+MaryMangan over there on Google+ made an interesting point about simple messages to refute the kinds of nonsense promulgated by vaccine denialists, among others.
Here’s my contribution:
+MaryMangan over there on Google+ made an interesting point about simple messages to refute the kinds of nonsense promulgated by vaccine denialists, among others.
Here’s my contribution:
I am TRYING to write an eBook on influenza, which stubbornly refuses to be finished – as part of a sabbatical project, which finished in December 2010. So, like my History of Virology, I am trialling the material on you, the Web community. Enjoy / comment / be enlightened / whatever!
NEW NOTE: The ebook is finished, and is available here on the iBooks Store: please try it out (you can read it on any Mac / iPad / iPhone using the free iBooks app)
A useful online history in pictorial form can be accessed here.
While they were not recognised as such at the time, major or pandemic outbreaks of influenza disease have occurred throughout recorded history. Medical historians have used contemporary reports to identify probable influenza epidemics and pandemics from as early as 412 BCE – and the term “influenza” was first used in 1357 CE, describing the supposed “influence” of the stars on the disease. The first convincing report of an epidemic of the disease was from 1694, and reports of epidemics and pandemics in the 18th century increased in quality and quantity.
The first pandemic that historians agree on was in 1580: this started in Asia, and spread to Africa, took in the whole of Europe in 6 months, and even got to the Americas. Subsequent pandemics with significant death rates occurred in 1729 and 1781-2; there was a major pandemic in 1880-1883 that attacked up to 25% of affected populations, and another in 1898-1900 that was probably H2N2. There is an excellent account here of the first “modern” pandemic, in 1890 – or at least, the first one to be followed essentially in real time via newspapers.
Influenza A pandemics in modern times. * = probably reintroduced from a laboratory from the H1N1 circulating from 1918 until 1957.
While the first reports of this pandemic were from Spain, this was largely because theirs was possibly the only uncensored press in Europe at the time because of the 1914-1918 War. In fact, it seems generally accepted that the virus originated in the United States, possibly in a military camp, and was then taken via infected personnel travelling by troop transport, to France by April 1918. The virus spread quickly across Europe, and via troop transports again to northern Russia, north Africa and India. Further spread then occurred, to China, New Zealand and The Philippines, all by June 1918.
Initially, there was nothing unusual: infections spread quickly for a while and then declined, and death rates were not higher than in previous pandemics. However, from August 1918 – marked by a ship-borne outbreak in Sierra Leone in west Africa – the virus seemed to have become markedly more virulent, and the death rate is supposed to have increased 10-fold. The virus quickly spread through Europe, to the USA, to India by October 1918, and to Australia by January 1919, all the while spreading through and around Africa.
Some countries had second and even third waves of infection, in 1918-1919 and 1919-1920. The pandemic was initially calculated as having killed some 20 million people: however, later estimates which took into account in particular the African, Indian and Chinese death tolls have increased the death toll to at least 50 million, and possibly up to 100 million.
The virus probably infected over one third of the humans alive at the time, with a case mortality rate of up to 5%. Some regions, like Alaska and parts of Oceania, had death rates of up to 25% of the total population. By contrast, the normal mortality rate for seasonal flu is 0.1 – 0.3% of those infected.
The pandemic was unusual in that it seemed to affect mainly young adults: The graph shows case mortality rates in percent for pneumonia and influenza combined for 1918-1919, and for seasonal influenza for 1928-1929, for different age groups. The “W” shape for the 1918-1919 figures is most unusual; the later seasonal data show a far more usual “U” curve. The green line shows what could have happened if – as is suspected – people over 30 had not had some immunity to the virus, due to prior exposure to the H1 and/or N1 – possibly during the 1880 or 1893 pandemics.
Although secondary bacterial infections of the lungs were common in fatal cases in 1918, and contributed significantly to mortality, there were also many cases of rapid death where bacterial infection could not be demonstrated – so these were due to a so-called “abacterial pneumonia”. Incidentally, the archiving of pathology specimens from especially military cases in the USA proved invaluable in “viral archeology” studies as late as 1997.
