Friday, January 19, 2018

CDC FluView Week #2 - Flu Still Rising

https://www.cdc.gov/flu/weekly/index













#13,085


Although there were hopes expressed last week that influenza was beginning to plateau across the nation, today's FluView report shows another hefty increase in outpatient visits for ILI (Influenza-like Illness), and cumulative hospitalizations (all ages) have jumped by nearly 50% (22.7 to 31.5) since last week.


https://www.cdc.gov/flu/weekly/index

Last week the P&I mortality rate (which lags other data) was at the epidemic threshold of 7.0% for week 51, while this weeks report has it at 8.2% (see below) - well above the epidemic threshold of 7.1% for week 52.


 https://www.cdc.gov/flu/weekly/index

P&I Mortality is a notoriously trailing indicator, and these numbers are subject to revision,  as severely ill patients may survive for days or weeks before succumbing and there are often delays in reporting adult flu deaths.

Sadly, another 10 pediatric flu deaths are reported for week 2. While nationally reportable, these numbers likely only capture 1/2 to 1/3rd of the pediatric flu deaths each year, and we often see belated reporting in this category as well.

https://www.cdc.gov/flu/weekly/index
 


 This week's summary from a much longer, and far more detailed report:
2017-2018 Influenza Season Week 2 ending January 13, 2018

All data are preliminary and may change as more reports are received.
Synopsis:

During week 2 (January 7-13, 2018), influenza activity increased in the United States.
  • Viral Surveillance: The most frequently identified influenza virus subtype reported by public health laboratories during week 2 was influenza A(H3). The percentage of respiratory specimens testing positive for influenza in clinical laboratories increased.
  • Pneumonia and Influenza Mortality: The proportion of deaths attributed to pneumonia and influenza (P&I) was above the system-specific epidemic threshold in the National Center for Health Statistics (NCHS) Mortality Surveillance System.
  • Influenza-associated Pediatric Deaths: Ten influenza-associated pediatric deaths were reported
  • Influenza-associated Hospitalizations: A cumulative rate of 31.5 laboratory-confirmed influenza-associated hospitalizations per 100,000 population was reported.
  • Outpatient Illness Surveillance:The proportion of outpatient visits for influenza-like illness (ILI) was 6.3%, which is above the national baseline of 2.2%. All 10 regions reported ILI at or above region-specific baseline levels. New York City, Puerto Rico, and 32 states experienced high ILI activity; 9 states experienced moderate ILI activity; the District of Columbia and six states experienced low ILI activity; and three states experienced minimal ILI activity.
  • Geographic Spread of Influenza:The geographic spread of influenza in Puerto Rico and 49 states was reported as widespread; Guam reported regional activity; the District of Columbia and one state reported local activity; and the U.S. Virgin Islands reported sporadic activity.

There are reports from some parts of the country that the intensity of flu may be starting to wane.  Even so, there is like another 6 to 10 weeks of flu activity ahead, and the potential for seeing a `second wave' of influenza B or H1N1 later in the spring.


PNAS: Infectious Virus Exhaled In Breath Of Symptomatic Seasonal Flu Cases


Youtube Video (no sound)

#13,084


Last weekend, in his Virology Down Under blog, Dr. Ian Mackay took a long look at the ways humans shed and spread influenza viruses (see Influenza virus transmission: with or without symptoms, you’re dropping Flu virus). It is an excellent review, well worth reading in its entirety,
Ian looked at both large droplet and fine aerosol transmission from coughing, sneezing and simply just breathing - along with fomite contamination - even from asymptomatic carriers
 While viral RNA had been detected simply from the exhalation of flu victims, Ian cautioned:
Viruses were not able to be grown in culture, or culture was not used in these studies and this is a limitation because we can’t say with certainty that viruses were breathed out during such studies could infect a susceptible person; we don’t know if the positive results mean infectious virus was present.
This is a topic I wrote about a couple of weeks ago myself, while reviewing a Journal of Infectious Disease study (see  J.I.D.: Asymptomatic Summertime Shedding Of Respiratory Viruses).
 
