Tuesday, 5 July 2016

E.coli O157 Outbreak Linked to Contaminated Mixed Salad Leaves in England

Hands being washed under running water.
There is an Escherichia coli (E. coli) outbreak affecting more than 100 UK people could be linked to eating contaminated mixed salad leaves according to public health England. To date, 109 people (figure correct as at 4 July 2016) are known to have caught the bug - 102 in England, 6 in Wales and 1 in Scotland with the South West of England particularly affected.
PHE has been working to establish the cause of the outbreak and has now identified that several of the affected individuals ate mixed salad leaves including rocket leaves prior to becoming unwell. Currently, the source of the outbreak is not confirmed and remains under investigation. PHE is now reminding people to maintain good hygiene and food preparation practices in response to the current outbreak.
E. coli O157 infection can cause a range of symptoms, from mild diarrhoea to bloody diarrhoea with severe abdominal pain. On rare occasions, it can also cause more serious medical conditions and can be caught by eating contaminated food or by direct contact with animals with the bacteria. It can also be passed from an infected individual to another person if hand and toilet hygiene is poor.
Dr Isabel Oliver, director of PHE's field epidemiology service, said: "At this stage, we are not ruling out other food items as a potential source."
PHE was first alerted to the outbreak at the end of June. Dr Oliver said people could help protect themselves from possible infection by washing their hands before eating and handling food and by thoroughly washing vegetables and salads that they were preparing to eat.
E. coli O157 is found in the gut and faeces of many animals, particularly cattle, and can contaminate food and water. Outbreaks of E. coli O157 are rare compared with other food-borne diseases.
Avoiding E. coli O157 infection
§  Wash hands thoroughly after using the toilet, before and after handling food, and after handling animals
§  Remove any loose soil before storing vegetables and salads
§  Wash all vegetables and fruits that will be eaten raw
§  Store and prepare raw meat and unwashed vegetables away from ready-to-eat foods
§  Do not prepare raw vegetables with utensils that have also been used for raw meat
§  Cook all minced meat products, such as burgers and meatballs, thoroughly

§  People who have been ill should not prepare food for others for at least 48 hours after they have recovered

Source - PHE & BBC

Sunday, 17 April 2016

Concerns over the spread of untreatable multi-antimicrobial resistant gonorrhoea strain

There is a huge concern by health sector and Doctors in England over wide spread of untreatable multi-antimicrobial resistant gonorrhoea strain widely across England and to gay men.
The new superbug prompted a national alert last year shared in this blog (Read it here), as one of the main treatments had become useless against it. Public Health England acknowledges measures to contain the outbreak have been of limited success.
Doctors fear the sexually transmitted infection, which can cause infertility, could soon become untreatable. There are now cases of this resistant gonorrhoea in the West Midlands, London and southern England. Only 34 cases have been officially confirmed in laboratory testing, but this is likely to be the tip of the iceberg of an infection that can be symptomless.
The outbreak started in straight couples, but is now being seen in gay men too. A consultant in sexual health based in Bristol, Peter Greenhouse said that we’ve been worried it would spread to men who have sex with men which is what we have now. The problem is that they tend to spread infections a lot faster simply as they change partners more quickly. They are also more likely to have gonorrhoea in their throats. Further resistance is more likely to develop as antibiotics get to the throat in lower doses and the area is also teeming with other bacteria that can share the resistance to drugs.
The bacterium that causes gonorrhoea is extremely adept at shrugging off our best antibiotics. Two drugs - azithromycin and ceftriaxone - are used in combination, but now resistance to azithromycin is spreading and doctors fear it is only a matter of time before ceftriaxone fails too.

The disease is caused by the bacterium called Neisseria gonorrhoeae and infection is spread by unprotected vaginal, oral and anal sex. Of those infected, about one in 10 heterosexual men and more than three-quarters of women, and gay men, have no easily recognisable symptoms. But symptoms can include a thick green or yellow discharge from sexual organs, pain when urinating and bleeding between periods.
Untreated infection can lead to infertility, pelvic inflammatory disease and can be passed on to a child during pregnancy.

