Calibrated response to emerging infections
BMJ 2009; 339 doi: https://doi.org/10.1136/bmj.b3471 (Published 03 September 2009) Cite this as: BMJ 2009;339:b3471
All rapid responses
There
cannot be any doubt that the new H1N1 virus is highly contagious but only
produces mild disease, probably is even less virulent than seasonal flu.
Dr.Scheibner has put it very succinctly 'Much ado about nothing'.
I have recently returned from India and what struck me was the
valuable resources diverted by the officials into the anti-flu campaign,
which at that time had reported only a single case of H1N1 flu in an
Airline passenger who had mild fever lasting for a day. Thousands of
casualties to preventable diseases like diarrhoea, malaria an
tuberculosis are a daily occurrence there.
Peter Collignon referred to the inappropriate fear which has pushed
us to inappropriate responses. May I refer to inappropriate information
which has been used to create unnecessary fear both by the WHO and the UK swine flu information leaflet: because it is a new virus no one will have
immunity to it (1,2).
H1N1 has been around since 1918. This is a new
variant, a fact that I don't argue.
But is it true that no one will have immunity to it? Millions have
been infected. Most patients had only mild symptoms. The death rate and
overall admission rate were the same or even lower than for seasonal flu. How
could this have happened if the infected population did not have any
immunity? In fact they had good immunity.
Two distinct immune systems operate in our body:innate immunity and
acquired immunity.
Innate immunity is a primitive but powerful immune system that comes
into operation immediately after infection and does not require
previous exposure to the invading microbe. Pattern recognition receptors
in the host cell recognise pathogen associated molecular patterns in a
general manner and signal the immune system to destroy the parasite. There
are also thousands of antimicrobial peptides which keep the pathogen in
check.
Acquired immunity operates by lymphocytes which specifically
recognise antigenic epitopes in the pathogen. Quite a large percentage of
these epitopes will be shared by the different flu viruses and the
vaccines already in use. In fact most of us have good immunity to the new
H1N1 virus as demonstrated by the epidemiology of the present Pandemic.
1.World Health Organization. Ten things you need to know about
pandemic influenza. 2005.
2.Important Information about Swine Flu. www.direct.gov.uk/swineflu
Competing interests:
None declared.
Competing interests: No competing interests
I thank Peter Collignon for providing links to the data regarding the
Australian wave of the pandemic H1N1 flu. The arguments for mass
vaccination may well be different for Australia where they are emerging
from the usual seasonal risk period, but in the Northern hemisphere it is
prudent to plan for a second wave in winter and it is sensible to ensure
that all vulnerable groups are offered the potential protection of a
vaccine when this is available and has completed its safety and efficacy
checks.
The recent BMJ article on lessons learned from Australia was
instructive; apart from the opinion voiced by Dr Collignon criticising the
overall response as being excessive there were other senior clinicians who
"believe the risks [of H1N1] are understated" and who indicate the demands
for critical care services in the Northern hemisphere are likely to be
overwhelming. It must be remembered that in this scenario it is not just
the deaths from influenza that may be "due to flu", but the deaths of all
those without flu who will be unable to access level 2/3 critical care can
also be indirectly attributed as deaths "due to flu".
With H1N1 certain groups are more at risk of death and complications
than others, and these groups should be prioritised for vaccination to
minimise the chance that they get infected and require admission/critical
care.
I must question some of Dr Collignon's own figures, however. He tells
us H1N1 has "a very low mortality rate (less than 1 per 10,000 infected)"
but the references he cites as evidence for this for this clearly indicate
there have been 150 deaths out of 34,172 cases. That makes a mortality
rate of 1 per 228 infected by my calculations. The reference cited also
states the number of notified flu deaths is an underestimate. Even
accounting for some underdiagnosis of mild disease increasing the
denominator, it is hard to know how he derives his estimate. If true it
would suggest that nearly one in ten Australians have already had H1N1
without realising it.
