VDU's blog

Monday, 12 October 2015

Jon Snow is remarkably well informed compared to us...

...because we clearly know almost nothing when it comes to the specifics of where Ebola virus (EBOV) can, in some portion of survivors, hide.

What triggers EBOV to come out of hiding? If indeed that is what it has done within PC, the United Kingdom nurse who seems to have recently become ill while (or due to) hosting a reappearance of EBOV in her blood - 9 months after her blood was defined as containing no detectable EBOV.

This is not a new infection - but a return of a virus that had not been cleared from its hidey hole(s).

There are obvious concerns to be discussed around this, including:

What triggered its re-emergence
Is this a strange and rare event or a more common one?
Was the virus hiding in PC's central nervous system (she has meningitis-like symptoms reportedly) or in another place or places?
Is the thyroid a site of persistence?
Did the mysterious antiviral treatment she was given alongside a plasma treatment in 2014/15 act to push the virus into hiding?
Has the activated virus mutated in any significant way during its holiday out of the bloodstream?
Can EBOV become truly latent or at least dormant (still producing proteins, but not infectious virus particles) when off the beaten track, or is it constantly replicating?
Is PC suffering from full-blown Ebola virus disease (EVD) now, or a disease due to tissue or organ damage from her earlier infection - although if she has detectable EBOV in her blood, one would assume it is EVD.
What the hell are a "lucky set of genes" in the context of a return to systemic EBOV infection?

Below are some known and some proposed/possible/unproven sites at which EBOV may linger, avoiding or not exposed to clearance by the full force of our immune response.

In the future, perhaps tomorrow, in a non-rich nation, will others become infected from a convalescent patient who experience a return of EBOV long after they were declared virus-free based on a their blood test results. Has that happened already? Will they be our colleagues, friends or family members? The sooner we hear more about what is going on with PC, the better prepared those on the ground will be to intervene. Also, those tending to convalescent health workers in countries around the globe.

Communication has always been a key issue for EVD and other emerging diseases. Have we been listening?

We know nothing but we can learn. Will we?

Saturday, 10 October 2015

Is the next Ebola virus revelation...reactivating infection?

Update #1 11OCT2015 AEST
Update #2 11OCT2015 AEST
Update #3 22OCT2015 AEST

Great. Are members of the Zaire ebolavirus (EBOV) species the most educational viruses of modern times or what? I mean, we've "known" about EBOV since 1976, but the West Africa Ebola virus disease (EVD) epidemic is the epidemic that keeps on giving - we seem to learn a brand new thing every few months.

And the latest is a doozy although we don't know many of the details yet.

So what do we know about this new finding of a seeming return of infection in a former EVD case? Or is this new disease because of damage from the old infection?

A 39 year old nurse, PC, was originally infected with EBOV while working for 3 weeks in the Save the Children’s Kerry Town Treatment Centre in Sierra Leone. She did not show signs of illness until after arriving home in Scotland [1,11]
PC was believed to have become infected while treating EVD patients in some way related to her use of a visor as part of her personal protective equipment, rather than goggles, [10]
PC entered a Gartnavel Hospital isolation unit on 29-DEC-2014, and was subsequently flown to the Royal Free Hospital (RFH) in Hampstead, North London on 30-DEC-2015. She stayed there for around a month [2,4]
During her time in the RFH, PC was treated with convalescent blood plasma and an experimental antiviral drug
PC was declared free of EBOV and discharged from the RFH on 24-JAN-2015 but continued to report thyroid problems afterwards as she described just a week ago [3,4,12]
On Monday evening, PC went to a GP service at Victoria Hospital with a temperature, headache, sore neck and sensitivity to light (photophobia). [15] She was sent home.
On Wednesday 07-OCT-2015, PC was admitted to the Queen Elizabeth University Hospital (QEUH) in Glasgow, Scotland. Tests revealed that EBOV (presumably) RNA was present.[13]
On Friday 09-OCT-2015, PC was admitted to the RFH, 8 months and 15 days after being declared free of Ebola virus and discharged.[16]
She is described as being in serious condition. However, it is unclear what her signs and symptoms were at presentation, or have become since.[4]
On Wednesday 14-Oct-2015, PC's conditions was described as having deteriorated and was now classified as in critical.[16,19,20]
On Monday 19-Oct-2015, PC's condition was described as improved.[16,21]
On Thursday 22-Oct-2015, at a press conference made possible because PC had given permission for her case to be publicly discussed, PC was described as having significantly improved. She had meningitis and has received a "highly experimental" drug, GS-5734, under development by Gilead Sciences, and proven highly effective in the lab and in monkeys post-infection.[22,23,25,26]