As early as 1901, investigators had shown that the agent of fowl plague was a “filterable virus”: however, this was not linked to human disease, as it was only shown to be an influenza virus in 1955.
Charles Nicolle and Charles Lebailly in France proposed in 1918 that the causative agent of the Spanish Flu was a virus, based on properties of infectious extracts from diseased patients. Specifically, they found that the infectious agent was filterable, not present in the blood of an infected monkey, and caused disease in human volunteers. However, many scientists still doubted that influenza was a viral disease.
A paper presented in 1918 to the Academie Francaise, describing the influenza agent as a filterable virus
In 1931, Robert Shope in the USA managed to recreate swine influenza by intranasal administration of filtered secretions from infected pigs. Moreover, he showed that the classic severe disease required co-inoculation with a bacterium – Haemophilus influenza suis – originally thought to be the only agent. He also pointed out the similarities between the swine disease and the Spanish Flu, where most patients died of secondary infections.
Pigs in the USA and elsewhere probably caught the H1N1 “Spanish Flu” from people – and it has circulated in them continuously until the present day
Patrick Laidlaw and others, working in the UK at the National Institute for Medical Research (NIMR), reported in 1933 that they had isolated a virus from humans infected with influenza from an epidemic then raging. They had done this by infecting ferrets with filtered extracts from infected humans – after an observation that ferrets could catch canine distemper – and then found that ferrets could transmit influenza to investigators by sneezing on them! The “ferret model” was very valuable, as strains and serotypes of influenza virus could be clinically distinguished from one another. Their serotype was named “influenza A”, and it was later typed as H1N1: this virus was a direct descendant of the Spanish flu virus, and had circulated in humans since 1918. It was the same subtype, incidentally, as that isolated by Shope from pigs.
Frank Macfarlane Burnet from Australia in 1936 showed that it was possible to do “pock assays” for influenza virus on the chorioallantoic membranes of fertilised chicken eggs, and subsequently said that:
“It can probably be claimed that, excluding the bacteriophages, egg passage influenza virus can be titrated with greater accuracy than any other virus.”
Historic picture on the wall in the routine influenza isolation laboratory at the National Institute of Communicable Diseases, Johannesburg.
This finding led directly to the development of the first influenza A vaccine – a killed virus preparation made in eggs – by Thomas Francis in the USAin late 1943. He had earlier, in 1940, isolated the first influenza B, which was made into a vaccine by 1945. It was then clear that seasonal influenza was caused by two viruses: the A H1N1 type, and influenza B.
After the influenza pandemic of 1918-1920, influenza went back to its usual seasonal pattern – until the pandemic of 1957. This started with the news that an epidemic in Hong Kong had involved 250 000 people in a short period. This was a unique event in the history of influenza, as for the first time the rapid global spread of the virus could be studied by laboratory investigation. The virus was quickly identified as an H2N2 subtype.
Except for people over 70, who had possibly been exposed to an influenza pandemic in 1898 – also probably a H2N2 pandemic – the human population was again confronted by a virus that was new to it – and again, the virus alone could cause lethal pneumonia. However, better medical investigation showed that chronic heart or lung disease was found in most of these patients, and women in the third trimester of pregnancy were also vulnerable.
The 1957 pandemic was the first opportunity for medical people to observe the vaccination response in the many people who had not previously been exposed to the novel virus. This was very different to the 1918 virus that had been circulating ever since, meaning that most people had no immunity to it at all. More vaccine was initially needed to give protective immunity than with the earlier type A vaccines. However, by 1960 as the virus recurred as a seasonal infection, immunity levels in the general population increased and vaccine responses were better, due to “priming” of the response by natural infection or first immunisation.
The death toll for this pandemic was around two million people – even though a vaccine was available by late 1957. Infections were most common among school children, young adults, and pregnant women in the early pandemic. Elderly people had the highest death rates, even though this was the only group that had any prior immunity, and there was a second wave in this group in 1958.