Dr Collignon is correct that fear pushes us to do things which may
not be appropriate, such as the overuse of oseltamivir. Yet there seems to
have been little in the way of clinical harm as a result of its use (side
effects, though frequent, were mostly mild/tolerable and less severe than
the flu) and fears of widespread resistance have proved to be unfounded
(only 18 cases have been reported worldwide). Yet concerns about
use/misuse of antivirals should not be used as a reason to deny protection
from H1N1 to those who need it the most.
Competing interests:
None declared
Competing interests: No competing interests
Mark McConnell’s wise young daughter recognises that there is no
swine flu pandemic just as there was no, and was not going to be, any SARS
or bird flu epidemic. The wise only see an attempt (doomed right from the
onset) to CREATE an epidemic. Once again, the babe recognised that the
emperor is naked. Para-phrasing a past US presidential campaign: “there is
no emerging swine flu pandemic, it’s the $$$economy stupid”, and what
would Shakespeare say? Much ado about nothing.
Competing interests:
None declared
Competing interests: No competing interests
Dear Editors
Mass vaccination against swine flu; could it cause more harm than
good?
Dear Sir,
Doshi (1) appropriately highlights the need for public health
responses to take into account the severity of any new infection as well
as its ability to spread. US Department of Health and Human Services, too,
in 2005 called for a graduated response in its pandemic preparedness plan
(2). It introduced a five-step "pandemic severity index" stratified by the
case fatality ratio (category 1 is for a pandemic with case fatality ratio
<_0.1. p="p"/> This “swine flu” pandemic, while it spread readily, appears to have a
very low mortality rate (less than 1 per 10,000 infected) (3,4). It thus
seems inappropriate that we should rush into what must be the world’s
largest ever mass vaccination program but with vaccines that have had
potentially less than optimal safety and efficacy studies performed.
Rolling it out in multi-dose vials also has the inherent increased risk of
cross infections with bacteria and blood borne virus infections (5,6).
We need to be sure with any vaccination program that the benefits
will substantially outweigh the risks. That is not at all clear with this
pandemic. Inappropriate levels of fear have already pushed us into
inappropriate responses. One example is the gross overuse of oseltamivir.
Fear has caused many people who should have stayed home and recovered
uneventfully with a mild illness, to seek medical help and treatment.
These actions likely spread infection in the facilities they visited and
while travelling. In addition such behaviour limits access to medical care
to those who had risk factors and did need to be seen promptly for either
therapy of prophylaxis.
The Northern hemisphere is about to enter the autumn and winter
seasons. There are now good data available from New Zealand (7) and
Australia (3,4) on what might be expected in winter when unvaccinated
populations are exposed to this new variant strain of influenza.
The best up to date data that is age stratified is from NSW Health
(3). It and the other Australian data (4) show now that this flu episode
is close to ending (it peaked early and unexpectedly in mid July). The
data show that this flu season has not been much worse overall than 2007
(although certain subgroups e.g. pregnant women have been overrepresented
in hospital and ICU admissions).
The death rate in the population was low, about 0.6 per 100,000
people (3,4).
Overall admission rates were not high either compared to seasonal
influenza (usually around 15 per 100,000 per). ICU admissions were 2.7 per
100,000 population. There are about 200,000 pregnant women at any one
time in Australia. My estimate for death was about 2 per 100,000 pregnant
women.
While hospital admission rates are available broken down by age
group, similar data is not available for deaths. My calculations of deaths
by age group are based on the data in these reports (Table 1).
Worldwide we are about to rollout one of the biggest and most rapid
vaccine campaigns ever undertaken. Reported inactivated vaccine efficacy
is between 50 to 80% (8). Thus for every 1 million people vaccinated we
will decrease the number of deaths from 6 to 2 or 3 people. We will also
prevent between 75 to 120 hospital admissions and 13 to 22 ICU admissions.
Given the relative lack of infections we are seeing in the elderly,
it appears that most people over 60 years are already immune (presumable
from previous H1N1 infection). Now also probably at least 20% of under-60
year old Australians have already been infected. Thus potentially only
about 60% of the Australian population may benefit from mass vaccination
if H1N1 returns next winter.