Well science marches on, and a new study published yesterday in the Journal PNAS (Proceedings of the National Academy of Science) provides additional evidence for, and gives considerable more weight to, the idea that flu carriers exhale substantial quantities of infectious influenza virus
Infectious virus in exhaled breath of symptomatic seasonal influenza cases from a college community

Jing Yana,b, Michael Granthama,1, Jovan Pantelica,2, P. Jacob Bueno de Mesquitaa, Barbara Alberta, Fengjie Liua,3, Sheryl Ehrmanb,4, Donald K. Miltona,5, EMIT Consortium6

Significance

Lack of human data on influenza virus aerosol shedding fuels debate over the importance of airborne transmission. We provide overwhelming evidence that humans generate infectious aerosols and quantitative data to improve mathematical models of transmission and public health interventions.
We show that sneezing is rare and not important for—and that coughing is not required for—influenza virus aerosolization. Our findings, that upper and lower airway infection are independent and that fine-particle exhaled aerosols reflect infection in the lung, opened a pathway for a deeper understanding of the human biology of influenza infection and transmission. Our observation of an association between repeated vaccination and increased viral aerosol generation demonstrated the power of our method, but needs confirmation.

Abstract

Little is known about the amount and infectiousness of influenza virus shed into exhaled breath. This contributes to uncertainty about the importance of airborne influenza transmission. 


We screened 355 symptomatic volunteers with acute respiratory illness and report 142 cases with confirmed influenza infection who provided 218 paired nasopharyngeal (NP) and 30-minute breath samples (coarse >5-µm and fine ≤5-µm fractions) on days 1–3 after symptom onset. We assessed viral RNA copy number for all samples and cultured NP swabs and fine aerosols. 

We recovered infectious virus from 52 (39%) of the fine aerosols and 150 (89%) of the NP swabs with valid cultures. The geometric mean RNA copy numbers were 3.8 × 104/30-minutes fine-, 1.2 × 104/30-minutes coarse-aerosol sample, and 8.2 × 108 per NP swab. Fine- and coarse-aerosol viral RNA were positively associated with body mass index and number of coughs and negatively associated with increasing days since symptom onset in adjusted models.
Fine-aerosol viral RNA was also positively associated with having influenza vaccination for both the current and prior season. NP swab viral RNA was positively associated with upper respiratory symptoms and negatively associated with age but was not significantly associated with fine- or coarse-aerosol viral RNA or their predictors. Sneezing was rare, and sneezing and coughing were not necessary for infectious aerosol generation. Our observations suggest that influenza infection in the upper and lower airways are compartmentalized and independent.
         (Continue . . . )

 The full, open access study can be read here, and it contains  a number of gems. 
  • Men shed influenza viruses in greater quantity than women through fine aerosols.
  • But women cough more frequently
  • Most surprisingly, they observed `6.3 (95% CI 1.9–21.5) times more aerosol shedding among cases with vaccination in the current and previous season compared with having no vaccination in those two seasons.'
This is the first detection of a possible vaccination connection and must be verified by additional studies, and then perhaps a reason can be attached.

In addition to releasing a short video, the University of Maryland School of Public Health published the following press release (see excerpt below) on this new study.  You'll also find a pretty good picture of the Gesundheit II machine they used in their study on their site.

Flu may be spread just by breathing, new study shows; coughing and sneezing not required

January 18, 2018
It is easier to spread the influenza virus (flu) than previously thought, according to a new University of Maryland-led study released today. People commonly believe that they can catch the flu by exposure to droplets from an infected person’s coughs or sneezes or by touching contaminated surfaces. But, new information about flu transmission reveals that we may pass the flu to others just by breathing.
 

(SNIP)

“We found that flu cases contaminated the air around them with infectious virus just by breathing, without coughing or sneezing,” explained Dr. Donald Milton, M.D., MPH, professor of environmental health in the University of Maryland School of Public Health and lead researcher of this study. “People with flu generate infectious aerosols (tiny droplets that stay suspended in the air for a long time) even when they are not coughing, and especially during the first days of illness. So when someone is coming down with influenza, they should go home and not remain in the workplace and infect others.”

Researchers from the University of Maryland, San Jose State University, Missouri Western State University and University of California, Berkeley contributed to this study funded by the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health.

(Continue . . . )

All of these tests were conducted on symptomatic, flu positive cases and illustrate why it is important to stay home when you are sick, even if you aren't coughing or sneezing up a storm.
What may be a `mild flu' for you could easily be deadly for someone else.
As we've discussed previously, people can spread influenza during the 24 hours before symptoms appear - or may have such minor symptoms as to not realize they are ill - (see PLoS One: Influenza Viral Shedding & Asymptomatic Infections).

While asymptomatic spread still provides a loophole for the virus to spread, this study lends  additional support to the idea of having and wearing simple surgical masks when you are home with the flu and are around other family members - even if you aren't coughing or sneezing. 