The new H2N2 virus completely replaced the previous H1N1 type, and became the new seasonal influenza type.
This pandemic started in mid-1968 in Hong Kong, and rapidly spread in a few months to India, the Philippines, Australia, Europe and the USA. By 1969, it had reached Japan, Africa and South America. Worldwide, the death toll peaked in December – January. However, although around one million people died, the death rate was lower than in 1957 – 1958 for a number of reasons, including the following:
The virus was similar in some respects to the Asian Flu variant – it was an H3N2 isolate, similar to the pre-1918 seasonal type, sharing N2 – meaning people infected then had partial immunity
The better availability of antibiotics meant secondary bacterial infections were less of a problem.
A vaccine to the new virus became available a month after the epidemic peaked in the USA – following a trend which had started with the 1958 pandemic, of vaccines becoming available only after the peak of the pandemic had passed.
An interesting development soon after this was the finding that waterfowl are the natural hosts of all influenza A viruses – and that there was a greater diversity of viruses in birds than in humans.
Between May and November of 1977, an epidemic of influenza spread out of north-eastern China and the former Soviet Union – hence the name “Red Flu”. The disease was, however, limited to people under the age of 25 – and was generally mild. It was soon found that virus responsible was effectively identical to the H1N1 that had circulated from 1918 through to 1958, and which had been replaced by the Asian flu, which was in turn supplanted by the Hong Kong flu. This was a most unlikely scenario, given that it was already known that influenza A viruses mutated rapidly as they multiplied – and it had been twenty years since the Spanish or H1N1 flu had been seen in humans. It also explained why infections were limited to young people: anyone who had caught the seasonal flu prior to 1958 was protected.
There has been speculation that the pandemic was due to an inadequately-inactivated or attenuated vaccine released in a trial; there has even been mention of escape from a freezer in a biological warfare lab. There is no firm evidence for either possibility; however, the result is that the virus that had reappeared then co-circulated with the H3N2 as a seasonal virus, continuously until the next pandemic. This was unusual, as a pandemic virus usually becomes the next seasonal strain.
The next major pandemic to follow on from the 1968 outbreak was again a type A H1N1 virus – which this time, originated in Mexico or the south-western USA, and probably came directly from intensively-farmed pigs. This had been an unusually long interval between pandemics, and warnings of the coming plague had been issued regularly for years: however, it had been expected that the next pandemic would involve the highly pathogenic avian influenza virus H5N1, which had been popping up since 1997, and had been established as an endemic virus in farmed chickens since 2004. This was therefore rather a surprise – but a reasonably welcome one, as the virus turned out to be relatively mild in its effects.
Intensive research on the origin of the virus threw up some very interesting results: it was effectively a direct descendant of the original Spanish flu H1N1 virus, but which had been circulating in pigs ever since 1918 – and had had contributions of genetic material from swine, humans and birds (see Chapter 3, here).
By June 2009 the World Health Organisation had raised the pandemic alert level to Phase 6 – the highest level, indicating that the virus had spread worldwide and that there were infected people in most countries. The “swine flu” pandemic was not as serious as had been feared, however: symptoms of infection were similar to seasonal influenza, albeit with a greater incidence of diarrhoea and vomiting. The virus was also found to preferentially bind to cells deeper in the lungs than seasonal viruses: this explained both why it was generally mild – it did not often get that far down – but also why it could be fatal, as it could cause severe and sudden pneumonia if it did penetrate deep enough, similar to the 1918 influenza. Binding to cells in the intestines also explained the unusual nausea and vomiting. It was also found that there were distinct high-risk groups, including pregnant women and obese individuals. In these respects it was similar to the 1918 flu, as this also predominantly affected young people, and pregnant mothers.
Vaccine manufacture was initiated in June 2009 by the WHO and manufacturers: while there was some concern over the slower-than-normal growth rate of the vaccine strains of the virus, this was rectified in a few months. However, as also happened with the other pandemics, there was not enough vaccine made soon enough to deal effectively with the pandemic – even though similarities between the pandemic virus and the 1977 outbreak virus meant that most middle-aged people had pre-existing immunity to it, which either prevented infection, or reduced the severity of infections. This also meant a single dose was sufficient in adults, similar to the seasonal vaccine.
