Doctors should recognise a broad and ill-defined range of symptoms that may signify depression in their primary care patients and should intervene appropriately, according to the results of a study reported recently in the Journal of General Internal Medicine.

RM Epstein and colleagues, from Rochester University Medical Center in New York, continue “…families, friends and the media can prompt people who have depressive symptoms to seek care by adopting a multi-faceted understanding of the experience of depression from the patient’s perspective — and helping them find the words to bring their experiences and concerns to the attention of [a] physician.”

Two things strike me here.

One is that this varied range of symptoms might, if considered analytically, using the Hamilton, Edinburgh or other rating scale, lead a clinician to an accurate mental health diagnosis. In the hands of others, the same information could lead the friends, family and the media to variously consider the potential patient as ‘just being himself’, ‘a bit down since John died’ or ‘dangerously psychotic’.

The point being that ‘families, friends and the media’ remain woefully ill-informed about the range of mental health conditions, their comparative severity and implications for patients’ lives.

Part of the solution to the above comes in the second feature.

Social amplification – the means by which the media press a concept or information into the public consciousness (for good or ill) – means that what is hyped in the press is expanded on talk shows until a proper sense of proportion can be lost.

Worries can be contagious, and mass media help to rapidly infect people within a social group. Family and friends – usually a solid source of support that keeps us alive through life’s ups and downs – are not immune. A year ago, pandemic influenza fed another misleading, damaging media feeding frenzy and, today, what quiet but sad middle-aged singleton would want to rely on a balanced diagnosis from friends or family, in the aftermath of the Cumbria shootings?

But, this can surely be harnessed for good as well as ill, can’t it?

Where Epstein and his colleagues are right is that the social actors around a patient need to know more about key features which point to a visit to the local surgery. This is easy with a broken arm. There is, usually, a clear cause and an obvious injury. Less so with mental health conditions like depression. Mental health conditions are complex, they overlap and they blur at the edges. Worst of all, they can be extremely hard to treat.

So what can we do to make sure that social amplification works for not against patients.

Increasingly, there is a need for a substantial proactive campaign of public information and education about the more common mental health conditions. In the UK, we never really accepted the mental part of health, preferring, perhaps, the philosophy of ‘Keep Calm and Carry On’. But that only carries you so far.

In many ways, we have only just come out of the Dark Ages in our treatment of mental health and we desperately need to widen public understanding with responsible and considerate reporting and discussion.

In this time of spending cuts, this is one area to stay hand of the axeman.

Epstein RM, Duberstein PR, Feldman MD, Rochlen AB, Bell RA, Kravitz RL, Cipri C, Becker JD, Bamonti PM, Paterniti DA. (2010); “I Didn’t Know What Was Wrong”: How People With Undiagnosed Depression Recognize, Name and Explain Their Distress; J Gen Intern Med. 15/05/10 [epub ahead of print].

Mad Cow (BSE, CJD) has been responsible for the deaths of 166 people in Britain and 44 elsewhere – and the bright sparks in Canberra have declared it’s okay to import beef products from countries that have reported CJD. For the record that is most countries in Europe and North America.

Some years ago I was shocked at the death of a close friend’s father who died as a result of bovine spongiform encephalopathy (BSE). More commonly known as Mad Cow’s disease when transmitted to humans it is a variant of Creutzfeldt Jakob Disease (CJD).

From Monday 1 March, beef import rules will be relaxed allowing countries including the US, UK, Canada and Mexico to export meat to Australia. What the hell for?

Here’s a little primer on the symptoms of CJD: First a fast and progressive dementia encompassing memory loss and personality change along with hallucinations. Then speech, impairment, balance and coordination dysfunction, jerky movements, seizures and ultimately certain death in anything from months to weeks.

We’ve already seen what panic the erroneously named swine flu – (H1 N1 flu strain) caused to the pork industry here and overseas. Just imagine the frenzy of hysteria to the local beef industry if the wheels fall off this genius initiative.

Already our tariffs and importation schemes have pretty well killed the clothing and footwear manufacturing industry here, they have had a damned good go at crucifying the pork industry by allowing subsidised frozen pork to monopolise the ham and bacon industry – so why wouldn’t we go a step further and open the flood gates for BSE infected countries to dump their dodgy beef products here.

If the subject didn’t sound like a line from the movie Kenny it would be otherwise laughable. But there’s also the sanitised (we hope) issue of the potential big dump of cheap Chinese toilet paper here to put another nail in the coffin of the Australian paper industry.

Statistically we spent $728 million buying 120,000 tonnes of poo ticket in 2007 and since then the market has grown by 25 per cent. With an influx of questionable beef products we could conceivably have a knock effect here with an even greater surge in usage and sales.

We are such good Joes at making Australia a level playing field for the world to score a litany of trade goals. And just to give them a solid head start we usually start the ball rolling with a couple of gratuitous own goals.

