Medical News Blog Information

H7N9 appears in a new north eastern Chinese province: Jilin

Click on image to enlarge.
...and the map expands a little more. 

It would be interesting to know if this case was acquired from a live poultry market stocked with birds sourced within the province or from the vast network of poultry movement that links the provinces and their markets across thousands of kilometres.

As I write this, there are 365 cases and 113 deaths, if I can add the latest Guangdong fatality to the 112 I wrote about, earlier today.

H7N9 deaths jump significantly....

Click on image to enlarge.
Twitter was buzzing this morning with news that several sources had announced a new total number of deaths in human cases of H7N9 infection.

It was not a total surprise that there were more deaths than we had heard about, and that is for several reasons:
  • In Wave 1, Spring 2013 in South east China, there had been a greater proportion of deaths than we have seen in Wave 2. That's seemed unusual.
  • After Wave 1, the proportion of fatal cases (PFC; see background here) sat up as high as 33%. Wave 2's high case numbers but few reported deaths had lowered that to 18% at one point. If the virus hadn't changed and human-to-human transmission had not changed then that was incongruous
  • The media were reporting higher numbers than we had data for in early Feb and in late Jan, Xinua reported 26 deaths in Zhejiang alone for 2014 - this far outstripped any publicly data available
So now we see that the tally is 112 fatal H7N9 cases among people infected with a laboratory confirmed H7N9 virus, since the outbreak began in 2013; that tally includes both waves of human cases. That makes the PFC among the 361 confirmed human cases at 31%. 

So this one new piece of news has bumped up the PFC by 10%. From 1:5 (22% last week) to nearly 1:3 cases dying after acquiring infection. 

Thankfully, H7N9 is not spreading efficiently among humans (or chickens according to reports). But these are numbers to care about.

For comparison, my Excel sheet has 64 cases with data that I can cross-check (I believe that agrees with the FluTracker's count also). 

The last media update I looked at had a tally of 77 fatal outcomes

So we have between 35-48 people have died without any ability for anyone outside China to link them to:
  • their age
  • when they became ill
  • where they were
  • how they may have acquired their infection
  • their sex
  • time to hospitalization and diagnosis
  • length of stay in hospital 
  • what contacts they had and how they have fared. 
I think that this is a ball that has been not just been dropped, but buried in a hole and covered over with feathers. I'm disappointed by such a gaping data loss. And don't get me started about the absence of H7N9 sequences from 2014 cases!

Sources...
  1. SCMP with higher death tallies than public data indicated
    http://www.scmp.com/news/china/article/1425289/january-worst-month-chinas-human-h7n9-outbreak
  2. Xinhua lists 26 deaths in Zhejiang alone for 2014
    http://news.xinhuanet.com/english/china/2014-01/21/c_133060657.htm
  3. VDU blog on missing deaths
    http://newsmedicalnet.blogspot.com.au/search?q=deaths+h7n9
  4. Mike Coston's Aviann Flu Diary take one the new data, with other sources
    http://afludiary.blogspot.fr/2014/02/chinas-moh-h7n9-fatalities-higher-than.html?m=1&utm_source=dlvr.it&utm_medium=twitter
  5. FluTracker's thread with links to eth WHO report
    http://www.flutrackers.com/forum/showthread.php?p=525996#post525996
  6. China's Ministry of Agriculture report of enlarged H7N9 death tally
    http://translate.google.com/translate?u=http%3A%2F%2Fwww.moa.gov.cn%2Fgovpublic%2FSYJ%2F201402%2Ft20140220_3791429.htm&hl=en&langpair=auto|en&tbb=1&ie=UTF-8
  7. The WHO report under the "vaccines" section
    http://www.who.int/influenza/vaccines/virus/recommendations/201402_recommendation.pdf?ua=1

H7N9 snapdate: epidemic curve as Wave 2 looks to be ending...