While the disease may have been mild in most cases, and initially the death toll was thought to be low, by 2012 it was calculated that 300 000 or more people probably died, mainly in Africa and Southeast Asia. A sobering quote: “since the people who died were much younger than is normally the case from influenza, in terms of years of life lost the H1N1 pandemic was significantly more lethal than the raw numbers suggest”. The virus has now become a normal seasonal strain, replacing the previously-circulating H1N1, but interestingly, has not replaced the H3N2 that has circulated since 1968.
All material Copyright EP Rybicki, except for the Camp Funston image, which is in the public domain.
The publication in this issue of these research papers on the airborne tranimssion [sic] of H5N1 marks the end of 8 months of controversy over whether some of the data, now freely accessible, should be withheld in the public interest.”
I think this is an important landmark in the so-called “dual use” debate: that is, the propensity of bodies in the US to attempt to regulate the release of information that MAY be usable in the making of bioweapons, or be usable in bioterror attacks.
Let us diffidently point out at this juncture that it is only really the superpowers who are definitively known in recent years to have had bioweapons programmes – apart from apartheid-era South Africa, that is! – and that damn nearly ANYTHING published on transmission or mechanisms of pathogenicity of human or animal pathogens (or even plant, for that matter) could be termed “dual use” if someone wanted to – and censored as a result.
It is also – as I tire of pointing out – possible to PROTECT against H5NX viruses using conventional vaccines right now – and the new universal flu vaccines coming on stream will almost certainly make this even more feasible.
The fact is that H5N1 flu is an ever-present threat to people living in Egypt, Indonesia, Cambodia, Viet Nam, Thailand and China – WITHOUT being weaponised. It is no more than a notional threat to the US or Europe – and keeping information that could help in understanding how or how soon the virus could mutate to pandemicity out of people’s hands, is simply stupid.
See on www.sciencemag.org
“A new Swedish study shows that all Swedes who developed narcolepsy from the swine flu vaccine Pandemrix received the vaccine from 12 of the 35 batches, despite the claim by the responsible agency that no such connection exists.”
There are some slightly disturbing connections between the H1N1 2009 pdm virus and narcolepsy: the virus itself seems to have caused narcolepsy in some of those infected; now a vaccine is implicated – is this an innate property of certain of the virus proteins, possibly?
See on www.thelocal.se
“The pandemic 2009 H1N1 vaccine can generate antibodies in vaccinated individuals not only against the H1N1 virus, but also against other influenza virus strains including H5N1 and H3N2.”
And a possible reason for this could be that the H1N1pdm virus’ haemagglutinin is a natural “ancestral” sequence – the kind that HIV vaccine researchers are looking for for gp120/160, which have been shown to elicit a wider spectrum of cross-reacting antibodies than “evolved” proteins, or ones that have been selected for antigenic escape in humans for a good few viral generations.
Flu vaccine graphic by Russell Kightley Media
See on www.eurekalert.org
Our (very) recently-published article on plant-made flu vaccines in BMC Biotechnology:
Elizabeth Mortimer, James M Maclean, Sandiswa Mbewana, Amelia Buys, Anna-Lise Williamson, Inga I Hitzeroth and Edward P Rybicki
During a global influenza pandemic, the vaccine requirements of developing countries can surpass their supply capabilities, if these exist at all, compelling them to rely on developed countries for stocks that may not be available in time. There is thus a need for developing countries in general to produce their own pandemic and possibly seasonal influenza vaccines. Here we describe the development of a plant-based platform for producing influenza vaccines locally, in South Africa. Plant-produced influenza vaccine candidates are quicker to develop and potentially cheaper than egg-produced influenza vaccines, and their production can be rapidly upscaled. In this study, we investigated the feasibility of producing a vaccine to the highly pathogenic avian influenza A subtype H5N1 virus, the most generally virulent influenza virus identified to date. Two variants of the haemagglutinin (HA) surface glycoprotein gene were synthesised for optimum expression in plants: these were the full-length HA gene (H5) and a truncated form lacking the transmembrane domain (H5tr). The genes were cloned into a panel of Agrobacterium tumefaciens binary plant expression vectors in order to test HA accumulation in different cell compartments. The constructs were transiently expressed in tobacco by means of agroinfiltration. Stable transgenic tobacco plants were also generated to provide seed for stable storage of the material as a pre-pandemic strategy.
