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Sunbathing and suicide

Sunbathing and suicide

Some comments on lockdown and exit strategies

The purpose here is not to object to the general concept of a ‘lockdown’ It is a valid strategy for containing an infectious disease. But there are some elements of the strategy that are worth comment, because it is not clear how they contribute to reducing transmission and/or because they might be counter-productive. We will also, sooner or later, need an exit strategy, and I hope the government is already considering the options.

  1. Exercise in the country.

We have been told that we are allowed to have one form of exercise per day, but it must be close to home. That is fine for those of us who live on the edge of open country, but for those who live in cities it means they are confined to parks and other urban open spaces, which runs the risk of those places becoming crowded, and posing a much greater risk of transmission of the virus than if they took a short car ride into open country. Granted that we do not want large collections of people in popular beauty spots (just close the car parks?), nor is it desirable for people to travel hundreds of miles to get their exercise (although I’m not sure what the problem is there, but I’ll let that go). This looks like a London-based rule, that ignores the fact that in many Northern cities, open countryside is only a short way away.

And now, predictably, we have some parks becoming sufficiently crowded that they are threatened with closure (and in some cases have been closed).

There has also been an element of ‘Eyam in reverse’ on some occasions. (Eyam, in case you don’t know, was the ‘plague village’ in Derbyshire which, when plague arrived there, decided to cut themselves off to prevent the spread of the disease to neighbouring villages.)  The comment from Derbyshire Police that some of the people visiting Curbar Edge came from Sheffield sounds rather like the reverse of Eyam’s action. So does the comment on the News tonight from a resident of the Lake District that visitors coming from Manchester were being selfish in that they might be bringing the virus with them. (But I do think that someone from Manchester has no need to go all that way when there are plenty of opportunities much nearer to home).

  1. Are we allowed to enjoy ourselves?

What is the problem with sunbathing, or having a picnic on a (deserted) beach? Provided of course that you keep your distance from everyone else. Yet we have seen police intervening to stop such activities. This looks like a rule that is designed to stop anyone from looking as though they might actually be enjoying themselves. I’ll come back later to the desirability of having fun.

  1. Do arbitrary and pointless rules matter?

At present, the vast majority of people seem to be going along with the rules (at least up to a point), but will it last? As the ancient proverb says “The tighter you screw the lid down, the sooner the boiler will burst”. (Actually, that’s not an ancient proverb; I just made it up. If anyone knows better, let me know!).

In an authoritarian culture, you would get away with it. But we’re not used to being told what to do in such depth, and if people start to think that the rules are unnecessary, it will be hard, if not impossible, to enforce them. Unfortunately, that might mean the sensible rules would be flouted as well as the pointless ones. This will become increasingly important once the peak of the epidemic has passed.

  1. Downsides of the lockdown.

The financial and social problems are sufficiently obvious that I don’t need to go over them. But there are other effects that are not well enough discussed publicly, mainly those associated with being cooped up all day in a small flat. We are starting to see evidence of an increase in domestic violence, mental illness, and apparently also in the number of suicides. There is not much public data yet, but the effects were predicted, so the small amount of evidence is credible.

A more subtle effect is the increased level of stress and anxiety in the population. Although a certain amount of anxiety is needed to ensure that the rules are kept, stress can also be counter-productive for attempts to control the epidemic. We know that factors like immune deficiency, respiratory problems, diabetes, obesity etc are risk factors for infection, and for the severity of the disease. It is less known that stress also reduces our resistance to infection. The precise mechanism of the interaction is imperfectly understood, but it has been shown in humans and in experimental animals, so it is a real effect.

This brings me back to point 3. If allowing people to have a bit of fun occasionally reduces their stress levels, it would go a long way to countering these negative effects of the lockdown.

So keep safe, but have some fun as well.

  1. An exit strategy.

Once the numbers start to come down in earnest, there will be increasing pressure to know when the brakes are coming off.  It will be essential to get this right. If we relax too soon, the epidemic could start off again. If it is delayed too long, apart from the unnecessary financial effects (both on industry and on the workers), there is the risk that people will start to take matters into their own hands.