Click on image to enlarge.
This image is another way of showing that the current wave of human cases of avian influenza A(H7N9) virus is ending and that we are solidly within a period of "tailing" (cases only ticking over at low levels in the lead-in or lead-out of the main peak).

BUT: These data are based on figures that are publicly available. As we learned overnight, those numbers can come in fits and starts, if at all. The addition of a large number of deaths without any identifying information linking to the case onset, supports what some have been suspecting for a while; we don't have a full picture of what's happening with H7N9. 

There are now up to 48 more deaths due to H7N9 infections, depending on where your base count is taken from (verified updates or or the media) than we knew about 12-hours ago.

More on that topic later today.

Allergy and viral infection: wheeze and more wheeze

I really liked this Letter by Karta and colleagues from the University of Wisconsin. Not just because it makes some sense to me but because it's not a long drawn-out immunology study written in alphabet soup with multiple 12-panel figures that make me cry.

Trying to understand how viruses (my thing) trigger asthma exacerbations (a clinical thing) via activation of multiple inflammatory pathways (an immunology thing designed to be impossible to follow unless you love keeping tract of tiny little initialisms and what each of them do, did and used to be called 5-minutes ago) is heavy going. This Letter somehow adds to the field without all of "that".

The authors obtained mononuclear cells from the lower respiratory tract of 10 volunteers with mild atopic (allergic) asthma, by bronchoalveolar lavage. That was Day zero (D0). At 48-hours (D2) the donors were given an allergen and cells were collected by BAL again. 

Macrophages were obtained from the D0 and D2 cells (they stick to the plastic culture flasks, other blood cells don't) and they were then challenged with 1 of 3 rhinoviruses (RV); either RV-A16, RV-B14 or RV-A2. I say challenged because rhinovirus doesn't replicate within macrophages (also written in shorthand as MF) but they do interact with them.

The team then looked at a bunch of initialisms which represent some potent chemicals called chemokines:


  • CXCL10 (IP-10)
    • C-X-C motif chemokine 10; formerly interferon gamma-induced protein 10
    • secreted by macrophages that have been activated by RV interaction
    • also secreted by endothelial cells and fibroblasts
    • secreted from cells in response to interferon gamma (IFN-?)
    • signal the recruitment of immune cells  (monocytes/macrophages, T cells, natural killer [NK] cells and dendritic cells) that take charge of getting rid of virus
  • CXCL11
    • C-X-C motif chemokine 11; formerly known as Interferon-inducible T-cell alpha chemoattractant (I-TAC) and Interferon-gamma-inducible protein 9 (IP-9)
    • also secreted by macrophages that have been activated by RV interaction
    • secreted in the pancreas and liver
    • secreted from cells in response to IFN-? and IFN-�
    • interacts with cell surface receptor, CXCR3
    • recruits activated T-cells
  • CCL2 
    • Chemokine ligand 2; formerly known as monocyte chemotactic protein-1 (MCP-1) or small inducible cytokine A2
    • can also be secreted by macrophages after RV exposure
    • also secreted by monocytes and dendritic cells and expressed by neurons, astrocytes and microglia
    • recruits monocytes and basophils
    • binds to the cell surface receptors CCR2 and CCR4
  • CCL8
    • Chemokine ligand 2; formerly known as monocyte chemoattractant protein-2 (MCP-2) 
    • can be secreted by macrophages after RV exposure
    • recruits mast cells, eosinophils, basophils, monocytes, T-cells and NK cells
    • binds to cell surface receptors CCR1, CCR2B and CCR5
Some key findings...
  • D2 samples that were not challenged with virus made less CXCL10, more CCL2 and nothing much changed in levels of CXCL11 or CCL8.
  • D0 samples incubated with RV saw a statistically significant rise in the amount of all 4 chemokines
  • D2 samples incubated with RV saw a rise in CCL2 but a drop in CXCL10 and CXCL11 but no effect on CCL8 
So the first batch of findings indicate that RV infection does not induce the same chemokine response from lower airway macrophages of people with allergy that have just been exposed to an allergen (think pollen or dust mite).