We need to weigh this against the risks of vaccination. There will
probably be between 1 to 2 additional episodes of Guillain-Barré syndrome
per million vaccine recipients (5,8). If we have a repeat of the 1976 US
swine flu vaccination roll-out then there may be 10 cases per million
vaccine recipients. We also need to estimate how many bacterial and blood
borne virus infections we might expect from the use of multi-use vials
(5,6).
Australia is approaching its spring. There is no need here to rush
into a mass vaccination programme particularly using multi-dose vials. In
the Northern hemisphere, rapid assessment of different age groups and at-
risk groups is needed re their risk and rates of death or severe
infection. This is to ensure that vaccination policy is appropriately
targeted to the threat of H1N1 and based on the extensive data now
available from winter in the Southern Hemisphere and the previous summer
in the Northern hemisphere. Mass vaccination will not be appropriate
unless likely benefits substantially outweigh likely risk in many of the
age groups.
Table 1 Number of admissions Deaths admissions rate deathrate Under 40 724 5 17.9 0.12 40-49 132 8 13.3 0.81 50-59 186 15 20.9 1.69 60-69 78 7 11.9 1.07 70+ 70 11 10.5 1.64 Total 1190 46 17.1 0.66 Rate per 100,000 population (NSW) (3)
References
1. Doshi P. Calibrated response to emerging infections. BMJ. 2009 Sep
3;339:b3471. doi: 10.1136/bmj.b3471.
http://www.bmj.com/cgi/content/full/bmj.b3471?ijkey=tKcb8W6KUoHXzPC&keyt....
[accessed September 11, 2009].
2. Interim Pre-pandemic Planning Guidance: Community Strategy for
Pandemic Influenza Mitigation in the United States. February 2007. CDC
Atlanta. http://www.flu.gov/professional/community/mitigation.html
[accessed September 11, 2009].
3. Weekly Influenza Epidemiology Report, NSW. Including H1N1
influenza 09
Prepared by the Population Health Division, 2 September 2009. NSW Health.
http://www.emergency.health.nsw.gov.au/swineflu/resources/pdf/case_stati...
[accessed September 11, 2009].
4. AUSTRALIAN INFLUENZA SURVEILLANCE SUMMARY REPORT No.16, 2009,
REPORTING PERIOD: 22 August 2009 – 28 August 2009.
http://www.healthemergency.gov.au/internet/healthemergency/publishing.ns...
5. Sweet M and Collignon P. Why can’t we have a rational discussion
about the merits of pandemic flu vaccination? August 31, 2009. Croakey.
http://blogs.crikey.com.au/croakey/2009/08/31/why-cant-we-have-a-rational-
discussion-about-the-merits-of-pandemic-flu-vaccination/?source=cmailer
[accessed September 11, 2009].
6. Drain PK, Nelson CM, Lloyd JS. Single-dose versus multi-dose
vaccine vials for immunization programmes in developing countries. Bull
World Health Organ. 2003;81(10):726-31.
7. Baker MG, Wilson N, Huang QS, Paine S, et al. Pandemic influenza
A(H1N1)v in New Zealand: the experience from April to August 2009.
EuroSurveill. 2009 Aug 27;14(34).
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19319
[accessed September 11, 2009].
8. Demicheli V, Di Pietrantonj C, Jefferson T, Rivetti A, Rivetti D.
Vaccines for preventing influenza in healthy adults (Review). Cochrane
collaboration. The Cochrane Library, Issue 2. Available online at:
http://www.cochrane.org/reviews/en/ab001269.html
[accessed September 11, 2009].