Furthermore, it will have to be a staged exit. You can’t suddenly say ‘Tomorrow, we’re all back to normal’. The Glossop Labour Club will need to know in advance when we can start ordering beer, and our suppliers, in turn, will need to know when to start making it. Apply that over the whole country, and you can see that chaos will ensue unless the exit is managed carefully.

Am I being too sanguine in hoping that the government is already producing such a plan?

 

 

 

 

Coronavirus – some information

Coronavirus – some information

A The virus

  • COVID-19 is the name of the disease. The name of the virus is SARS-CoV-2. Not very snappy, but it identifies its relationship to the virus (SARS-CoV) that caused the SARS outbreak in 2002. The virus that caused the MERS outbreak in 2012 (MERS-CoV) was also a coronavirus, although a different type. (see below for more about these diseases).
  • It is a virus, not a bacterium. Therefore antibacterial disinfectants will (probably) not be effective. Alcohol (70%) and hypochlorite (bleach) will kill it.
  • Coronaviruses in general are not uncommon – for example, they are estimated to cause about 10% of colds.
  • The genetic material of coronaviruses is RNA, not DNA. This is significant because RNA genomes tend to mutate more rapidly.
  • The RNA is contained in an envelope, which is surrounded by an array of spikes. These are glycoproteins (proteins with sugar molecules attached). The spikes are necessary for attachment to human cells, by binding to specific receptors. The spikes are the likely target for an immune response,
  • After attachment of the virus, the RNA enters the host cell and uses the protein synthesis machinery of the cell to produce the proteins needed for copying the RNA and formation of new virus particles.
  • The cell then dies and releases the new virus particles which go on to infect other cells.

B. COVID-19 and other coronavirus diseases

  • When you cough or sneeze, or, to a lesser extent, speak or just breathe, you shed droplets of various sizes. If you are infected, these will contain virus particles, depending on their size. Bigger droplets are more likely to contain virus.
  • The larger droplets will fall quite quickly (and may contaminate surfaces); smaller ones may remain airborne for some time. These droplets are mainly water. Because of the large surface-volume ratio, the water evaporates readily, forming tiny ‘droplet nuclei’ which can consist of a virus particle and not much else. They may remain airborne for a long time.
  • Incidentally, those droplet nuclei are too small to be intercepted by a mask, so even a well-fitting mask will offer imperfect protection against infection. However, the particles emitted by an infected person are larger, and can be intercepted by a mask. So wearing a mask will reduce the infectivity of someone with the disease.
  • For most respiratory pathogens, it is these droplet nuclei that are the problem, as they are small enough to bypass the mechanical barriers in the respiratory tract and penetrate right into the lungs. SARS-CoV-2 seems to be unusual in that picking it up from contaminated surfaces seems to be more common, and also in that it can infect through the eyes. Hence the advice to decontaminate surfaces and wash your hands frequently
  • The vast majority of infected people show few if any symptoms. This may be due to a level of non-specific immunity to coronaviruses, from previous infections with other coronaviruses, and/or the body’s natural resistance to infection.
  • A small proportion develop severe disease, and some die. In part this it thought to be due to an over-reaction by the immune system. Most of those who die have some underlying health condition, including reduced immunity and pre-existing respiratory tract conditions.
  • There is uncertainty about the real mortality rate (primarily because of uncertainty about the actual number of infections), but the general consensus is that it is about 1%. The mortality rate increases with age, from 50 onwards. This could be due not to age itself but the higher prevalence of underlying conditions, especially the reduction in immunity as you get older.
  • SARS (Severe Acute Respiratory Disease) started in China in 2002. There were over 8000 cases, mainly in China and Hong Kong, plus a number in other countries in the region (e.g., Taiwan, Singapore, Vietnam.) Apart from an outbreak in Canada (257 cases, traced to a traveller from Hong Kong), there was only a sprinkling of cases in the rest of the world. The apparent mortality was quite high (about 10%).
  • MERS (Middle East Respiratory Syndrome). The first case was identified in Saudi Arabia in 2012. Most subsequent cases were in Saudi Arabia, plus smaller numbers in other middle-Eastern countries. There were few cases elsewhere in the world. The disease has reappeared repeatedly in Saudi Arabia, and there was an outbreak in South Korea in 2015 (traced to a man who had visited Saudi Arabia). MERS appears to be more severe, with mortality rates estimated as high as 40%.
  • Why have SARS and MERS (in contrast to COVID-19) not spread more widely? That is a very interesting question, and I wish I knew the answer!