Further, it identified that in macrophages, a key immune cell in controlling viral infections in the airways, may not respond as effectively to RV infection in the body if such infection follows an allergen hit. At the same time, increasing CCL2 may increase inflammation by attracting those types of cells (eosinophils, neutrophils and more macrophages).

The team also went on to look at the levels of the 2 known RV cellular receptors, intercellular adhesion molecule I (ICAM-1) and the low density lipoprotein receptor (LDLR) and LDLR-related protein-1 (LRP-1). Receptors have been used as a way to categorise RVs in the past and some adhere to this when making choices in the design of their immunology research relating to RVs.
  • D2 macrophgaes had raised levels of ICAM-1 on the cellular surface but lowered levels of LDLR and LRP-1
  • Other blood cells showed no difference in receptor levels
  • Allergen-induced effects on RV receptor expression are distinct from its effects on chemokine levels
Great to know that RVs are ubiquitous and so are allergens!

References...
  1. Information on some cytokines and cell signalling following viral infection
    http://www.jleukbio.org/content/74/3/331.full.pdf+html
  2. Wikipedia as a starter for detail on cytokines

Wheezing after respiratory virus infection...

Takeyama and colleagues from Japan delved into the viruses present among young children (= 3-years of age) hospitalized with a clinically defined lower respiratory tract infection.

This exemplifies what many such studies do; sample from the upper respiratory tract to find signs of replicating virus in order to study a disease of the lower respiratory tract

It's a stretch but if you go along with it you are implying that an upper respiratory tract infection either triggers the symptoms from afar or that the virus travels into the lower respiratory tract to directly cause inflammation and/or cell destruction.

Viruses were detected by PCR-based methods.

Some key findings...
  • Respiratory syncytial virus (RSV) was the virus detected most often (51/102 samples from 153 children) in children who were admitted with wheezing followed by rhinoviruses (RV; 21 or 14%), RSV+RV (12 or 8%) and then parainfluenza virus 3 (PIV3; 8 or 5%), influenza virus (IFV; 5 or 3%) or human metapneumovirus (hMPV; 5 or 3%)
  • A similar pattern was observed in 259 children who were admitted without wheezing (RSV-25%; RV 9%; IFV 7%; RSV+RV-4%; PIV3-3%; hMPV-1%)
  • 67% of children with wheezing were virus positive (POS)
  • Children with an allergic predisposition (IgE antibody levels >30IU/mL at admission and a parental history of asthma) POS for RSV more often had wheezing later
  • Children who were wheezing & RV POS when they were admitted were more likely to wheeze again than were those who were RV POS without wheeze at admission.
So [allergic predisposition + RSV] or [wheeze/clinical severity + RV] were 2 factors related to subsequent wheeze.

The authors also raised the spectre of RV positivity occurring in asymptomatic individuals in other studies. However, that can happen to some extent with all respiratory viruses. No other virus has 160 distinct type like the RVs...but that's another story.

Article...

Humans unlikely to infect poultry with H7N9? Data please!

The United Nations Food and Agriculture Organization (FAO) has said that poultry is not at risk of being infected by humans carrying H7N9 virus.
In fact, we have no evidence that affected people could transmit the virus to other species, including birds. The highest risk of virus introduction is uncontrolled live poultry trade between affected and unaffected areas.
But absence of evidence is not evidence of absence.

We have seen studies, like this one, that use a human H7N9 virus and use it to successfully infect chickens. So the virus is capable of replicating even if it is inefficient at spreading to other chickens or even ferrets ( a human surrogate of influenza infection). But then we do know that humans get infected from exposure to something in poultry markets.

I agree (for what that's worth), that the risk of spreading virus is more in the area of moving infected birds around, as well as their own migration movements. But I think it is too early be early to issue strong denials that humans may infect poultry until we find some data to support them.