Descriptions note that PC is "not thought to be contagious". Presumably this means she is not symptomatic with EVD and if so the testing that must have identified EBOV somewhere in her system must have does so from a part of her system that is not readily in contact with the environment. In one report, laboratory staff in Glasgow who handled PC's samples, were not wearing the most basic of personal protective equipment (PPE) for lab staff-gloves.[24] All of that side, she is once again isolated at one of the world's best infectious diseases hospitals.[4]

There are also recent reports of PC having had thyroid problems after recovering-perhaps virus has been replicating in this tissue. PC's "condition is a complication of a previous infection with the Ebola virus".[4] Which leaves a lot of room for idle speculation but could just be that she is ill because of what the fallout from what EBOV previously did to a tissue/organ rather than because of EVD itself. Perhaps follicles in the scalp have been a site for virus replication, relating to her earlier hair loss. Another site may be the central nervous system...

@amymaxmen I've heard she has a meningitis like syndrome, probably CSF is where #Ebola virus is replicating
— Ahmed Tejan-Sie MD (@AhmedTejanSie) October 9, 2015

@MackayIM @amymaxmen CSF and blood (later) positive
— Ahmed Tejan-Sie MD (@AhmedTejanSie) October 15, 2015

All speculation. Again, nothing is known about PC's signs and symptoms of disease when she presented herself to the QEUH, what tissue(s) are involved in her current illness, which samples tested positive first, whether viral culture has been conducted or just RT-PCR and where the virus may have been replicating all this time. While we understand that some tissues are sites for EBOV persistence, there is clearly much more to learn about the frequency and full range of tissues that harbour infectious EBOV once it becomes undetectable in the blood.

Apart from how shocking and scary this must be for PC herself, another issue is how this will impact on the fragile processes of accepting of EVD survivors back into their West African communities. Extending the length of time that some male survivors are known to harbour EBOV already put pressure on their acceptance by some, but the potential for virus to return to the blood or other tissues - if indeed that is what has happened here - even after that time frame, will require a lot of communication to explain. It will be vitally important for this process that the facts underpinning what's happened here are deduced soon and communicated in ways that can be understood in West Africa. This is a chance for the World Health Organization to show off their shiny new intent to do better at communicating and reacting.

This is not the first time EBOV has been found to persist in a convalescent former EVD case.[5,6,7,8,9] But this may be the first documented time that the virus has re-emerged from an immune privileged site and returned to the blood, possibly causing EVD symptoms in the same former EVD case (recent media article mentions that this is the 2nd such case[15]).

The comments about PC's photophobia are similar to those from Dr Ian Crozier - who was found to have persistent infectious virus in the aqueous humor collected by needle from the anterior chamber of his eye causing uveitis-14 weeks after his EVD diagnosis.[6,17] His blood did not become EBOV positive again.[17] The virus found in his blood earlier and his ocular fluid 14 weeks later were nearly identical-just five mutations differentiating the genomes. Could the eye be a site of PC's hidden virus also? Perhaps the central nervous system the reservoir given the meningitis-like symptoms PC's family mentioned early and which was confirmed 22OCT.[15,18] Again, lots of speculation.

Shingles has been thrown up as an example of a similar disease that results from a virus recurring but it's not the same thing at all. Although, we don't know that with absolute certainty. The viruses are very different - that we know for certain. Varicella zoster virus (VZV) is the herpesvirus that first causes chickenpox (doctors call it 'varicella'), usually in childhood. The virus then goes dormant in your nerves. In this state, the virus is not producing full virus particles and so VZV no longer excites our (cellular) immune system, which can eventually "forget" it. Decades later (again, usually) after lying dormant and because of triggers and a lack of suitable immune memory VZV may arise from dormancy (reactivate) to produce lots of whole virus and cause shingles (doctors call this 'herpes zoster' - still the VZV though).[14] As far as we know, EBOV does not go dormant or become latent, but remains active at some sites, like the testes and the eyeball,[5,7] where our immune system is programmed not to venture in full force, so as to protect those sites from unwanted inflammation (in a nutshell). There may well be other sites.