C. Testing

  • The commonly used test is a molecular one technically known as RT-PCR (Reverse Transcriptase- Polymerase Chain Reaction). This copies the RNA into DNA and then amplifies it to an extent that it can be detected. It is very sensitive, but it detects the RNA and not the whole virus. So you may remain positive for a short while after the virus has been eliminated, and you are therefore no longer infectious. Conversely, it may not pick up the infection in the very early stages, when only a few cells are infected.
  • This test requires sophisticated materials and equipment, and skilled technicians. All of these are in short supply, which limits the number that can be done. Some countries were better prepared than others and/or were quicker to react and get everything in place.
  • How important is testing? It is useful for essential staff (esp NHS workers) to know whether or not they are infected, so they can continue to work. Widespread testing would be useful, as getting a better handle on the actual number of cases would inform policy decisions, but I’m sceptical as to how important this is. The traditional view, that finding cases enables the identification of contacts who can then be quarantined, becomes untenable with large number of cases, at least without a degree of surveillance that might well be unacceptable except under authoritarian rule.
  • A different test, that relies on the detection of specific antibodies, is much discussed. Such tests are being evaluated. However, they tell you whether someone has had the disease, not whether they are infected.

D. Interpreting the data

  • We are showered with statistics – numbers of cases or deaths, in various countries. These are a few points to consider when we look at those numbers, especially when comparing data from different countries.
  • Are the numbers adjusted for the population size? Very often they are not, or they don’t say one way or the other. Clearly, a large country would expect more cases than a small one.
  • Do they refer to the cumulative number (the total number of cases/deaths during the epidemic) or the number that day/week?
  • If considering the number of cases, the definition of a ‘case’ may vary between countries. In particular, consider the impact of testing. A country like Germany (which is doing a lot of testing) will identify a large number of cases with few if any symptoms that may not be counted by other countries – and hence will be expected to have a large number of ‘cases’.
  • The number of deaths is often regarded as a more reliable comparison, but this may also have problems. Does it include those who die outside hospital? And remember that many who die as a result (probably) of coronavirus infection actually die from e.g., pneumonia, heart failure, multiple organ failure, etc. How are these deaths recorded? Procedures may vary between countries.
  • To overcome these difficulties, it is best to look at the trends in different countries, i.e., the number of cases/deaths over time. This assumes that the practice in each country is consistent, which is not always true – the UK figure of deaths suddenly jumped today (3 April) after a change in reporting procedure.
  • Bear in mind that there is a delay between ‘cases’ and ‘deaths’ – so you might expect the death rate to continue to go up while the infection rate is levelling off.
  • The trend line will also show where the countries are on the epidemic curve. Italy for example had its first case earlier than Germany did, so comparing those two countries needs to take account of that, in effect looking at where Italy was a short while ago.
  • When considering deaths, it is important to remember that many deaths are among the very old or those who have other serious conditions. Trying not to be callous about this, we have to remember that some of them would be expected to die anyway in any given period. To get a true picture of the impact, we should look at excess deaths – i.e., the number of deaths above the number that would be expected to happen anyway. Bear in mind that there are normally about 0.5 million deaths per year (England and Wales).