Competing interests:
None declared
Competing interests: Table 1Number of admissions Deaths admissions rate deathrateUnder 40 724 5 17.9 0.1240-49 132 8 13.3 0.8150-59 186 15 20.9 1.6960-69 78 7 11.9 1.0770+ 70 11 10.5 1.64Total 1190 46 17.1 0.66Rate per 100,000 population (NSW) (3)
Peter Doshi presents some interesting thoughts on the current H1N1
outbreak and its wider ramifications for future outbreaks of newly emerged
human pathogens (1).Distilled, the central themes of the paper are:
1. That the response to the pandemic may have been unnecessarily
aggressive;
2. That early response was driven by concern generated by
inappropriate diagnostic laboratory testing producing potentially biased
prevalence estimates; and
3. Response to future outbreaks of novel and emerging infections may
be better targeted by use of a two-dimensional framework, which classifies
such events on disease severity and numbers infected.
Starting with the last of these first, whilst the framework is
interesting as a piece of reflection, as a construct for planning an
urgent response to a newly emerged agent it is, I would argue,
impractical.
Firstly, values that would allow one to place an outbreak correctly
in any four of the described planes are not available at the time a
response is required. For disease severity, even Doshi acknowledges that
decisions on the initial response were being made at a time when such
information was incomplete. In the US a nationwide public health emergency
was declared on April 26 with 20 cases and no deaths, but evidence of
severe disease from Mexico. With the information available at that time,
when response measures were required and public health officials would
have been derelict not to act, where on the x-axis does this pandemic go?
Clinical severity is even more troublesome. There are two qualities
that make the y-axis variable different to the x-axis: the number of cases
is both outbreak duration dependent and reliant on the success of control
efforts. Placement on this axis too early in an outbreak, when cases are
few, may result in an insufficient response resulting in continued disease
transmission and human suffering that may have been stopped with early,
aggressive intervention. At what time-point during the 2003 global SARS
outbreak did it become clear that cases would not exceed 10,000? I would
argue it was many months after the time when action was required and
taken, and that said action greatly limited the spread of the outbreak.
These are features we can only be certain of in the comfort of hindsight.
Doshi implies that the response to the H1N1 pandemic may have been
unnecessarily aggressive. But even now he appears unprepared to place H1N1
pandemic on his framework for guiding action. H1N1 may prove (my emphasis)
to be type 3: if we can’t definitively characterise H1N1 some four months
after the first cases were identified, in what time frame will this
construct allow us to calibrate response?
Finally, Doshi suggests that the increase in diagnostic laboratory
testing may have led to misperceptions about the outbreak and may even
have biased our understanding. Laboratory testing has greatly assisted our
understanding of influenza epidemiology. No distinction could be made
between seasonal and pandemic influenza in 1918 as the viral cause of
influenza was first reported in 1931 (2). The advent of highly sensitive
and specific nucleic acid tests has, in recent years, revolutionised
virology, and real-time RT-PCR assays were available for pandemic (H1N1)
2009 virus within weeks of the discovery of this new variant (3).
Laboratory testing played an important role in informing national response
in Australia during our winter season, including the declaration of phases
and planned responses, in line with the National Pandemic Plan (4).
Doshi suggests that results of laboratory testing drove concern and
anxiety about the H1N1 outbreak and that this, rather than the pandemic
itself, forced potentially unnecessary action. Even a pandemic influenza
virus that causes typical influenza disease will have substantial impact:
in Australia over our flu season we have had 162 identified deaths, and
despite being at the end of our outbreak, 334 people remain in hospital
(5). Indigenous Australians and pregnant women were disproportionately
affected. Laboratory testing reflects what is happening in the community;
it doesn’t generate but merely confirms cases, and given deaths and
hospitalisations occur, it would be unreasonable not to provide this
information to the public, particularly those at increased risk. At the
height of our H1N1 outbreak in Australia influenza was detected in 67% of
specimens submitted, and 91% of typed influenza viruses were the pandemic
strain (6). There was little influenza B around removing a role for point-
of-care testing in artificially increasing the proportion of specimens
positive (1). The worried well effect described would increase the number
of negative specimens collected thereby reducing the proportion of all
specimens positive for the agent of interest. The Swedish data Doshi cites
account for only 79 people coming from endemic countries – this compares
with tens of thousands of specimens collected and tested in such
countries. Whilst interesting, their importance should not be overstated.