But most of all, this study shows us just how easily influenza can spread in the community, even from someone who doesn't appear all that sick.




Thursday, January 18, 2018

Eurosurveillance Review: Association Between Acute Flaccid Myelitis (AFM) & Enterovirus D68 (EV-D68)

AFM Surveillance United States 2014-2017  - Credit CDC














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Acute flaccid myelitis (AFM) is a rare polio-like illness that affects a person’s nervous system - specifically the spinal cord - and is characterized by sudden weakness in one or more arms or legs, along with loss of muscle tone and decreased or absent reflexes.

AFM is a subset of conditions that fall under a broader `umbrella' of syndromes called Acute Flaccid paralysis (AFP), which may include myelitis, peripheral neuropathy, myopathy, Guillain-Barré syndrome (GBS), toxic neuropathy, and other muscle disorders.

While the exact causes of Acute flaccid myelitis aren't fully understood, it has been linked to a number of viral infections, including West Nile Virus, Adenoviruses, and a number of (polio and non-polio) enteroviruses, including EV-71 and more recently, EV-D68
A nationwide outbreak of EV-D68 was linked to a concurrent spike in AFP cases across the United States in the fall of 2014, and while a pretty strong circumstantial case has been made over the past couple of years (see EID Journal Enterovirus D68 Infection in Children with Acute Flaccid Myelitis, Colorado, USA, 2014), no definitive causal link to EV-D68 has been established.
Since then we've seen a number of EV-D68 outbreaks around the world (see here, here & here) where a concurrent spike in AFM cases have also been reported. 
Today the ECDC's Eurosurveillance Journal has a review of the literature, and an examination of the available evidence using the Bradford Hill criteria, that attempts to establish a potential link between EVD68 infection and AFM.

http://www.eurosurveillance.org/content/table/10.2807/1560-7917.ES.2018.23.3.17-00310.t1?fmt=ahah&fullscreen=true


The authors found that analysis based on the Bradford Hill criteria suggested good evidence for EV-D68 being a cause of AFM.  Today's review is a lengthy, detailed one, which most of my readers will want to read it in its entirety.

The link and a few small excerpts follow:
The association between acute flaccid myelitis (AFM) and Enterovirus D68 (EV-D68) – what is the evidence for causation?  

Amalie Dyda1, Sacha Stelzer-Braid2,3, Dillon Adam1, Abrar A Chughtai1, C Raina MacIntyre1,4
         (EXCERPT)
Discussion
Historically, the incidence of EV-D68 has been low, with sporadic cases and small clusters of mild illness reported. Whether this represents under-ascertainment or true low incidence in the past is unclear, but active EV surveillance studies in several countries including Germany in 2013-14, Hong Kong in 2014, France in 2014 and China in 2011-15 suggest that EV-D68 was a rare cause of clinical infection in the past [18-21]. Since 2014, the number of reported infections and clusters has increased. In addition, severe complications including AFM have been reported since 2014 [3]. Several clusters of AFM in recent years were associated with EV-D68 and a large outbreak of EV-D68 in 2014 in the US was associated with severe respiratory illness.

Our application of the Bradford Hill criteria suggested good evidence for EV-D68 being a cause of AFM. While EVs in general are neurotropic, AFM has never previously been associated with EV-D68. It could be that incidence of EV-D68 was genuinely been much lower in the past, so that rare complications of infection have not been apparent. An analogous example is the association between Zika virus and microcephaly which was only recognised during a large-scale epidemic in Brazil in 2015 [62,63]. However, retrospective analysis of a large outbreak of Zika virus in French Polynesia two years earlier showed the same association with microcephaly but was not recognised at the time [64]. In addition, clades A, B and B1 of EV-D68 were highly neurovirulent in animal studies, with specific tropism for motor neurons [47]. It appears that these strains which evolved after the year 2000 are capable of causing AFM, as demonstrated in a mouse model, while the original Fermon and Rhyne strains do not cause AFM [47].

There is a need for phylogeographic epidemiology to ascertain temporal and geographic changes in the virus and whether such changes could explain why AFM is newly associated with the virus. Genetic changes in the virus which have rendered it more neuropathic could explain the association, and several clades have been shown to be highly neurovirulent. Phylogenetic studies have demonstrated that strains isolated in recent outbreaks are very divergent from the original Fermon strain isolated in 1962 [15]. Clades B1 and B2 caused the 2014 outbreak [30] and clade B3 caused an outbreak of severe EV-D68 infection in the Netherlands in 2016 [17]. Strains in clade B1 have mutations in structural and non-structural proteins, which could play a role in the reported neurovirulence of these strains [12], and all EV-D68-infections in human AFM cases were attributed to clade B. However, mouse studies showed that multiple clades (A, B and B1) cause paralysis [47]. The observation that clade B1 was associated with AFM in 2014 may be due to the much higher incidence of clade B1 infection in 2014. More research is needed to study biological gradient and to quantify measures of association between EV-D68 and AFM.