Hopefully, more official key information will be made clear soon (as opposed to in the scientific literature weeks or months from now) as it will be vitally important for the continued management and support of EVD survivors in West Africa. It is also important knowledge for communicating real risks, and informing and toning down perceived but unrealistic ones. What falls into which category is however becoming harder and harder to discern.

I'll update this blog post as more information comes to hand.

References...

Updates...

Added dates for PC being initially released from the RFH and that she was tested at the QEUH; described "dormant" and qualified that chickenpox and shingles can occur at any times but usually as a child and adult respectively; provided references about chickenpox
Updated information from Ref 15 including dates, new calculation of time between RFH 1st discharge and admission and some symptom information from family
Added CSF+Blood Tweet; some tiny bits of new info from the RFH press conference; links to GS-5734 info

Monday, 5 October 2015

A place to be critical...

Around May/June 2015, the Middle East respiratory syndrome (MERS) coronavirus escaped its Arabian Peninsula bonds and exploded...still associated with the circumstances created under lax hospital conditions...into another part of the world entirely - South Korea.

About 20% of South Korean MERS cases were fatal. In contrast, nearly twice that proportion have died after MERS-CoV infection among 26 countries (36% fatal).[1] Meanwhile, a little over twice the SOuth Korea proportion of fatal cases occurs in the Kingdom of Saudi Arabia (KSA; 42%).[2]

It is interesting to look at another possible measure of clinical impact - how often a MERS patient is publicly described via official channels as being in "critical" condition. I suspect that this term could be applied as arbitrarily as anything else used by humans, nonetheless, see the figure below.

Total MERS-CoV detections (mustard bars; left-hand axis)
and mentions of cases in "critical" condition (red bars; right-hand axis).
Taken from the MERS-CoV data visualizations page.[3]
Click on image to enlarge.

A few things:

Sadly, you have to ignore the biggest peak - the Jeddah-2014 hospital outbreak (March to June) - as data during that time were rare and detail was mostly absent both from the KSA Ministry of Health and the World Health Organization
If we look at the South Korea peak (May/June 2015) versus the most recent Riyadh outbreak (July/August 2015), there seem to be a lot more mentions of critical cases. There is also more red visible during the Eastern Region/Ar Riyadh region peak around January/February 2015.

There may be little to conclude from observations such as this, but it is yet another interesting pattern to muse upon.

Older males with comorbidities are heavily represented among MERS disease cases that present to hospitals (younger people among those with mild or no notable disease) and older males and females with comorbidities among the fatal outcomes. A shared risk is that comorbidities are preyed upon by MERS-CoV.

Comorbidities include diabetes mellitus, cirrhosis and various lung, renal and cardiac conditions. All of these are diseases of concern among countries with abundant unhealthy food options, weight issues and ageing populations. Is your country one of those? Even familiar old viruses could re-emerge as threats to this subgroup as the years go by. In the meantime, emerging newly identified viruses create an atmosphere of concern.

MERS-CoV detections broken down by age bands and into total cases
(left hand graphs), and those with a fatal outcome (right-hand grpahs).
Taken from the MERS-CoV data visualizations page.[3]
Click on image to enlarge.

References..

http://www.who.int/csr/don/01-october-2015-mers-jordan/en/
http://www.moh.gov.sa/en/CCC/PressReleases/Pages/Statistics-2015-10-04-001.aspx
http://virologydownunder.blogspot.com.au/2014/08/mers-cov-daily-monthly-and-cumulative.html

Sunday, 27 September 2015

Corona counts continue to clarify...

From Mackay & Arden [1]
Click on image to enlarge

The Kingdom of Saudi Arabia's (KSA) Ministry of Health (MOH) has, over the past week, made a few changes to its Middle East respiratory syndrome coronavirus report layout. Good changes. Nice additions. And I say bravo. In fact - as we've said in the scientific literature [1] - the KSA data are far better than those we have seen from other recent emerging infectious outbreaks. In particular, China's efforts for the avian influenza A(H7N9) virus cases over many months or Egypt's communication about its avian influenza A(H5N1) virus outbreak(s), have been relatively simplistic, uninformative and hidden from public view, by comparison.