Read more at http://www.bbc.co.uk/news/health

Polio Vaccination: Vaccine switched in a bid towards ending polio

Over 150 countries have begun switching to a different polio vaccine which has been hailed by health campaigners as an important milestone towards polio eradication. The new vaccine will target the two remaining strains of the virus under a switchover 18 months in the planning. There were just 74 cases of the paralysing disease in 2015 and there have been 10 so far this year. All of the cases were in Afghanistan and Pakistan. Africa has been free of polio for more than a year. Switching the vaccine from one successfully used to fight polio for more than 30 years is a huge logistical exercise.
Thousands of people will monitor the changeover in 155 countries during the next fortnight. It is taking effect mainly in developing countries, but also in richer ones such as Russia and Mexico. The new vaccine will still be given as drops in the mouth, so healthcare workers will not need fresh training. It will no longer include a weakened version of type 2 polio virus, which was eradicated in 1999.
Dr Stephen Cochi, from the US-based Centers for Disease Control (CDC), said that the current vaccine contains live weakened virus relating to three types of polio. But we don't need the type 2 component, as it's not in the world any longer. And in very rare cases it can mutate and lead to polio, through what's called circulating vaccine-derived virus. So removing type 2 from the vaccine takes away that risk - and ensures we have a vaccine which will work better dose by dose.
The planning involved in the switchover has included dealing with a global stockpile of 100 million doses of vaccine targeting just type 2, built up as an insurance policy in case of any outbreak. The World Health Organization denied some media reports that millions of doses of the old vaccine would need to be destroyed, by incineration or other approved means. Its director of polio eradication, Michel Zaffran, said some will need to be destroyed, but this will be a few vials, not trucks full of vaccine. This has been carefully planned because of the huge amount of resources, so countries have been using up the old vaccine, to minimise leftover quantities. We're closer than ever to ending polio worldwide, which is why we are able to move forward with the largest and fastest globally synchronised vaccine switchover.

Read more at http://www.bbc.co.uk/news/health

Sunday, 10 April 2016

PHE Update on rising Scarlet Fever across England

Group A streptococcus (GAS) on Blood Agar
Following the Public Health England (PHE) warning on the rise in cases of scarlet fever in England, they have reported a continued increase in cases of scarlet fever across England with 1319 new cases between 21 to 27 March. This is the highest weekly total recorded in recent decades (data available from 1982 onwards). Since the season began in September 2015, there have been a total of 10,570 reported cases of scarlet fever. Scarlet fever is a seasonal illness which should be treated with antibiotics and cases of the illness usually peak at this time of year.
An increase in invasive disease caused by the same bacterium Group A streptococcus (GAS) which causes scarlet fever has also been seen in England. A total of 593 cases of invasive Group A streptococcus infection, such and bloodstream infection or pneumonia, have been notified so far for 2016 compared to 440 cases for the same period last year (January to March). Group A streptococcus seasonal activity this year coincides with the seasonal influenza activity owing to the late flu season. Influenza and invasive Group A streptococcus co-infection is a rare but well-recognised occurrence. Whilst the elderly remain most at risk of invasive Group A streptococcus infection, increased levels of disease compared to last year have been seen in young adults and children less than 5 years old, the age groups most affected by influenza in recent weeks. There’s no suggestion of an increase in invasive Group A streptococcus infection in patients diagnosed with scarlet fever.
This is the third season in a row in which elevated scarlet fever activity has been noted. A total of 15,637 notifications were made in England and Wales in 2014, rising to 17,590 in 2015. Weekly activity so far this season has been similar or slightly above for that last year.
Group A streptococcus bacteria are spread by direct person-to-person contact with an individual carrying the bacteria or indirectly through contact with bacteria in the environment. The act of keeping wounds clean and practising hand hygiene can decrease chances of catching a Group A streptococcus infection.
Dr Theresa Lamagni, PHE’s head of streptococcal infection surveillance, said that while we hope that the Easter school break will assist in slowing down transmission of the bacteria causing scarlet fever, we cannot assume or rely on this being the case. As such, our investigations and assessment of the impact of this extraordinary rise in scarlet fever continue.
As we reach peak season for scarlet fever, health practitioners should be particular mindful of the current high levels of scarlet fever when assessing patients. Close monitoring, rapid and decisive response to potential outbreaks and early treatment of scarlet fever with an appropriate antibiotic remains essential, especially given the potential complications associated with Group A streptococcal infections. PHE strongly urges people with symptoms of scarlet fever, which include a sore throat, headache and fever accompanied by a characteristic rash, to consult their GP. Scarlet fever should be treated with antibiotics to reduce risk of complications. Once children or adults are diagnosed with scarlet fever we strongly advise them to stay at home until at least 24 hours after the start of antibiotic treatment to avoid passing on the infection.
Scarlet fever is mainly a childhood disease and is most common between the ages of 2 and 8 years. It was once a very dangerous infection, but has now become much less serious, thanks to the use of antibiotics. There is currently no vaccine for scarlet fever.
Below is the PHE regional breakdowns for scarlet fever seasonal activity in England between September and March (for 2014 to 2015, and 2015 to 2016; weeks 37 to 13)
Scarlet Fever Notifications
2014 – 2015 (weeks 37 – 13
2015 – 2016 (weeks 37 - 13)
Area name
Anglia and Essex
Avon, Gloucestershire and Wiltshire
Cheshire and Merseyside
Cumbria and Lancashire
Devon, Cornwall and Somerset
East Midlands
Greater Manchester
Kent Surrey and Sussex
North East
South Midlands and Hertfordshire
Thames Valley
West Midlands
Yorkshire and Humber
Grand Total