Last Tuesday I attended a Royal Society discussion meeting titled ‘Pandemic influenza: frontiers in research‘ which I hoped might provide some answers as to where research is headed in the wake of the emergence of a pandemic influenza strain.  Organized by Neil Ferguson and John Skehel it was a packed schedule, with the highlights for me being talks on the origins of the H1N1 influenza A strain that has swept the globe, the uncertainties that modellers grapple with when attempting to provide the best possible picture of the dynamics of an emergent epidemic (focusing of course on H1N1 influenza A), research into a universal ‘flu vaccine, surveillance of serological responses over the course of the pandemic in the UK by the Fluwatch project and a final word from Charles Penn discussing the WHO response to the H1N1 influenza A outbreak.

Gavin Smith discussed research published in June of last year in which a team of researchers carried out an evolutionary genomics study that showed that reassortment of swine ‘flu virus genes can result in emergence of a pandemic strain. The team of authors,  scattered in Oxford, Edinburgh, Hong Kong and Arizona, collaborated using a wiki to share their data and write a paper. Apparently we don’t have anywhere near enough data on ‘flu strains circulating in pigs, or how ‘flu viruses are transported by the pig trade. One big issue for policymakers and researchers alike is garnering the funding and political will to carry out surveillance of ‘flu strains in domestic pigs — clearly farmers might not be happy about such initiatives and moreover, as pointed out by Nick Phin, Head of pandemic flu planning at the HPA in the UK, would we be able to spot a new strain that had pandemic potential? Policymakers would need to decide whether allocating resources to routine ‘flu surveillance in animals was warranted, according to Dr. Smith, but he speculated that it might be possible (if monitoring  in animals and humans) to ’spot unusual gene flow in humans’.  Avian ‘flu on the other hand is transmitted by wild birds and its politically easier to establish surveillance in wild bird flocks, but, Robert Webster, also speaking at the meeting, cautioned that a global network of surveillance was needed and that current levels of surveillance are inadequate either to spot emergent strains, or to provide the level of genomic data needed to accurately determine the origins of new pathogenic strains that emerge in humans.

Neil Ferguson highlighted the differences between what the ‘flu modellers expected from a ‘flu pandemic (high attack rates, and emergence of a H1N1 strain from somewhere in Asia) with what they got (lower attack rates and emergence in Latin America) and pointed out that a lack of information on seroconversion rates in the first wave of the epidemic affected the ability of modellers to accurately predict the severity of the second wave of H1N1 infection. He also pointed out that making predictions is much easier with severe strains than with mild strains of ‘flu because surveillance often fails to spot the majority of mild cases. The biggest obstacles to accurate predictions during the early days of the H1N1 outbreak were limited serosurveillance (essentially only for those seeking care, who were by definition likely to have more severe symptoms), lack of information on H1N1 seasonality, and lack of mechanisms for sharing epidemiological data. Tellingly,  he asked ‘what is a reasonable worst case scenario’ and of course its very important to remember that messaging changing outputs, by both scientists,  politicians and the media, is a key challenge that need to be addressed. Similar views were echoed by John Edmunds at a CRAASH meeting (Healthy Futures: Medical Regulation and human agency) that I went to in January of this year. Regarding the thorny issue of widespread serological surveillance, Ferguson felt that whilst baseline data on serological responses to different ‘flu subtypes might have been helpful, he was concerned over whether gathering such data was cost-effective.

Are we anywhere near a universal ‘flu vaccine? Peter Palese has been working towards this goal for a long time now and reported on recent work in which his team generated cross-subtype specific antibodies (published in PLoS Pathogens) and a new mouse study investigating the protection offered against death and disease caused by a variety of subtypes by a headless HA vaccine, published in the new open access journal from the American Society for Microbiology called mBIO.

Charles Penn drew the meeting to a close and discussed general themes of the pandemic commenting that the only region currently showing an upwards trend in cases is West Africa so he felt that there was insufficient information to say that ‘we’re over the pandemic’.  He also commented that the word ‘pandemic’ is loaded as a pandemic can be severe or mild and that the WHO will soon be publishing revised guidance for the clinical management of H1N1 influenza. This has apparently been derived from clinicians sharing clinical notes, although the mechanism for data-sharing wasn’t clear to me. In response to some strong questions regarding recent data that contended that there was a paucity of evidence supporting the cost  effectiveness and safety of oseltamivir (Tamiflu), and questions over whether advice received by the WHO was impartial,  Dr. Penn was very clear that WHO actively manage conflicts of interest, whether ‘real or perceived’.

Labour MP, Paul Flynn suggested unused supplies of Tamiflu should be used to grit the UK’s icy roads after the overzealous stockpiling of the antiviral left the UK with surplus supplies of the drug.

As the UK has invested such a large sum on the medication, the MP took to his blog to state:

‘Unless an alternative use can be found for them, the Government stand condemned. They would be great for gritting the icy roads.’

Flynn’s remark is obviously witty for a number of reasons firstly the government bought a ridiculously large amount of antivirals for a pandemic which never actually happened. And secondly the government failed to purchase a satisfactory supply of grit for a big freeze which very much did happen.