Since the 17th of September, the reports have been undergoing constant change. These range from the subtle tweaks in colour, the addition of pie charts (I particularly like the strong colours in the latest!), inclusion of a marker to identify an asymptomatic MERS-CoV positive sample (are these now included as a "cases" by the MOH?) and the breakdown of how MERS-CoV positives were likely to have acquired their infection.

Some things I'd still very much like to see added...

In the 'Deaths' table, a column for the date that the deceased person was first described by the MOH - that is, the reporting date. Currently there is not always enough information to go back and say with conviction which e.g. "60 year old male Saudi from Riyadh" died when there may have been several cases with the same description, listed over the preceding days and weeks (even months as some MERS cases have been hospitalised for a very long time before eventually dying of complications)
The number of samples tested each week, as listed by the Infection Prevention and Control-KSA webpage
Details added retrospectively for those 'found' cases. Those data are clearly in the system somewhere as they were summarised back on the 3rd June 2014 [4] and the 18th September 2014. This would be a nice 'rounding off' of all the data to date.
An explanation for what constitutes a "primary case". Currently, the suggestion is that over a third of cases are primary cases. To my mind, after excluding healthcare acquisition, this implies infection from animals. But only a touch over 7% (91 of over 1200 virus detections) of cases reported publicly have any animal contact described. So what does a primary case" mean to eh KSA MOH?
A single, regularly updated and downloadable line list of these deidentified detections, each with a unique identifier, for all 1200+ detections (akin to what the World Health Organization did for the South Korea cases...but better). This would be a resource that could be of use to future publications (which should cite the source appropriately), conversations whereby we could all discuss the same case using the same code, for student projects and for those number nerds the world over

Screen captures from the KSA MOH Command and Control Centre (CCC)[2]
Date of report is shown below each screen capture.
Compiled using Adobe Photoshop
Click on image to enlarge

But that little wishlist aside, it is fantastic to see this response from the MOH. I have no problem at all with the formats changing, even if it is day by day by day. I'm just happy to see a responsive data sharing outlook. And the willingness to put these changes up, and leave each version in public view is also a promising sign of openness from the MOH. There is nothing wrong with showing the process.

These website is becoming a great example of how we can and should communicate outbreak data in the future.

References...

The Middle East respiratory syndrome puzzle: A familiar virus, a familiar disease, but some assembly still required
Mackay IM, Arden KE. J Infect Public Health. 2015 Sep-Oct;8(5):405-8. doi: 10.1016/j.jiph.2015.07.001.
http://www.ncbi.nlm.nih.gov/pubmed/26278813
http://www.moh.gov.sa/en/CCC/pressreleases/pages/default.aspx
http://www.gdipc.org/
http://www.moh.gov.sa/en/CCC/PressReleases/Pages/mediastatement-2014-06-03-001.aspx
http://www.moh.gov.sa/en/CCC/PressReleases/Pages/Statistics-2014-09-18-002.aspx

Friday, 18 September 2015

Happy 3rd birthday Middle East respiratory syndrome coronavirus (MERS-CoV)...

It has been 3-years since Prof. Ali Mohamed Zaki sent his email to ProMED notifying them, and the world, of a novel coronavirus (15-Sept-2012). That email was published 20-Sept 2012.[1,7,8]

Two years ago at this time we had 138 cases and 58 deaths, last year 856 cases with perhaps 306 fatal (36%). Today, we have heard of 1,588 cases worldwide of which at least 551 (35%) have been fatal.[2,3] A higher proportion of fatal cases occur in the Kingdom of Saudi Arabia (KSA) than were recorded in the 2015 South Korean outbreak. The type and extent of a nation's community that has comorbidities may play a role in these differences. The young seem nearly untouched by MERS. To date, 26 countries have harboured a MERS-CoV infected person and 13 of those have hosted ongoing transmission.[4]

Thankfully, the diagnostic tools described very early on are as useful today as they were in 2012.[5,6]

Three years on we still see no sign of that virus patenting issue manifesting into a real problem.[3]