For both transient and transgenic expression systems the highest accumulation of full-length H5 protein occurred in the apoplastic spaces, while the highest accumulation of H5tr was in the endoplasmic reticulum. The H5 proteins were produced at relatively high concentrations in both systems. Following partial purification, haemagglutination and haemagglutination inhibition tests indicated that the conformation of the plant-produced HA variants was correct and the proteins were functional. The immunisation of chickens and mice with the candidate vaccines elicited HA-specific antibody responses.
We managed, after synthesis of two versions of a single gene, to produce by transient and transgenic expression in plants, two variants of a highly pathogenic avian influenza virus HA protein which could have vaccine potential. This is a proof of principle of the potential of plant-produced influenza vaccines as a feasible pandemic response strategy for South Africa and other developing countries.”
I have mentioned time and again that going green is the sensible thing to do: here is a concrete example of how my research group is trying to go about it. This is a very sensible technology for rapid-response vaccine production, and especially for emerging or orphan or pandemic virus threats. We got really good expresion levels of H5N1 HA protein via transient expression in plants, and have already started on pandemic H1N1 HA expression. Let’s hope some governmental types in SA take some notice!
I thank Russell Kightley Media for the specially-commissioned graphic of budded HA-only VLPs.
Seeing as it’s officially over – well, the odd people still dying might dispute this, but the WHO Has Spoken – I thought I would share this with you, seeing as I agree 100% with the sentiments (I wanted it called Mexico Flu). Arvind Varsani, my one-time PhD student now in The Land of the Long Black White Cloud, sent me this link today – thanks Arv! You win a free ViroBlogy article! I expect it within a month.
I have been waiting with great interest to see what would happen in the wrong northern hemisphere 2009-2010 winter season with the Mexican – sorry; politically incorrect, aka pandemic H1N1 – flu – and it has pretty much happened, and it wasn’t nearly as bad as it could have been.
INFLUENZA PANDEMIC (H1N1) (05): VACCINE UPDATE
A ProMED-mail post
Date: Mon 11 Jan 2010
Source: Reuters News [edited]
Countries re-think swine flu vaccine orders
The United States said on Monday [11 Jan 2010] it had cut in half its order for influenza pandemic (H1N1) 2009 virus vaccine from Australia’s CSL Ltd, but said it is not certain how far orders from other suppliers will be trimmed. While U.S. officials are still calculating how much swine flu vaccine they will need, it is becoming increasingly clear that the United States will not need all 251 million doses it ordered from 5 companies. …
Several other governments have started to cut orders for [pandemic] H1N1 vaccines because the pandemic has not turned out to be as deadly as originally feared and most people need only one dose, not 2, to be fully protected.
…Germany’s Bild newspaper reported that the German government had agreed to cut its vaccine order with GlaxoSmithKline Plc by one-3rd. The newspaper said the agreement would save states about 133 million euros (USD 193 million). On Friday [8 Jan 2010], Britain said it was in talks with Glaxo about reducing supplies. ….
…While the pandemic is slowing down in North America, the World Health Organization said on Monday [11 Jan 2010] the virus was still active in parts of central, eastern and southeastern Europe, North Africa and South Asia. Governments are torn between trying to encourage companies to make influenza vaccine and wasting money on doses that are never given. But bulk antigen — the vaccine before it is put into a syringe – — can be stored and might be used in next year’s seasonal vaccine.