Given that the association of AFM with EV-D68 is recent, there is a strong case for systematic and enhanced EV surveillance, which will enable investigation of epidemiological data for measures of association. While past studies and EV surveillance showed that EV-D68 was a rare cause of EV infection, there has been a change in disease epidemiology since 2014, including a rise in the incidence of clade B infections. The lack of association between AFM cases and EV-D68 in the US in 2015 and 2016 [11] does not detract from our analysis, as AFM is a clinical syndrome with multiple possible aetiologies. More recent AFM cases could be due to a different aetiology, as other EVs continue to cause AFM, or could reflect the difficulty in isolating the virus from tissue and CSF. The Bradford Hill criteria are a tested and systematic method for evaluating causality and could be applied to other EVs.
 Conclusion
In summary, the application of the Bradford Hill criteria suggests that EV-D68 causes AFM. AFM has not previously been associated with EV-D68, and a mouse model shows that the original Fermon strain does not cause AFM, whereas the 2014 outbreak strain does [47]. It appears that the incidence of this infection and the clade-specific epidemiology have changed. Phylogeographic epidemiology will further our understanding of the temporal and spatial spread of increasingly neurovirulent clades and improve risk analysis. Further investigation into this relationship is important because of the severity of AFM, ongoing outbreaks of AFM and because there is currently no treatment for AFM related to EV-D68, and no vaccine to prevent infection [24,65].
        (Continue . . .)

Hong Kong Flu Express: Influenza B Ramps Up











#13,082


Hong Kong, which saw a relatively mild winter flu season last year - followed by an unusually severe H3N2 summer flu (see chart above) - entered back into their 2018 winter flu epidemic a little over a week ago, this time with influenza B leading the charge. 
Although Influenza B is generally regarded as being less severe than Influenza A, it can still exact a heavy toll, particularly on small children and the elderly. 
Today the HK CHP released their week 2 Flu Express report, and it shows increasing flu activity.  During week 2 and the first 4 days of week 3 (January 7th - 18th), Hong Kong has seen 24 flu deaths, including 1 pediatric fatality.


FLU EXPRESS
 
Flu Express is a weekly report produced by the Respiratory Disease Office of the Centre for Health Protection. It monitors and summarizes the latest local and global influenza activities.

Local Situation of Influenza Activity (as of Jan 17, 2018)
Reporting period: Jan 7 – 13, 2018 (Week 2)

  • The latest surveillance data showed that the local influenza activity continued to increase. Currently the predominating virus is influenza B.
  • Influenza can cause serious illnesses in high-risk individuals and even healthy persons. Given that seasonal influenza vaccines are safe and effective, all persons aged 6 months or above except those with known contraindications are recommended to receive influenza vaccine to protect themselves against seasonal influenza and its complications, as well as related hospitalisations and deaths.
  • Apart from adopting personal, hand and environmental hygiene practices against respiratory illnesses, those members of the public who have not received influenza vaccine are urged to get vaccinated as soon as possible for personal protection.
  • The Vaccination Subsidy Scheme (VSS) and the Government Vaccination Programme (GVP) for the 2017/18 season have been launched on Oct 18 and Oct 25, 2017 respectively. The VSS continues to provide subsidised vaccination to children aged 6 months to under 12 years, elderly aged 65 years or above, pregnant women, persons with intellectual disabilities and recipients of Disability Allowance. Eligible groups for free vaccination are the same as those of 2016/17 under the GVP. For more details, please refer to the webpage
(http://www.chp.gov.hk/en/view_content/17980.html)
         (SNIP)
Since the start of the 2017/18 winter influenza season in week 2, 41 adult cases of ICU admission/death with laboratory confirmation of influenza were recorded, in which 23 of them were fatal (as of January 17). Among them, 34 patients had infection with influenza B, 5 patients with influenza A(H1N1)pdm09, one patient with influenza A(H3N2) and one patient with influenza A pending subtype.
         (SNIP)
In week 2 and the first 4 days of week 3 (Jan 14 to 17), there were three cases of severe paediatric influenza-associated complication/death, in which one of them was fatal.               