For me, this past year in MERSville has been about:

How amazing it was that MERS cases didn't occur during or as a result of one of the world's largest mass gatherings, the Hajj. Really. Amazing.
The absence of asymptomatic cases included in reporting from KSA. The World Health Organization's (WHO) definition of a case does not rely on the presence of symptoms but on the presence of virus or past viral infection. Withholding or not seeking these data produces an overstated value for the proportion of cases that die from infection and could confound efforts to interrupt transmission during an outbreak. In reality, the higher percentages may just be what we should expect among infection of older males and females with one or more comorbidities
The continuing appearance of large hospital-based MERS-CoV outbreaks driven by circumstances we create through unsatisfactory understanding of respiratory viruses, as well as poor preparation for their arrival in an emergency department. This occurred again in South Korea and Riyadh over the past year as it did in Jeddah the year before. In South Korea, the financial, economic, social and trust impacts were significant; communication once again a big loser from public health authorities and governmental agencies
The big question over our MERS-CoV antibody detection tools' capabilities. Can they detect the prior presence of a MERS-CoV infection when that infection did not result in symptoms in its human hosts, or caused only very mild symptoms? A 4-week study enrolling the contacts of confirmed cases and collecting daily nose/throat swabs, weekly bloods, filling in a daily symptom and temperature diary, followed by an 8-week blood sample, would help address this I think
Slow acceptance that camels are the main, albeit sporadic, source of MERS-CoV spillover infections of humans. Bats may have been involved in the distant past but for 30 or more years we have strong data to say that a MERS-CoV (or closely related virus) has resided in and spread among dromedary camels in Africa and or the Arabian peninsula causing mostly a 'common cold' like upper respiratory tract illness. The precise role of importation on moving MERS-CoV around the region remains poorly explored
Other animals, on paper, look like they could host MERS-CoV, but experimental infection studies are still lacking. Similarly, a camel birth cohort study (h/t @newprof1) would add additional information to the story of how this virus spreads between camels in herds or holding pens after importation or during festivals
We did not see any resolution to the missing data from 2014 - despite assurances from the KSA MOH.[12] Comprehensive data on cases that were just 'found' - remained incomplete.[11] Also, trying to identify deaths from among previously announced MERS cases is a task fraught with frustration, despair and dismay. And then there are the unexplained errors and differences in reporting when comparing MOH data to World Health Organization data. Yes, those cases that are reported are likely to be the tip of an iceberg of indeterminate size, but at least get right what is being reported-or...GASP...fix it up later
It was reported that among those humans listed as being 'asymptomatic' - over three quarters of such cases, when later interviewed, recalled having symptoms.[6] This, to me, casts a darker shadow over the quality of other clinical and epidemiology data too
We still have not seen any data from the testing of human samples, prospectively or retrospectively, from non-Arabian countries that play host to high numbers of MERS-CoV antibody-positive camels, for example, Egypt, Sudan, Somalia or Ethiopia
In the past year we learned that MERS-CoV variants, like other CoV variants, can recombine when multiple variants co-infect the same host (probably in camel herds but perhaps in crowded hospital outbreaks in places like Riyadh which appears to be a nexus for mixing of variants [13,14]) producing a new variant.[9,10] To date there has been no proven impact on clinical presentation or course, virus reproduction or immunomodulation or transmission. But have wee looked hard enough lately? While it is not immediately obvious from observing whole genome sequences - most of the kind of sequencing produced since MERS-CoV was discovered - sites of recombination can be predicted when we look with more specific software tools. Yet, what happens if this recombination happens between a contemporary human/camel variant and a more ancestral camel variant? Could the resultant recombinant virus change in transmissibility or become more or less clinically severe? Is that recombination scenario even possible? Are even older bat variants too genetically distinct to allow easy recombination? It is important we find out more about the diversity of MERS-CoV and CoVs among camels outside the Arabian Peninsula and seek them out in other animals there too. Just as it is important to measure what is happening in people there
Advances in therapeutic antibody preparations and in vaccine candidates. It remains to be seen whether camels will respond as immunologically required for a camel-based vaccine to prove effective, but as Ebola virus disease showed us, there is obvious benefit to having a ready-to-deploy arsenal of weapons in case of invasion by a viral foe that just 'shouldn't be capable of doing that thing'

It would be stupid to predict what will happen with MERS and MERS-CoV in the next 12 months. We can take some educated guesses though.