Without further detail it is difficult to understand how the suggested
“ongoing randomised sampling” should be performed: is the sampling frame
the entire population or just symptomatic people? If the later, how is
this group to be identified and sampled without feeding into the concern
bias Doshi is attempting to prevent?
Most things are clearer on reflection. Public health authorities
attempting to deal with emerging infections that may have catastrophic
effects on human health and safety need to act promptly with available
information to hand, including laboratory testing data. In such
emergencies, the calibrated response is assessed and adjusted daily.
Doshi’s framework is interesting, but can only be accurately completed in
hindsight, it is not a tool to guide immediate response.
References
1. Doshi P. Calibrated response to emerging infections. BMJ
2009;339:b3471.
2. Shope RE. Swine influenza I: Experimental transmission and
pathology. J Exp Med 1931;54:349-359.
3. Whiley DM, Bialasiewicz S, Bletchly C, et al. Detection of novel
influenza A(H1N1) virus by real-time RT-PCR. J Clin Virol 2009;45:203-204.
4. Commonwealth of Australia. National Action Plan for Human
Influenza Pandemic. 2009. The Department of the Prime Minister and
Cabinet, One National Circuit, Barton ACT 2600 Australia.
http://www.dpmc.gov.au/publications/pandemic/docs/NAP.pdf
5. Commonwealth Department of Health and Ageing. Pandemic (H1N1) 2009
update bulletin. 09 September 2009.
http://www.healthemergency.gov.au/internet/healthemergency/publishing.ns...
6. Kelly H, Grant K. Interim analysis of pandemic influenza (H1N1)
2009 in Australia: surveillance trends, age of infection and effectiveness
of seasonal vaccination. Eurosurv 2009;14:1-5.
Competing interests:
SBL is a co-investigator in a CSL sponsored paediatric swine flu vaccine study and was the WHO team leader in Singapore during the 2003 SARS outbreak.
Competing interests: No competing interests
Dear Editor,
Nobody thinks in information society was the firm opinion of Michael
Chrichton, a US trained physician!
There is a novel way of testing new vaccines in an emergency
pandemic, we are told, by bypassing the regular mandatory human testing. I
wonder if the WHO has permitted this to be done by the drug companies!
The new European procedure, which was established by the Commission and
implemented by the EMEA, allows manufacturers to gain an authorisation for
a ‘mock-up’ vaccine before a pandemic has occurred. EMEA explains, in a
question answer document, thus: (http://www.emea.europa.eu/pdfs/gene)
“A mock-up pandemic influenza vaccine is a vaccine that mimics the
future pandemic influenza vaccine in terms of its composition and
manufacturing method. However, because the virus strain causing the
pandemic is not known, the mock-up vaccine contains another flu strain
instead. This is a strain that is not circulating in humans, and to which
humans have not been exposed in the past. This enables the company to test
its vaccine in preparation for any flu pandemic that may occur in the
future, by carrying out studies with the mock-up vaccine that predict how
people will react to the vaccine when the strain causing a pandemic is
included.”
I am a bit concerned, may be the wiser ones amongst us would allay my
fears, about a couple of things here. The “mock-up” uses a new strain of
‘Flu vaccine. Does this mean that we have stockpiled many unknown but,
potentially dangerous, ‘Flu strains in our laboratories? Is this a normal
practice? If the virus has not been exposed to humans thus far, how are we
sure that the few individuals that we expose to this new strain are not
being made guinea pigs?
Even assuming that all the above are fine, when the pandemic hits in
future the virus strain would again be a new one like the mock up virus
and its reactions could be as unpredictable as that of the mock up virus.
Each virus would produce its own individual way of attacking humans. How
then are we sure that the mock up bypass is of any guidance? Reminds me of
bypassing the coronary epicardial arteries in chronic angina where the
culprit is the reduced coronary reserve in the millions of perforating
muscular vessels inside the myocardium. Are all bypasses in medicine
basically money spinners? This bypassing will give permission to
manufacturers to get new vaccines as and when they think fit using
whichever strain they think is needed. To me it looks as if we have put
the cart before the horse. Long before the pandemic has arrived efforts to
make vaccines have begun; rather vaccine manufacturing seems to be our
primary concern in a pandemic.