Thursday, 24 March 2016

Detection of Helicobacter pylori antigen by enzyme immunoassay (EIA)

Helicobacter pylori antigen test was performed using Premier Platinum HpSA PLUS enzyme immunoassay (EIA). The kit used was purchased from Meridian Bioscience Inc. The Premier Platinum HpSA PLUS enzyme immunoassay (EIA) kit is an in vitro qualitative procedure for the detection of Helicobacter pylori antigens in human stool. Test results are intended to aid in the diagnosis of H. pylori infection and to monitor response during and post-therapy in patients. Accepted medical practice recommends that testing by any current method, to confirm eradication, be done at least four weeks following completion of therapy.
Helicobacter pylori which is previously known as Campylobacter pylori, is a gram negative, microaerophilic bacterium usually found in the stomach. It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren, who found that it was present in a person with chronic gastritis and gastric ulcers, conditions not previously believed to have a microbial cause. It is also linked to the development of duodenal ulcers and stomach cancer. However, over 80% of individuals infected with the bacterium are asymptomatic, and it may play an important role in the natural stomach ecology. According to research, more than 50% of the world's population harbour H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. H. pylori's helical shape and its flagella is used to penetrate the mucoid lining of the stomach to reach the epithelial cells underneath, where the pH is more neutral. They also neutralise the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. The ammonia, which is basic, then neutralizes stomach acid. This ammonia produced to regulate pH is toxic to epithelial cells, as well as other biochemicals produced by H. pylori such as proteases, vacuolating cytotoxin A (VacA) and certain phospholipases. Cytotoxin associated gene CagA can also cause inflammation and is potentially a carcinogen.
Most people infected with H. pylori are asymptomatic but in acute infection may appear as an acute gastritis with abdominal pain or nausea. If the infection develops into chronic gastritis, the symptoms may include nausea, belching, stomach pains, bloating, black stool and sometimes vomiting
Individuals infected with H. pylori have a 10 - 20% lifetime risk of developing peptic ulcers and a 1 - 2% risk of acquiring stomach cancer. Inflammation of the pyloric antrum is more likely to lead to duodenal ulcers, while inflammation of the corpus (body of the stomach) is more likely to lead to gastric ulcers and gastric carcinoma. However, H. pylori possibly plays a role only in the first stage that leads to common chronic inflammation, but not in further stages leading to carcinogenesis. A meta-analysis conducted in 2009 concluded the eradication of H. pylori reduces gastric cancer risk in previously infected individuals, suggesting the continued presence of H. pylori constitutes a relative risk factor of 65% for gastric cancers and in terms of absolute risk, the increase was from 1.1 - 1.7%. H. pylori have been associated with colorectal polyps and colorectal cancer and may also be associated with eye disease
The faeces sample should be received in an airtight transport container and stored at 2-8oC until tested. The specimen should be tested as soon as possible, but may be held up to 72 hours at 2-8oC prior to testing. If testing cannot be performed within this time frame, specimens should be frozen immediately upon receipt and stored frozen (-20oC to –80oC) until tested. Specimens may be frozen and thawed twice.
Stool in transport media, swabs, or preservatives are inappropriate for testing.
1. Using a pipetting device, add 500μL of Sample Diluent to a clean test tube.
2. Mix stool as thoroughly as possible prior to pipetting.
a. Liquid or semi-solid stools - Using the supplied transfer pipette, add 100μL (second mark from the tip of the pipette) of stool into Sample Diluent. Using same pipette, gently withdraw and expel the stool suspension several times, then vortex 15 seconds. Save the transfer pipette in the sample for later use.
b. Formed/Solid stools - Using a wooden applicator stick, transfer a small portion (5-6 mm diameter) of thoroughly mixed stool into Sample Diluent. Emulsify stool using the wooden applicator stick, then vortex 15 seconds.
3. Stool specimens may be centrifuged after dilution. Centrifuge at approximately
2750 x G for five minutes or until solid matter separates from liquid. Proceed with the assay after recovering supernate.
1. After the pouch has reached temperature, break off the required number of
microwells (1 well for each specimen, plus 1 positive and 1 negative control well per
batch). Place the microwells in the microwell strip holder and record the location of
all wells. Unused microwells must be resealed in the pouch immediately.
2. Using the specimen transfer pipette, add 100μL of diluted stool (second mark from the tip of the pipette) to the appropriate well. (Place the pipette tip halfway into well and let the sample slowly run down side of well.)
3. Add 2 free falling drops of Positive Control and 100μL of Sample Diluent /Negative Control to the appropriate wells.
4. Add 1 free falling drop (approximately 50μL) of Enzyme Conjugate to each well.
Firmly shake/swirl the plate for 30 seconds.
5. Cut plate sealer to size and press firmly onto top of microwells to seal. Incubate the plate for 1 hour at 19-27oC
6. Carefully remove the plate sealer and wash wells:
a. Manual method:
i Dump plate contents firmly into a biohazard receptacle.
ii Bang the inverted plate on a clean stack of paper towels.
iii Fill all wells with 1X Wash Buffer I, directing stream of buffer to the sides of the wells to avoid foaming.
iv Repeat wash cycle (dump, bang on fresh towels, fill) 4 times for a total of 5 wash cycles. After the last fill, dump and bang plates on fresh towels hard enough to remove as much excess wash buffer as possible, but do not allow wells to completely dry at any time.
b. Semiautomated method using validated equipment
i Aspirate the contents of the well.
ii Fill the wells to the top (approx. 300-350μL/well) with 1X Wash Buffer I then aspirate. The washer manifold should be adjusted to ensure no foaming occurs during the filling of the wells and that the wells are thoroughly aspirated after each wash.
iii Repeat step ii a minimum of 4 more times. Following the last wash, test wells should be thoroughly aspirated to remove as much moisture as possible.
7. Clean the underside of all wells with a lint-free tissue.
8. Add 2 free falling drops (approx. 100μL) of Premier Substrate Solution I to each well. Firmly shake/swirl the plate for 30 seconds. Incubate for 10 minutes at 19-27 oC.
9. Add 2 free-falling drops (approx. 100μL) of Premier Stop Solution I to each well.
Firmly shake/swirl the plate for 30 seconds.
Initial colour of positive reaction is blue, which changes to yellow upon addition
of Premier Stop Solution I.
10. Inspect and record reactions. Test results can be read visually or using a
spectrophotometric reader.
a. Visual Determination - Read within 15 minutes after adding Premier Stop
Solution I.
b. Spectrophotometric Determination - Zero EIA reader on air. Wipe underside
of wells with a lint-free tissue. Read absorbance at 450 nm or 450/630 nm
within 15 minutes of adding Premier Stop Solution I.
The following interpretations apply to both initial diagnosis and monitoring of anti-H. pylori therapy.
Visual Reading
Negative = colorless to faint yellow
Positive = definite yellow color
To be called positive, a faint yellow color must be confirmed by a spectrophotometric reading. If a spectrophotometer is not available, the cut-off must be determined by an alternative method.
Spectrophotometric Single Wavelength (450 nm)
Negative: < 0.140
Positive: ≥ 0.140
Negative Control: < 0.140