         (SNIP)
Global Situation of Influenza Activity
  • In Mainland China (week ending Jan 7, 2018), the influenza activity in both southern and northern provinces was at the seasonal level for winter influenza season, and was still on an increasing trend. In southern provinces, the proportion of ILI cases in emergency and outpatient departments reported by sentinel hospitals was 6.0%, higher than that reported in the previous week (5.5%) and that in the corresponding period in 2014-2016 (3.0%, 3.2%, 3.3%). In northern provinces, that proportion was 5.8%, higher than that reported in the previous week (5.5%) and that in the corresponding period in 2014-2016 (4.1%, 2.9%, 3.8%). The proportion of influenza detections in the week ending January 7, 2018 was 44.8%. The most common influenza virus detected currently was influenza B.
  • In Macau (week ending Jan 6, 2018), the proportions of ILI cases in emergency departments among both adults and children increased. The proportion of influenza detections was 32.2%, an marked increase from 17.0% in the previous week.
  • Taiwan (week ending Jan 13, 2018) was at influenza season. In the week ending January 13, the proportion of ILI cases in emergency department was 13.18% which was above the threshold of 11.4%. The predominating virus was influenza B.
  • In Japan (week ending Jan 7, 2018), the influenza season has started in late November 2017. The average number of reported ILI cases per sentinel site slightly decreased to 16.31 in the week ending January 7, 2018, which was higher than the baseline level of 1.00. The most frequently identified influenza virus type in the past five weeks was influenza A(H1N1)pdm09, followed by influenza B and A(H3N2).
(Continue . . . )

The Lancet: Genomic Characterisation Of Human Monkeypox Virus In Nigeria

http://www.ncdc.gov.ng/themes/common/files/sitreps/56aa487b4dd7426a7f46860ae9fef651.pdf













#13,081


Beginning in September of 2017 - after an absence of nearly 40 years - Nigeria began to report scattered cases of suspected human Monkeypox (see map above).  By December 22nd - the date of the last Nigerian CDC Update -  the number of suspected cases across 23 states was nearing 200 (see chart below).

http://www.ncdc.gov.ng/themes/common/files/sitreps/56aa487b4dd7426a7f46860ae9fef651.pdf

The name `monkeypox’ is a bit of a misnomer. It was first detected (in 1958) in laboratory monkeys, but further research has revealed its host to be rodents or possibly squirrels. It produces a remarkably `smallpox looking'  illness in humans, albeit not as deadly.

Humans can contract it in the wild from an animal bite or direct contact with the infected animal’s blood, body fluids, or lesions, but consumption of under cooked bushmeat is also suspected as an infection risk. Human-to-human transmission is also possible.
According to the CDC: There are two distinct genetic groups (clades) of monkeypox virus—Central African and West African. West African monkeypox is associated with milder disease, fewer deaths, and limited human-to-human transmission.
Monkeypox is most commonly found in the Central Africa countries of the DRC and the CAR - where outbreaks have been on the rise for years (see here and here) - presumably because smallpox vaccinations (which provided up to 85% protection) were halted in the late 1970s.
While Nigeria's Monkeypox outbreak appears to be waning, the obvious question remains : how did the virus reappear nearly 40 years after the last recorded outbreak in Nigeria?
The two most likely possibilities are an imported case from the DRC or the CAR, where outbreaks remain common, or a recent zoonotic spillover from local reservoir hosts.
To try to answer that question, 29 isolates were sent to an outside lab which sequenced them in order to determine their origins. 
As an excerpt from the following Lancet correspondence explains, this appears to be the result of a local zoonotic spillover. First a link to the report, after which I'll return with a postscript.

Genomic characterisation of human monkeypox virus in Nigeria

Ousmane Faye, Catherine B Pratt, Martin Faye, Gamou Fall, Joseph A Chitty, Moussa M Diagne, Michael R Wiley, Adesola F Yinka-Ogunleye, Sola Aruna, Ebitimitula N Etebu, Neni Aworabhi, Dimie Ogoina, Wari Numbere, Nwando Mba, Gustavo PalaciosEmail the author Gustavo Palacios, Amadou A Sall, Chikwe Ihekweazu


Published: 16 January 2018
PlumX Metrics

DOI: http://dx.doi.org/10.1016/S1473-3099(18)30043-4
 
(EXCERPT)


Phylogenetic analysis (appendix) indicates that the closet relative of the three outbreak isolates were the two Nigerian strains available on GenBank (KJ642615 and KJ642617), within the west African clade. The isolates grouped most closely to KJ642617, a genome isolated from a human MPXV case in Ihie, Abia State, Nigeria, in 1971, which is relatively close to the epicentre of the current outbreak.