Sources...

Why I think the 2nd wave of human influenza A(H7N9) virus infections has broken...


If you look at the chart above, it shows declining:

  • Average cases per day (blue data points) in 2014
  • Less noticeable but consistently declining average cases per day when calculated across all of Wave 2 (oranges data points)
  • And importantly, a drastic decline in the number of new cases being announced after the 27-Jan peak. 

From 5-Feb, we have not seen more than 2 cases/day whereas in Jan we were regularly seeing 5-6 cases/day (peaking at 12/day).

The last time we saw this steep a drop in cases was 19-Apr 2014; the end of H7N9's 1st wave of human infections. 


That doesn't mean the virus has gone away or that the outbreak has been "solved". I learned that lesson last year. H7N9 is still out there. 


If these latest case numbers accurately reflect what is happening in China, then it looks like closing poultry markets did the same job in 2014 that it did in halting the 2013 Spring outbreak in southeast China. It will be down to the poultry industry and perhaps the Ministry of Agriculture in China to find evidence that specifically disproves a role for poultry in human infections; and it seem clear that changing from fresh to processed poultry has some even more safety data to support it.

We still have no data that lets us point the finger at chickens, or ducks or song birds or pigeons or geese or some other animal in the markets as the source. 

We just know there is a strong association between humans getting infected after being in the presence of "live poultry" usually in a market setting. With reports suggesting better growth of H7N9 in song birds compared to chickens as well as poor spread of virus between infected chickens, there is much work to be done outside of chickens to track the source of the virus down.


I care what the H7N9 numbers are...


This was the Tweet from Crawford Kilian (hereafter "Crof") a couple of days ago. 

I respect Crof. He has been as much of a mentor in my year doing this as has anyone. He even sent me his book on "Writing for the Web". I immediately changed a few things that I did after reading parts of it. Unfortunately nothing can help my appalling typing skills.

So when I saw that Tweet I thought it must have been a hook to get people to come read the full story. Twitter is a great way to attract readers to my blog; its a top referring site. Among other things, it's an important tool for promoting what we write to a wider audience. Sometimes a catchy title can be as good a bait as something more straight down the line. So, hooked, I dutifully read on.

What I found has been disappointing me ever since I read it 2 days ago, because I care about these numbers, and I thought you did too, Crof.

The article is of a type that I have read several times from Crof. It reminds those of us getting carried away with small, confined disease outbreak that hey, it's a great big world of misery out there and many more people are suffering and dying of all manner of diseases, a lot of which we forget about. Sometimes we don't forget though, we just focus on other things for a time.

I think it is a very valid point to make; and to make it over and over again is also fine with me. Points made in a blog post are very quickly forgotten, if they are ever read in the first place. At least a search engine may lead some back to that post or online newspaper story, unlike a printed newspaper which if not read may never have existed.

What really disappointed me I think...and I've been trying to work out why this has stuck with me for 2-days now, even causing me to give up on writing this last night or on blogging about viruses at all...is that Crof's post never did back away from the message of that original Tweet. Who cares about those numbers? It continued to hammer home that to follow such small numbers of deaths needed a special kind of justification, even for Crof. He said....
When I see WHO's H7N9 updates extending to 10 or 15 cases, it looks a bit alarming, I grant you. But let's put it in proportion.
and
Yes, I pay more attention to avian flu than to lung cancer and malaria. So, unfortunately, does everyone else...if you define "everyone else" as affluent, educated, vaccinated individuals living in countries with excellent public health systems and drinkable tap water.
and 
For us, it's the implicit threat of some clever virus that holds our attention: we don't have a vaccine for this one, so we ourselves are as vulnerable as some kid in Cit� Soleil or Asunci�n or Gorakhpur.
and
I suppose we can justify our interest by arguing that by studying these new diseases, we learn more about other diseases, and ourselves, as well. And that's a plausible argument.