The U.S. government was still promoting vaccination, reminding people that influenza is unpredictable and that [pandemic] H1N1 could come back in a 3rd wave. One potentially large market for the vaccine is children. Children under 10 need 2 doses of vaccine to be fully protected and some U.S. school districts were planning more vaccination clinics this week to get children a 2nd dose. …
[Byline: Maggie Fox]
ProMED-mail Rapporteur Mary Marshall
Well, “The Big One” that we have all been waiting for since 1968 – or 1977, if you count the accidental re-release of the original humanised H1N1 as a pandemic – is well and truly here. A nice little animated graphic for depicting how it arose, while a bit simplistic, is available here.
And what have we learned? Has civilisation fallen; have populations been decimated?
Paris – More than half the fatalities from H1N1 swine flu have been among young adults, according to one of the first surveys to gather mortality data from across the globe for the new A(H1N1) virus.
The analysis of 574 pandemic deaths from 28 countries through mid-July, released this week, also found that being diabetic or obese significantly boosted the risk of dying.
Neither children nor the elderly are as vulnerable as initial reports indicated, found the study, published by Eurosurveillance, the monitoring arm of the European Centre for Disease Prevention and Control.
“Most deaths (51%) occurred in the age group of 20-to-49 year-olds, but there is considerable variation depending on country or continent,” the researchers reported.
Only 12% of those who died were 60 or older.
All of these features – high mortality among young adults and the obese, but not the very young or elderly – are sharply different than for the seasonal flu.
More than 90% of deaths from seasonal flu – which claims 250 000 to 500 000 lives annually according to the WHO – are in people over 65.
By contrast, with the pandemic H1N1, “the elderly seem to be protected from infection to some extent, perhaps due to previous exposure to similar strains”, the study conjectured.
Persons born before 1957, other studies have suggested, were almost certainly exposed to the milder seasonal A(H1N1) viruses that evolved from the terrible pandemic of 1918, which left some 40 million dead.
With the 2009 strain, “when infection does occur, however, the percentage of deaths in elderly cases seems to be higher that in others”.
One common target across both pandemic and season strains is pregnant women, according to the study, led by Philippe Barboza of the French Institute for Public Health Surveillance….
And that’s the sinister part…here in South Africa, of 18 fatalities known to have been associated with pandemic AH1N1 infection, NINE were pregnant women, mostly in the third trimester of pregnancy. In a report published yesterday, SA’s Minister of Health Dr Aaron Motsoaledi said the following:
“We find it very worrying that there is an increasing number of pregnant women who are succumbing to this pandemic,” Motsoaledi said.
“The directive to all health care workers… is to put pregnant women with flu-like symptoms (even if they are mild) on Tamiflu treatment.
“Doctors should not wait for any tests before such treatment is administered.”
Further on in the same report:
On Monday, the National Institute for Communicable Diseases [NICD] also said pregnancy had been identified as a particular risk factor for severe H1N1 flu.
It said that in the second and especially the third trimester, urgent treatment with antiviral drugs should be considered even before any laboratory results were received.
The institute added however that most H1N1 flu cases in South Africa remained mild and “self-limiting”.
Routine H1N1 testing for everyone with flu-like illness was still not recommended.
Nationwide, there had been 5 118 laboratory-confirmed cases of H1N1 flu, it said.
The figure is essentially meaningless, given that most suspected flu cases are not laboratory-diagnosed (it costs R700, or ~US$70, for a single test) and the pandemic flu is pretty much indistinguishable from seasonal, and may in fact have supplanted the normal flu. It certainly has in Australia and Argentina, which remain the two worst-hit southern hemisphere countries, and probably has in South Africa too: the CDC has a very useful map illustrating this, accessible here.
International news, via the CDC site, is the following:
As of August 13, the World Health Organization (WHO) regions have reported over 182,166 laboratory-confirmed cases of 2009 H1N1 influenza virus (2009 H1N1) with 1,799 deaths. The laboratory-confirmed cases represent an underestimation of total cases in the world as many countries now focus surveillance and laboratory testing only in persons with severe illness. The 2009 H1N1 influenza virus continues to be the dominant influenza virus in circulation in the world.