But for now the focus is still largely on what the KSA will do about the problem on their doorstep. It may also be that MERS-CoV cases are percolating outside the Arabian Peninsula without our knowledge. Let's not leave this virus to its own device any longer. Let's act to make sure it doesn't comes back to bite us. The clues are all there. There are patterns that are clearly visible. Let's get the work done ahead of the panic for a change. How about we meet back here this time next year, same batch channel, same camel topic?

References...

http://www.promedmail.org/direct.php?id=20120920.1302733
https://flutrackers.com/forum/forum/novel-coronavirus-ncov-mers-2012-2014/146270-2012-2015-case-list-of-moh-who-novel-coronavirus-mers-ncov-announced-cases?t=205075
http://www.who.int/csr/don/17-september-2015-mers-saudi-arabia/en/
http://virologydownunder.blogspot.com.au/2015/09/mers-around-world.html
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20285
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20334
Happy 1st birthday Middle East respiratory syndrome coronavirus (MERS-CoV)
http://virologydownunder.blogspot.com.au/2013/09/happy-1st-birthday-middle-east.html
Happy 2nd birthday Middle East respiratory syndrome coronavirus (MERS-CoV)...
http://virologydownunder.blogspot.com.au/2014/09/happy-2nd-birthday-middle-east.html
http://biorxiv.org/content/early/2015/06/12/020834
http://mbio.asm.org/content/6/5/e01280-15
http://virologydownunder.blogspot.com.au/2015/03/where-did-mers-cov-comorbidity-and.html
http://virologydownunder.blogspot.com.au/2014/09/mers-cov-data-request-response-from.html
http://www.ncbi.nlm.nih.gov/pubmed/24055451
http://mbio.asm.org/content/5/1/e01062-13.abstract

MERS around the world...

China was the 26th country to host a MERS-CoV infected person, when a 44-year old symptomatic male (onset 21-May-2015) travelled from South Korea, through Hong Kong to Huizhou in Guangdong Province, China on 26-May-2015.[1]

Click on it!
It gets bigger!!!

Reference...

http://www.who.int/csr/don/30-may-2015-mers-china/en/

MERS by month, camel and mass gathering...

I haven't updated this figure in a long while but recently had the chance to add some new camel calving season data [1] and another festival to my earlier lists [2-4] - the Um Ragaiba festival.[6]

The Um Ragaiba festival is purportedly the largest of the human|camel gatherings, located north of Riyadh and near Buraidah and Hafr Al-Batin - interestingly, are all sites of infamy among the tales told in MERSville.[5]

MERS-CoV detection in humans by month. Also showing spring and
summer seasons in the Kingdom of Saudi Arabia and some key
camel and festival dates.
Click on image to enlarge

The latest version of this figure highlights a few things to me:

I don't see a seasonality here which is not surprising. Most human cases are due to human error creating the circumstances by which health care related outbreaks take off. These happen at different times. It is hard to remove that very loud noise and see if a seasonality remains. A seasonality that is presumably due to times when there are more active camel infections increasing the risk of human infections through proximity and direct contact with infected hosts
The Kingdom of Saudi Arabia has at last taken the threat posed by MERS-CoV infected camels seriously. In 2015, two big festivals which had camel involvement, Janadriyah and Um Ragaiba were not held. Take note China and avian influenza
The bulk of human cases occur within a timeframe bracketed by camel calving season - so, keeping in mind what I said above, rather than season, perhaps we can agree that the period in which higher numbers of MERS-CoV cases occur, seems to be in the Arabian Peninsula's spring and summer - even if that outbreak is in South Korea! When virus activity rises at the source, so does the risk of death and significant economic and social impact beyond the borders of that source

Reference...

Thursday, 10 September 2015

Ignore mild and asymptomatic cases at your peril...

Infected but apparently well people may be key points along the transmission chain - not just in spreading infectious virus, but also in contaminating surfaces.

Or they may have no role in transmission at all.

When you have problems that weren't solved by the easy answers - look harder.

Study. Test. Find out. Communicate.