Finishing with
Meanwhile, since I posted a few minutes ago that 768 mothers died in childbirth today, the number has risen to 775.

So Crof, are there so few people on the planet that some cannot keep an eye on one disease, some on another? I get that we do have to prioritise certain diseases over others. We have limited resources and human nature seems such that we never get everyone to pull in the same direction for long enough to truly solve our problems. But there is no definition of a suitably attention-worthy number of lives lost to infection. Every infection that takes a life, or even those that make life miserable, are worthy of our attention, our study, our understanding and eventually, our efforts in defeating it. I care about those numbers.

You cited a number of examples of other causes of far greater human death and disease. I remember a post or comment of yours with similar information that has always sat in the back of my mind as a check and balance of over-reacting.  Yet I have also read many other posts from you that champion the need for better information about MERS and MERS-CoV cases, for example. You often provide "granular" (my word of the month) detail on individuals with infections. You followed the story of a single French MERS patient for many weeks. And so did we because of you. So I simply don't "get" how this post fits, if not to remind us that ALL the numbers are always worthy of our care. 

Yes. There are very few cases of H7N9 compared to the world�s population. But there could be many more, as I know you are more aware than many, with only a few bits of bad luck and circumstance lying between "sporadic" and "sustained". Why not have more eyes rather than fewer on such risks?

There were very few cases of SARS, H5N1 or even now, few new cases of polio or measles compared to such a huge denominator. But each and every one of those diseases has been and should be watched, followed, tracked and its every aspect quantified. 

Every death that could be prevented now with vaccination or in the future by better education, better research, better understanding of the patterns and changes to those patterns, and better awareness by the public themselves, is one more person who remains a living family member. I don't dwell on every death I've reported but I know what it would be like if it happened to someone close to me.  


So I leave you with these 2 thoughts...

And if a little pandemic porn helps all of us protect our health, and outgrow the need for such porn, then maybe it's worthwhile.
..the attention we pay to these fringe viruses is certainly worth the effort..

...and I hope to read many more like them in the future Crof. 

Just like you care about the words that you masterfully write, I think you like me, also really do care about what the H7N9 number are.

H7N9 human case #1 - 1-year ago...

A year ago, on the 18-Feb-2013, the first human case of avian influenza A(H7N9) virus infection started showing signs of an illness; coughing with sputum. 

That person was an 87-year old retired male with hypertension and chronic obstructive pulmonary disease (COPD). By the time he presented a week later he had fever and shortness of breath. He sadly died of acute respiratory distress syndrome (ARDS).

No other cases of infection were noted to have resulted. 

He was treated with oseltamivir, an antiviral flu drug to which H7N9 is generally susceptible, 7-days after he became ill. He was in hospital for 6-days. 

His infection, along with those of 2 others, were reported to the World Health Organization on 31-March (2)


  1. NEJM Article on First 3 human cases of H7N9.
    http://www.nejm.org/doi/full/10.1056/NEJMoa1304459
  2. WHO Overview. 31-05-2013.
    http://www.who.int/influenza/human_animal_interface/influenza_h7n9/WHO_H7N9_review_31May13.pdf?ua=1

Collaboration in Pediatric Medical Education and Clinical Care in Mbarara, Uganda

I walk into the admissions room for the �Toto� Pediatric Ward at Mbarara Regional Referral Hospital in Uganda and the intern on-call looks up at me with an anxious smile.  In this room there is a small bench, where two mothers sit with their toddlers, prostrate on their laps, one tachypneic, the other pale with visible scleral icterus.  The intern is admitting both children - checking vitals, writing admission notes, placing orders, inserting IV catheters, and ensuring these two patients receive their medications promptly.  I glance over at the single exam table where there is a small bundle � I lift the blanket and find two premature twins, each less than 1kg, swaddled together under a bare bulb for warmth.