Positive Control: ≥ 0.640

Meningococcal C (MenC) vaccine schedule in infant to be changed by July 2016 - PHE

The Public Health England (PHE) will implement the recommendation by The Joint Committee on Vaccination and Immunisation (JCVI) which is that infants no longer require vaccination against meningococcal serogroup C (MenC). Therefore, from 1 July 2016, infants should no longer receive the dose of MenC conjugate vaccine currently given at the second primary immunisation visit at around 12 weeks of age. The Hib/MenC vaccine (Menitorix) dose given at 12 months of age and the MenACWY conjugate vaccine dose given at around 14 years of age are unaffected by this change and should still be given.
The JCVI also said that, because of the successful MenC programme introduced in 1999, there are now very few cases of invasive MenC disease. Vaccination of adolescents with MenC conjugate vaccine which began in the 2013/14 academic year, and later, MenACWY conjugate vaccine should sustain good herd protection and therefore the risk to infants will remain low. The dose of combined Hib/MenC offered at 12 months of age will provide good protection to toddlers and younger children. In addition, the introduction of Bexsero® (i.e. MenB vaccine) in to the infant programme may provide a degree of protection against some cases of invasive MenC disease.
The revised routine schedule for MenC-containing vaccinations from 1 July 2016.

Dose and Vaccine
12 – 13 months old
One dose of Hib/MenC Vaccine
Around 14 years old (ideally at the same time as Td/IPV)
One dose of MenACWY Conjugate vaccine

The routine MenC booster dose that was offered to pupils in school year 9/10 was replaced with the MenACWY conjugate vaccine from September 2015, to offer additional protection against meningococcal capsular group A, W and Y in response to a national outbreak of invasive MenW disease. As part of a time limited catch-up campaign, those aged up to 25 years entering university as undergraduates for the first time, should be offered a MenC-containing vaccine. A comprehensive MenACWY catch-up programme was introduced last Autumn through general practice and schools to vaccinate all adolescents aged 14-18 years in response to an increase in meningococcal W (MenW) disease.