E. In defence of ‘herd immunity’

  • The course of an epidemic is determined by a parameter known as R, the Reproduction Number, which is the number of people infected by a single case. At the outset, for COVID-19, R has been estimated as about 2.5.
  • R itself depends on a number of factors; I’ll just consider two of them. Firstly, the number of contacts a person has while they are infectious, and secondly how likely it is that those contacts are actually susceptible to the virus.
  • ‘Social distancing’ (or in extreme cases, isolation) is obviously a way of reducing the first of these.
  • The second factor comes into play when a significant number of people have had the disease (and are, we hope, immune to re-infection). This is the natural way in which an epidemic becomes self-limiting. As more people become infected, and hence immune, R falls. When it gets down to less than 1, the epidemic stops, even though there are a number (possibly a large number) of people still susceptible. This is ‘herd immunity’.
  • The point at which herd immunity kicks in (the Herd Immunity Threshold or HIT) is related to the initial value of R (Ro). Mathematically, the proportion still susceptible at the HIT is 1/Ro. So, if Ro is 2.5, we would get herd immunity with 40% still sensitive, or 60% having been infected. That’s a lot of people. But if we combine it with other measures, effectively reducing the value of Ro, say to 1.5, we get herd immunity after 33% have been infected. And if we reduce Ro still further, to 1, then we get herd immunity straightaway.
  • This is all a gross simplification! In particular, it assumes a homogeneous population, which is obviously not true. Someone living in London, especially if they still travel on public transport, will pass on the virus much more often than someone in the Highlands of Scotland. But it demonstrates the principle.

I hope this all makes sense. If you want to ask anything, or disagree with me, feel free to email me. You might also like to read my book Understanding Microbes which amplifies some of the basic issues (although not COVID-19 as it was published in 2013)

Coronavirus – has the Emperor got any clothes?

It seems to be universally agreed, by journalists, politicians, scientists and everyone else, that China, and potentially the rest of the world, is in the grip of a devastating infectious disease epidemic. I have seen no comments questioning this. But there are questions that should be asked.

1. Is this a new disease? Although this virus is a new one, at least as a cause of human disease, coronaviruses as a group are very common, causing perhaps 10% of common colds, and most people have been infected with one or more of them at some time. But as this is a previously unidentified form of coronavirus, we are justified in regarding it as a new disease.

2. How infectious is it? One estimate that I have seen put its ‘reproductive number’ at 3. That is, each case would infect three other people. While that is plenty for the establishment of an epidemic, it is well short of that seen in a number of other infectious diseases – for example the corresponding number for measles is estimated at 15-20. (That is admittedly an extreme example; estimates for most common infectious diseases lie in the range 2-7).

So it is infectious, but not wildly so – which calls into question the need for the extreme measures being adopted.

Face masks are one form of protection widely used Are they needed? Are they any use? Answering this question needs an understanding of how such infections spread. An infected person will liberate droplets carrying the virus – not just when coughing or sneezing, but when talking or even just breathing normally. Most of those droplets can be trapped by a face mask, as they are relatively large. But they are mainly water, which will evaporate rapidly in the air, leaving tiny particles (known as ‘droplet nuclei’). These carry the virus, and it is this form that is breathed in by others who thus become infected. But these droplet nuclei are too small to be trapped by a simple face mask. So a face mask will cut down the extent to which an infected person will pass on the disease, but offer virtually no protection against becoming infected. (There are also other limitations to a simple face mask, but one will do.)

3. How dangerous is it? While there have been a large number of deaths in China, that needs to be related to the number of cases. That is done by dividing the number of deaths by the number of cases (giving the ‘mortality rate’). The reports from China indicate a mortality rate of between 2 and 3%. That needs to be qualified. While we can be reasonably confident of the number of deaths, we are much less sure of the real number of cases. When a new disease occurs, and/or when there is pressure on resources, it is inevitable that the necessary tests are more likely to be done on subjects with serious disease. Those with a milder disease – and even more so those with no recognisable symptoms – are less likely to be investigated. If we include these subclinical cases, the number infected will be higher, and hence the actual mortality rate will be lower than this estimate. It is repeatedly seen, when a new disease emerges, that initial estimates of mortality are very high, but then drop substantially as more of the less severe cases come to light.

Even if we accept a level of 3%, this does not make it the ‘deadly virus’ that has been reported. This is similar to the mortality rate of a typical outbreak of influenza.

4. Are the resources being devoted to this disease justified?  The world is still suffering from many other infectious diseases, with many more deaths than those caused by this coronavirus. These diseases could be controlled or even eliminated if sufficient resources were available – cholera, malaria, tuberculosis for starters. If a fraction of the resources being poured into controlling this epidemic were applied to, for example, providing clean water and proper sanitation across the planet, we would eliminate cholera (and other water-borne diseases).

