately 5-fold higher than exon 8a expression.
There is one mutation found in patients with classical Cack syndrome, G406R, located just past the 6th membrane spanning segment of domain 1 (D1S6). The conserved glycine at this position seems to be vital for proper voltage dependent inactivation as the mutant is lacking in this respect.[3] Atypical Timothy syndrome mutations are similar, one being the identical G406R mutation in the other splice form and the second mutation being G402S, located a few amino acids upstream. The affect of these mutations on channel function is identical to the G406R mutation in classical Timothy syndrome.[4] The lack of proper voltage-dependent inactivation in these mutants causes prolonged inward current and depolarization during cardiac action potentials. This leads to long QT syndrome and resultant arrhythmia. Because exon 8 has greater expression in the heart versus exon 8a, patients with atypical Timothy syndrome have worsened cardiac defects compared to those with the classical form.

[edit]Treatment

Surgery is typically used to correct structural heart defects and syndactyly. Propanolol or beta-adrenergic blockers are often prescribed as well as insertion of a pacemaker to maintain proper heart rhythm. With the characterization of Timothy syndrome mutations indicating that they cause defects in calcium currents, it has been suggested that calcium channel blockers may be effective as a therapeutic agent.[4]

[edit]Prognosis

The prognosis for patients diagnosed with Timothy syndrome is very poor. Of 17 children analyzed in one study, 10 died at an average age of 2.5 years. Of those that did survive, 3 were diagnosed with autism, one with an autism spectrum disorder, and the last had severe delays in language development.[3] One patient with atypical Timothy syndrome was largely normal with the exception of heart arrhythmia.[4] Likewise, the mother of two Timothy syndrome patients also carried the mutation but lacked any obvious phenotype. In both of these cases, however, the lack of severity of the disorder was due to mosaicism.

[edit]History

Some of the abnormalities observed in Timothy syndrome were described in the 1990s. However, it was linked with calcium channel abnormalities in 2004, and the disorder was thence named "Timothy syndrome" in honor of Dr. Katherine W. Timothy, who was among the first to identify a case and performed much of the phenotypic analysis that revealed other abnormalities.[3]

[edit]See also

[edit]External links

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