One very important piece of information further down this report is the following:
There have been no significant changes detected in the 2009 H1N1 influenza virus isolated from persons in the Southern Hemisphere as compared to viruses isolated from persons in the Northern Hemisphere.
This is important because the frantic rush to make vaccines to combat the expected northern hemisphere upsurge in infections in their autumn season – October or so – depends upon the virus not having changed much from the seed material which was derived from virus isolated earlier this year. This could negate some of theh fears that the much-anticipated “second wave” of virus infections could be a lot worse than the first.
Good news on the vaccine front – for Australians at least – is that an Australian company, CSL Ltd, has the world’s first data from human trials of a pandemic strain vaccine, and looks set to be able to provide Australia with 21 million doses of vaccine – and 2 million doses of the vaccine at the end of the month.
Other vaccine news is also fairly encouraging, notwithstanding a rather alarming report in New Scientist recently about the new strain growing only half as well in eggs as seasonal flu types: while this remains a worry, newer, faster-growing variants have been derived and distributed – though possibly not in time for a northern hemisphere autumn roll-out.
Mind you, all of this production relies on the well-proven-but-seriously-archaic 1930s technology of growing live virus in hen’s eggs: we are still trapped, in the 21st century, into having to use early 20th century methods to produce vaccines for fast-adapting pathogens. Things ARE changing: various pharma companies are diversifying into mammalian and insect cell culture; people (including us!) are investigating making recombinant subunit vaccines in plants (see here) – and there is at least the tantalising possibility that “universal vaccines” may become available in the not-too-distant future. These will exploit all or part of the highly conserved M2 “ion channel” protein of influenza viruses as recombinant subunit vaccines.
However, all of this is at least six months in the future for conventional vaccines, and many years hence for newer offerings. Meantime – there is disturbing news concerning trans-species transmissions of pandemic AH1N1 viruses.
ProMED Mail (ProMED Digest V2009 #394) reports that “Chile finds H1N1 swine flu in turkeys“:
Chilean health authorities announced on Thursday night [20 Aug 2009] that they had detected and controlled an outbreak of swine flu in 2 turkey farms, according to a communication from the Agricultural and Livestock Service (SAG).
“The presence of an influenza type A virus was detected in 2 farms in the Valparaiso Region, and immediate precautionary measures were adopted to prevent the dissemination of the disease and to protect the population’s health,” said the text.
And again from ProMED on 20th August, quoting The Straits Times and AFP:
A 2nd Australian piggery was placed in quarantine due to swine flu on Wednesday [19 Aug 2009] as the number of human deaths from the virus reached 121.
Authorities ordered a biosecurity lockdown at the piggery in Victoria state amid concerns the virus could mutate and return to humans in a more deadly form.
Another piggery in New South Wales state has been quarantined since late July , although the state government said most of the animals had recovered from the disease.
Victoria Agriculture Minister Joe Helper said tests confirmed the presence of influenza at the piggery after its owners reported earlier this week that the animals were not eating.
‘It is important to stress that this is not a human health issue and that national and international food authorities continue to advise that pork and pork products are safe to eat,’ he said.
Media reports said the pigs were believed to have contracted the virus from workers at the property who were suffering the human form of the disease.
Health experts fear swine flu in humans, which is easily spread but has a relatively low fatality rate, could mutate in other animals and emerge in a more virulent form. [my emphasis]
So: two independent incidents, on different continents, of pandemic AH1N1 viruses getting into different species of farmed livestock – and luckily controlled.
What would have happened if domestic fowl and/or pigs had been infected in places like Vietnam, Thailand, Indonesia, Turkey and Egypt – where highly pathogenic avian H5N1 influenza viruses appear to be endemic, and not well controlled? Given the complex origins of the current pandemic virus – from several swine, avian and human viruses – it could be a recipe for disaster, on a scale even greater than the 1918 pandemic.
The REAL Big One. Let’s all help get a vaccine, people!!
…as I think I do…
Thanks Michael Rolfe!