I strongly feel the whole science of vaccination needs a re-look in
view of the fact that only one viral disease, small-pox, has been
successfully eradicated so far by human effort. Every other vaccine could
be explained as only a partial success in so far as the virus has only to
mutate to bounce back with greater vigour. The vaccine will, of course, be
useless in that scenario. Edward Jenner used cow pox virus on James
Phipps. Cow pox virus is genetically different from small pox virus. It
was T. Z. Holwell, FRCP (London), FRS, who studied the protective power of
the Indian Ayurvedic vaccination system prospectively for twenty years in
"The Bengall" in the eighteenth century to suggest universal vaccination
that has eradicated small pox for ever. (1) Hopefully, all laboratories
will have destroyed their stock of that deadly small pox virus.
Holwell in his paper to the President and Fellows of the London Royal
College in 1767 AD did write that the Indian vaccination was not only
effective but done with great care and sophistication. Holwell even noted
that the vaccination system existed for “times out of mind” in India, and
has been effective for hundreds of years, which he strongly recommended
for universal use! I think that his original papers are preserved in the
library archives in Regents Park. Recently Douglas C Wallace, a noted US
geneticist, who has discovered some extra nuclear mitochondrial DNAs
(mtDNA) that are more useful for drug testing and disease prevention in
contrast to our conventional Mendalian genetics where only nuclear DNAs
are taken into consideration. (2)
Using his MITCHIP he has been able to find that Asian herbal
medicines are not only effective against many diseases including some
infections like malaria that he had tested, but has also shown that the
western pharmacology of chemical compounds for a target might even damage
the cell in the bargain. Could this be the bane of all our problems with
the deadly adverse drug reactions? We might have to take a leaf out of
Wallace’s work to think of a new science of vaccination.
Another point that worries me is the possibility of multiple
vaccinations confusing the human immune system. Children get nearly 20
vaccinations in infancy and many more after that. To cap it, now we have
the “mock-up” vaccines also getting ready! Real immunity comes from real
disease only. Vaccines create a mild form of the disease and we do not
know how effective that mild (forme frustae) disease would be in producing
anti-bodies. Lately frequent tetanus toxoid injections have been shown to
be useless if not dangerous. One could easily understand the anxiety and
enthusiasm to produce vaccines. The latter is the best business as the
whole world becomes vaccine customers for the business. My worry is: could
the recent spurt in auto-immune diseases have anything to do with this
preventive strategy of modern medicine? I could be wrong but, just in case
someone has an answer!!
One lead here seems apt. African Americans have the highest incidence
of autoimmune diseases compared the Caucasians, while Africans in Africa
have very low incidence of autoimmunity. While there could be many
imponderables, but one that might connect the two is that Africans have
many kinds of germs that their immune system has to fight against for
survival. Their nearly 150 odd genes that oversee the immune system are
busily engaged. While African Americans live in a relatively germ free
sterile environment in the US compared to Africa. May be the genes have no
work to do. Could they become naughty and produce anti-bodies against
their own body cells? (Horror auto-toxicus of Paul Ehrlich?)
Yours ever,
bmhedge
References:
1) Hegde BM. Vaccination system in India. 1998; 46: 472-473.
2) Wallace DC. Mitochondrial Chi. Genetics 2008; 179: 727-735.
Competing interests:
None declared
Competing interests: No competing interests
I wonder whether Peter Doshi apreciates that employing a measured
approach to such events could result in frustrating pharmaceutical
industry growth targets? We might get a different view of all this if we
looked at the financial models rather than the medical ones.
For instance, a report from PriceWaterhouseCoopers last year
envisaged a pharmaceutical industry in 2020 which is more than double the
size of the present global industry, in which the primary shift of focus
is from "treatment to prevention"[1]. This is a lot of prevention.