As I begin to help him assess the needs of these tiny twins in respiratory distress, a nurse walks in carrying another bundle.  Lifting the cloth we find another set of premature twins.  These are larger and breathing on their own, so while they will need IVs placed, infusions to prevent hypoglycemia, antibiotics, and a full assessment in time, for now we re-wrap them and place them next to the first set of twins.  The intern returns to rapidly completing his assessment of his other patients, but only a few moments pass before a mother brings her child over from the ward � she is a toddler with cerebral palsy, severe acute malnutrition, and now a rash that appears to be disseminated varicella.  She is concerned and there is nowhere else for her to go, so she places her crying child in the last few inches of space on the exam table.  Just outside the room, caregivers sit patiently on a bench with their children, many of whom appear quite ill and have travelled a great distance to seek medical care, awaiting a doctor�s attention so their child may be triaged and treated as well.

Admissions Room in Pediatrics Ward at MRRH

This is a fairly typical day at Mbarara Regional Referral Hospital (MRRH), a governmental district referral hospital in Southwestern Uganda affiliated with the Mbarara University of Science and Technology (MUST).  Many departments from MGH have well established partnerships with our colleagues here with ongoing research, education, and patient care collaborations.  Given the partnership between the Pediatrics Department at MRRH/MUST and MGH is newer and continuing to grow, I feel fortunate as a resident in the MGH combined Internal Medicine-Pediatrics residency program to have the opportunity to work and participate in medical education initiatives here. The majority of my time thus far has been spent working in the Pediatrics ward, specifically the acute inpatient and malnutrition wards alongside the Ugandan post-graduates (residents), interns, and medical students.  My mornings consist of rounding with the team and co-teaching with the post-graduate, and the remainder of my time is focused on medical education.  Practically speaking, the greatest need has been in precepting the medical students on their presentation skills, reviewing case write ups, teaching physical exam skills, reviewing the approach to generating a differential diagnoses, and discussing management strategies for the myriad diseases being treated on the ward.  Additionally, I have been assisting the interns, who have just started their pediatrics rotation, with developing their skills in performing assessments and determining initial management of critically ill children newly admitted to the wards. 
View of the Mbarara Regional Referral Hospital on arriving in the morning

The pressures placed upon this already resource limited system are unbelievably high.  The �Toto� Pediatrics ward functions as the pediatric emergency room as well as the inpatient ward for all medically ill neonates and children at MRRH.  They admit anywhere from 15-25 children daily, many of whom are critically ill with conditions including cerebral malaria, severe sepsis, cyanotic congenital heart disease, severe acute malnutrition, ingestions, HIV/AIDS, and complex rheumatologic and oncologic conditions.  Each morning the interns report on whether or not supplies were adequate to provide care to the patients.  It is not infrequent that they report inadequate antibiotic coverage due to the hospital supply being depleted, lack of oxygen when the power driving the concentrators shuts off, shortage of forms for documentation and lab requests, inavailability of blood for transfusion, or absence of proper tubes needed for lab specimen collection. Many sub-specialty services or supplies not available at MRRH are accessible privately in town or in Kampala, however, this oftentimes is not an option financially or logistically for many families. 
Room for care of premature infants - currently empty for cleaning, the infants were waiting outside with their caregivers.

I cannot overstate how devastating it is to watch children die from diseases you know could have been prevented with earlier evaluation or treated with increased access to resources.  You can�t help but be struck by the inequity in the disease burden here � a mortality rate of 90/1,000 for children under 5, 76% of which has been estimated to be caused by preventable or treatable infections (WHO, Uganda ICCM Implementation Guidelines 2010).  But in truth, the most prominent thought I have on a daily basis is how smart, resourceful, and resilient my Ugandan colleagues are.  Despite being faced with a healthcare system that can be so complex and unpredictable, each day the post-graduates arrive smiling, inquisitive, and enthusiastic (albeit fatigued at times) about teaching, learning, and caring for an endless flow of patients.  Each day on rounds the post-graduates relentlessly push the medical students to definitively characterize an abdominal mass on palpation, rate the severity of digital clubbing, or outline the WHO algorithm for the inpatient management of malnutrition.  Modern medical advances and technology have certainly revolutionized the way we care for people to tremendous benefit, but I can�t help but wonder whether in more financially resourced settings we underestimate the power of our human resources.  There are limitations and frustrations encountered daily here, but the vast majority of the providers I have worked with find a way to maintain perspective, care for each child to the best of their capacity, and try to learn from the adverse outcomes.  These resilient, dedicated individuals are invaluable, and certainly have all the skills to be the leaders of future systems improvement. 