So just what would happen if we did grit the UK’s icy roads with Tamiflu?

Firstly the cons, when a new more dangerous flu pandemic develops people would realise that the Tamiflu they desperately need is not in the pharmacies but is sitting on the roads.

Frantic coryzal victims will then begin to consume the grit, this would lead to a salt overload and imminent death. Now in my opinion anybody that is stupid enough to eat road grit would die in a ‘survival of the fittest’ type death: the kind that eliminates the brainless.

There are more positives of gritting the road with the medication though, most importantly it would solve the insufficiency of grit dilemma.

Furthermore influenza pandemics begin when a new variant of the virus mutates, this usually occurs when the flu virus in an animal mutates allowing it to pass directly from animal to human and then again to pass from human to human.

If we give the original animal the antiviral then that would alleviate the potential pandemic before it even passes to the first human. Through putting Tamiflu on the roads we are providing a supply to British wildlife thus preventing a future strain of bird flu and if lorry drivers continue to veer off the motorway, we could prevent future strains of swine flu as well.

So using the antivirals to grit the road seems like a ideal idea, there is just one small problem, by giving the drug to an abundant amount of animals, a new virulent strain of influenza will evolve, so dangerous it would knock out the entire worlds population. But damn it, nobody said resource allocation was easy.

Image: Salvatore Vuono / FreeDigitalPhotos.net

Teenage Girl Left Blind and Disabled by Tamiflu

Cher Thornhill
UK Daily Mail
January 21, 2010

A teenage girl left disabled by the swine flu treatment Tamiflu did not even have the virus, it was revealed today.

Samantha Millard, 19, became critically ill after suffering a severe allergic reaction to the tablets, which she took on the advice of the controversial NHS helpline.

Within 72 hours of taking three pills, doctors put her on life support.

Samantha spent a month in hospital after developing the life-threatening Stevens Johnson syndrome, which causes the skin to peel off, and later developed toxic epidermal necrolysis syndrome, which has damaged her sight.

Read Full Article Here

by revere, cross-posted from Effect Measure

It was some time after the pandemics of 1957 and 1968 that we were able to judge their severity and it will likely be some time after this one has finally burned itself out, most likely to become “just another” seasonal flu, that we will be able to gauge the 2009 swine flu pandemic. A lot of data is being generated but it will take time to harvest it and send it to the scientific market for consumption. A report in today’s Lancet reminds us that we aren’t seeing all there is to see, even with unprecedentedly rapid means of communication and better surveillance than ever in the history of our long battle with the influenza virus:

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The distribution and uptake of antivirals and vaccination was in the news quite a bit before Christmas. H1N1 swine flu didn’t turn out to be the Armageddon some commentators were forecasting, but I don’t think it’s overstating the case to say that we dodged a bullet there. In cases like this we might expect the government to give a clear message, based on the best possible epidemiology. No, please, stop laughing. After all, the UKian government was right about the MMR combined vaccine, even if they did handle the situation incredibly poorly.

And that’s a problem, isn’t it? In our culture we don’t trust what the government tell us anymore. That may or may not be a good thing, but it certainly creates problems for public health policy, especially in a potential epidemic situation. Sometimes it’s quite clear what the right thing to do is, but how do we get them to do it?

A paper just published in PNAS and reviewed on f1000 (link free for three months) sets out an economic framework for controlling transmissible and evolving diseases. Now, I’m not an epidemiologist (you should possibly go and talk to my mate Bill if you’re that interested), and the argument therein apply more to a healthcare system that is not free at point of care (Obama’s reforms notwithstanding), but it’s an interesting paper nonetheless.

“public policies such as taxing and subsidizing goods are frequently used to correct (for public benefit) the private actions of individuals when externalities, or side effects, of these actions exist.”

By comparing four different scenarios and addressing negative externalities, the authors predict where financial dis/incentives should be applied for maximum public health benefit. The scenarios discussed here are

1. Tetanus: infectious but not transmissible between humans, and no herd immunity
2. Measles: infectious, effective vaccination that generates a herd effective by reducing transmission
3. Otitis media: non-transmissible, but unnecessary antibiotic treatment can lead to the negative externality of antibiotic resistance
4. Pandemic influenza: antiviral treatment generates negative (resistance) and positive (reduced transmission) externalities.

There’s a whole heap of math in this paper, and although (or perhaps because) I’m supposed to be coming up with robust formulae for our rankings on the main site, it makes my brain hurt.

I find the thesis that economic impact can be leveraged to get maximum public health benefits an interesting one. I’m not sure how that would apply to the UK, for example, where the cost of healthcare is more-or-less invisible.

Infectious diseases tend to evolve quite rapidly when we attempt to control them, whether we use antibiotics, other drugs or prophylactic vaccinations. The framework expounded in this paper should prove to be readily applicable to a wide range of such diseases. Assuming, of course, that the authorities responsible for public health have the appropriate fiscal executive power, and access to current and accurate scientific information…

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