These findings support the hypothesis that the index case of the current outbreak in Nigeria was not imported, but probably originated from a spillover event or events involving reservoir hosts. These results emphasise the value of local surveillance for the early detection of viral spillovers and the need for advanced characterisation to help determine the origins of outbreaks.

(Continue . . . )


As the percentage of smallpox vaccinated members of the community dwindles, the risks of human MPXV outbreaks is only expected to increase (see 2010 PNAS study Major increase in human monkeypox incidence 30 years after smallpox vaccination campaigns cease in the Democratic Republic of Congo).

A 2016 study (see EID Journal:Extended H-2-H Transmission during a Monkeypox Outbreak) looked at a large 2013 outbreak of Monkeypox in the DRC and suggested that the virus's epidemiological characteristics may be changing (possibly due to the waning smallpox vaccine derived immunity in the community).
The DRC had reported a 600% increase in cases over both 2011, and 2012.  The authors also cite a higher attack rate, longer chains of infection, and more pronounced community spread than have earlier reports.
Like all viruses, Monkeypox continues to evolve and diversify, as discussed in the 2014 EID Journal article Genomic Variability of Monkeypox Virus among Humans, Democratic Republic of the Congo,  where the authors cautioned:

Small genetic changes could favor adaptation to a human host, and this potential is greatest for pathogens with moderate transmission rates (such as MPXV) (40). The ability to spread rapidly and efficiently from human to human could enhance spread by travelers to new regions.
Although Monkeypox is normally restricted to small outbreaks in Africa, in 2003 we saw a rare outbreak in the United States when a Texas animal distributor imported hundreds of small animals from Ghana, which in turn infected prairie dogs that were subsequently sold to the public (see MMWR Update On Monkeypox 2003).
By the time this outbreak was quashed, the U.S. saw 37 confirmed, 12 probable, and 22 suspected human cases. Among the confirmed cases 5 were categorized as being severely ill, while 9 were hospitalized for > 48 hrs; although no patients died (cite).
A reminder, as if we needed one, that in this highly mobile 21st century that outbreaks of rare and exotic diseases - even those occurring the most remote areas of the world - can be exported to anywhere on the globe in a matter of hours or days.

And so we watch outbreaks, such as this one in Nigeria, with considerable interest.

UK: DEFRA Expands Bird Flu Prevention Zone As More Infected Birds Are Found



















#13,080

Just over a week after 17 dead birds were discovered in Dorset (see UK: DEFRA Announcement On H5N6 In 17 Wild Birds In Dorset), the UK's DEFRA today has announced the discovery of 13 dead birds in Warwickshire, nearly 200 km to the north.

We also learn today that the total number of birds found infected in Dorset has risen to 31. As a result, DEFRA announced that the entire nation is now declared a bird flu prevention zone.
— News story

Bird flu prevention zone extended to cover whole of England

Legal requirement for all bird keepers in England to follow strict biosecurity measures.
A bird flu prevention zone has been declared across the whole of England, Chief Veterinary Officer Nigel Gibbens has confirmed today.

This means it is a legal requirement for all bird keepers to follow strict biosecurity measures. It comes as 13 dead wild birds were confirmed to have the virus in Warwickshire.

Last week 17 wild birds tested positive in Dorset and a total of 31 infected birds have now been identified at that site. Defra took swift action to put a local prevention zone in the area on Friday (12 January). However, as these latest results show the disease is not isolated to a single site the decision has been taken to extend the prevention zone across the country on a precautionary basis.

Testing of the birds found in Warwickshire is ongoing, however, it is highly expected that this will be the same H5N6 strain of the virus which has been circulating in wild birds across Europe in recent months. Public Health England have advised the risk to public health remains very low and the Food Standards Agency have said that bird flu does not pose a food safety risk for UK consumers.
        (Continue . . . .)


The UK has joined The Netherlands, Germany, and Switzerland in reporting this recently arrived H5N6 (reassorted from last year's H5N8 epizootic) virus, along with similar reassorted H5N6 viruses reported in Japan, South Korea, and Taiwan.

Three days ago DEFRA released a detailed Rapid Risk Assessment On H5N6 In Wild Birds In Dorset which drew comparisons to this year's relatively slow spread of H5N6 (at least compared to H5N8 during the winter of 2016-17) to H5N8's subdued first appearance in Europe four winters ago.