Here are two other interesting financial reports: 'Kids' vaccine
market set to quadruple'[2] from November 2007 which projects a
quadrupling of the juvenile vaccine market over the period of a decade,
and the more recent 'New report forecasts more than doubling of vaccine
sales by 2014'[3].
Presently in the UK we already administer 25 vaccines by 13 months of
age[4] so you might have thought that the room for expansion was limited.
I believe there is an ethical imperative at this juncture to stand
back and ask what is happening, and why?
[1] PriceWaterhouseCooper, 'Pharma2020: Which path will you take?'
[2] http://www.drugresearcher.com/Research-management/Kids-vaccine-
market-set-to-quadruple
[3] http://www.marketwatch.com/story/new-report-forecasts-more-than-
doubling-of-vaccine-sales-by-2013
[4]
http://www.immunisation.nhs.uk/Immunisation_schedule/Full_immunisation_s...
Competing interests:
None declared
Competing interests: No competing interests
On hearing the news of the "pandemic" this past spring, my medically
naive
daughter asked, "Dad, isn't this the same thing they said about SARS and
bird
flu?"
Her question brought to mind thoughts so nicely articulated in
Doshi's article.
I am happy that he is such a fine writer as I can refer my dear daughter
to this
as well as sharing it with patients and staff who are wrestling with how
to put
well intended information about H1N1 into a useable context.
I fully support the idea of categorizing pandemics so that the term
has more
meaning. I suspect government officials must assume a "worst-case
scenario"
but we all must, as Doshi reminds us, recognize the costs of our
preparation
and try to maintain balance.
The content and tone of this piece offer me a resource I can share
with patients
(and my daughter!) to help promote the prudence of practical preparedness
without the panic of pandemic.
Competing interests:
None declared
Competing interests: No competing interests
Using information available from New Zealand and New York City it
would appear that 20-30,000 people are infected with this pandemic
construct for each death.
Given that there have been approximately 3,000 confirmed deaths that
would suggest that between 60 million and 90 million people have already
been infected by the 2009 H1N1 pandemic influenza virus.
Given the USA has 595 deaths that would equate to 12 million to 18
million infections in the USA alone.
By any measure this is a very benign influenza virus. New Zealand,
for example, normally has 400 influenza deaths each year... (according to
official's statements). This year we had 17 deaths so it could be argued
that the pandemic has resulted in 383 lives being saved which makes it
more effective than any influenza vaccine.
Competing interests:
None declared
Competing interests: No competing interests
Flu stats vs PR
Dear Mr. Doshi,
This is the second of your articles that I have had the happy
opportunity to read, the first being - ‘Are Flu Death Figuress More PR
than Science?”.
For 10 years now I have read (and practiced what I've learned, i.e.
eschewing vaccinations altogether) - voraciously on the subject of
vaccines. I found yours - in the above referenced article - to be a long
overdue common sense voice, in contrast to the CDC’s unfathomable style of
reporting flu deaths, and the hysteria that is clearly (to some of us)
tacked on to the subject and racheted up systematically every few years or
so.
Lately I have been searching the CDC web site to get their figures on
just how many people they are alleging to have died this year from H1N1 in
the US (I say 'alleging' since actual testing for this specific ailment
stopped late summer) and how it compares to their mantra of ’36.000 flu
deaths annually' for ‘seasonal flu’. It would appear to me that if you
'do the math', that providing the reported figures for H1N1 deaths is
accurate, that no one has had the regular flu at all. Getting an actual
tally from the CDC web site though I discovered, is as easy as finding
Osama Bin Laden since 1997.
I do have a question that I would like to ask you. Are there any
reliable statistics for the number of flu deaths (in any age group or any
nation) relative to the percentage of these victims having been
innoculated, or not?
Any feedback is welcome. I’m obliged in advance.
Victoria Christine Bingham
Alexandria VA
EMAIL: artistry@bfresco.com
Competing interests:
None declared
Competing interests: No competing interests