Knowing the full story of how a virus spreads is hard work. But transmission is not necessarily a simple process. Like everything biological, it may be more complex than we care to acknowledge. Such a complex scenario is shown here. Completely fictitious.
Or maybe not.
Testing can answer questions. Communication can provide answers.Click on image to enlarge.

Friday, 4 September 2015

To (type) B or not to (type) B...

Image adapted from Geoscience Australia,

The Australian Government.[13]

The latest weekly influenza statistics for Queensland were made public today.[1] Unfortunately there are no hard public numbers to support claims about the proportion of strains from the two influenza B lineages that affect humans that have been circulating in Queensland - for either July or August.
I was hoping to find some support for comments in the media this week which included...

The Brisbane strain has accounted for 27 per cent of influenza B cases in the year to August 23 [2]

This is in the latest report,[1] but these are year-to-date proportions -almost pointless for the spike in cases that happened more recently i.e. 48% of 2015 influenza cases occurred in the past 3 weeks [12]. Also not helpful when considering how few influenza Bs seem to be 'lineageanated' (have a lineage determined-further characterised - ?term)

..it was 25 per cent higher this year[3]

Talking about B/Brisbane strain's rise

Whatever. The upshot is that Australia has had a big influenza B virus-dominated winter in 2015.

At least some proportion of those Bs have been due to strains of Influenza B virus Victoria-like lineage. That lineage was not included in the sponsored trivalent vaccine - namely the Brisbane strain (first characterised here in Brisbane back in 2008).[3,4,5,6]

I had expected, based on the earlier Eurosurveillance article from our southern labs[9], that an influenza virus with an already decent presence that had not predominated in a number of years and which was not covered by the current vaccine would take off and cause a big season. But it seems like that hasn't happened. And yet we've had a huge influenza B season here in Queensland, and across Australia, nonetheless.

Seems a strange mix to me but I'm no flu expert so perhaps this is all very normal for this Rubik's cube of a virus. Here's hoping for some literature on this down the track.

Despite the completely unavoidable mismatch event there remain a bunch of influenza A virus subtypes and the Phuket strain of the other influenza B virus lineage (Yamagata) that are indeed catered for by this season's trivalent vaccine. While the flu season may be taking a turn downwards,[1] you may want to consider a vaccination if you or your family hasn't had one yet-talk to your GP!

The newer (to us in Australia anyway), less common and not (yet?) sponsored quadrivalent vaccine caters for both influenza B virus lineages.

Figure from most recent State of Queensland (Queensland Health) report found here includes data up to 30th August 2015.[1]
Images excised from PDF and saved using Adobe Photoshop CC 2015.0.0
Click on image to enlarge

Oh, and those age bands I've discussed previously [10,11], are still the highest - school aged kids (5-19 years) got a lot of influenza B in 2015. Compare that to my earlier comparison - those age bands have really shot ahead.[11]

References...

Thursday, 3 September 2015

Where do these 'primary' MERS cases come from?

I was just dropping by the General Directorate for Infection Prevention and Control's Middle East respiratory syndrome (MERS) statistics website ([1]; Kingdom of Saudi Arabia) and noticed this graph which I've snipped and labelled below.

What strikes me as very strange is the listing of so many "primary" MERS cases (green). Keep in mind that the Command and Control Center of the KSA Ministry of Health has a case definition that does not allow for a person who has no symptoms as a Case-even if they are laboratory confirmed as being infected [2]. A strict clinical-based definition. In a more real-world definition for reporting a MERS Case, the World Health Organization (WHO) has, since at least July 2014, included any laboratory confirmed person (which includes suitably serologically confirmed) as a Case.

In other words, the green bars represent KSA-defined Cases that have not acquired MERS-CoV infection from family, friends or house mates (yellow), not from healthcare workers or the healthcare facility (nosocomial; red and purple) and that are not unclassified (magenta).

Excerpted figure from the General Directorate for Infection Prevention and
Control website.[1]
Blue labelling by me using Photoshop.

Doesn't that just leave camels?

But camel exposures are not being listed in WHO Disease Outbreak News (DONs) in anything like that number. It's very rare to see a camel contact listed in the current Ar Riyad province outbreak at all (just one, early on).

So where do these primary cases acquire their infection from?

Reference...

Static pages