Outside the Toto Ward, caregivers have washed and are drying clothes.
Many caregivers will sleep out here at night, or on a mat on the ground near their child's bed.
I have only been here a few weeks and have just two weeks remaining, but even in this short period of time it has been a privilege to have the opportunity to support my colleagues here in Pediatrics.  I will have the opportunity next week to travel to Bugoye and work in a rural level three healthcare center where I will be able to learn more about the work of the clinical officers and village health workers, who are the backbone of the healthcare network for so many Ugandans.  As much as I spend my time teaching and sharing whatever I may have to offer, I hope my Ugandan colleagues have learned half as much from me as I have learned from them and am very thankful to the Partners Center of Expertise, MGH, and MRRH/MUST for providing me with this incredible opportunity.  

Best,
Meredith Eicken MD
Internal Medicine-Pediatrics, PGY-3
Massachusetts General Hospital

Shanghai and Hangzhou to permanently stop live poultry markets.

According to the report on CNTV.com ENLGLISH linked below, the poultry industry in Shanghai and Hangzhou (the capital of Zhejiang province) is about to change significantly (h/t Crawford Kilian's H5N1 blog post and Tweet on this).

A new plan for the use of processed poultry in place of live or freshly butchered birds will be rolled out in late February.

Brilliant news!

As you can see in the short news video, some (n=1) of the public see the sense of a change as well as the benefits of not having to deal with slaughtering and plucking chickens while others (n=1) complain that there will be a taste difference. 

I've never known much truly fresh chicken (I'm more a fan of the flavours its cooked in) so in my ignorance I don't know whether I'm missing something special or not. 

I do know what it is to miss a bad bout of the flu though. That's something I'd go the long way around to avoid crossing paths with.

This change seems so much more in concert with a China made of glass and steel. Good work. I hope it catches on elsewhere.

Sources...

  1. CNTV Report
    http://english.cntv.cn/program/newsupdate/20140215/103244.shtml
  2. H5N1 blog
    http://crofsblogs.typepad.com/h5n1/2014/02/china-hangzhou-to-build-h7n9-prevention-system.html


Looking at the age and sex difference between H7N9 Wave 1 and Wave 2...

Thanks to CIDRAP's Dr. Nicholas Kelley for asking the question of whether I'd looked at the epidemiology of the H7N9-related deaths between Waves 1 and 2.

So that led to the charts below.


Click on image to enlarge.
Only laboratory confirmed cases and the fatal cases with enough data to identify them are shown.
Wave 1 was defined as from weeks beginning 18-Feb-2013 to 20-May-2013.
Wave 2 as from Week beginning 7-Oct-2013, until today.
Top row: total cases; surviving and fatal.
Bottom row: fatal cases. Approximately 17 are missing sufficient data to identify.
If we look at numbers, because eyeballing these charts can be misleading we see some differences, although not huge.

The average age (in years) is divided as below:

  • Wave 1
    • All cases: 56.9
    • Fatal cases: 64.5
  • Wave 2
    • All cases: 52.8
    • Fatal cases: 63.0
The proportion of Males (%) is divided thus:
  • Wave 1
    • All cases: 72.0
    • Fatal cases: 75.0
  • Wave 2
    • All cases: 66.3
    • Fatal cases: 82.1

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