5. Why are these questions not being asked?  That brings me back to the title of this blog.

The Emperor’s New Clothes  is a short tale written by Hans Christian Andersen, about two weavers who promise an emperor a new suit of clothes that they say is invisible to those who are unfit for their positions, stupid, or incompetent – while in reality, they make no clothes at all, making everyone believe the clothes are invisible to them. When the emperor parades before his subjects in his new “clothes”, no one dares to say that they do not see any suit of clothes on him for fear that they will be seen as stupid. Finally a child cries out, ‘But he isn’t wearing anything at all!’” (Wikipedia).

No further comment necessary!

Why Labour lost

Various reasons have been put forward as to why Labour lost the recent General Election. Let’s look at some of them.

1. The Labour Party has moved too far to the left. Actually, the policies put forward in the manifesto were far from being extremist. Many of them reflect the current situation in some other European countries, and have also been shown in opinion polls to attract public support. It is a measure of how far the country has moved to the right that such a manifesto could be labelled as extremist. The problem was that the Labour Party never succeeded in shifting the debate onto such policies.

2. The Labour Party has been taken over by metropolitan elites and has lost touch with its core voters. Ever since I’ve been involved in politics (dating back to the 1960s) the Party has been a coalition of people with different backgrounds, and different perspectives – and it remains so. I doubt if an analysis of Jeremy Corbyn’s shadow cabinet would show a significant difference in class background from those of Attlee, Wilson or Blair. But there is some truth in the second part of the above statement. It was apparent in 2017, and even more so in 2019, that the Party has lost a considerable amount of previously automatic support in a number of constituencies.  Despite what many pundits are saying, this is not a recent phenomenon. Taking one constituency, Hartlepool,  the Labour vote varied between 22,000 and 27,000 in every election from 1974 to 2001. Then it went down to 18,251 in 2001 (Tony Blair’s 3rd victory) and again to 16,267 in 2010 and to 14,076 in 2015  Then it bucked the trend, going up to 21,969 in 2017 (under Jeremy Corbyn). In 2019 it was back down, to 15,464,  but this was still higher than achieved in 2015. Nevertheless, it is still far behind the vote achieved in the elections from 1974 to 2001, lending some support to the concept of ‘losing touch with the core voters’, even if that dates back to 2001 rather than recently. In my opinion, this is largely a consequence of the Thatcherite policies of dismantling heavy industry (shipbuilding, steel, coal etc) coupled with the emasculation of the Trade Unions. This has destroyed the social cohesion of these areas. This matters because previously, through those links, the workers in those areas were exposed to a variety of opinions, and discussions, that helped to counter the right-wing propaganda they were fed through the media. So Labour has lost touch with those communities, not through any actions by the Party, but through other factors that the Labour Party has failed to counter. In this context, it can be said that a major failure of the Blair administration was that they did nothing to reverse Thatcher’s anti-Trade Union legislation. In addition, I remember, when I first joined the Party, back in the 1960s, that there were a number of very able people who had missed out on formal education for various reasons, and had worked their way up through the Trades Unions, coupled often with self-education. I suspect that this is less common now, partly because of better educational opportunities (including the expansion of the Universities) – which is obviously a good thing – but also because there are fewer opportunities for ‘working-class’ people to rise through involvement through the Trade Union movement.

3. Brexit.  It is undeniable that a large slice of the population was (is) completely fed up with the Brexit issue and wanted it to go away. Hence the success of the ‘Get Brexit done’ slogan. Labour thought that the debate could be shifted onto other issues, but this proved to be impossible. The policy that they (eventually) went into the election with made sense, theoretically, but was open to the criticism that it would prolong the acrimonious debate – which proved crucial. Labour was too ‘nice’ to point out that it was Johnson and his cronies who were responsible for dragging it out so long.

4. Corbyn. JC was subjected to a continuous barrage of abuse and misinformation, which undoubtedly struck home with some electors. Unfortunately, some of this came from Labour MPs and others who claim to be on the same side. It is very difficult to fight an effective campaign when you are repeatedly stabbed in the back by your own side. This factor was present in 2017 as well, but was to some extent countered by the excitement of having someone new who, when they saw him on the television, came over as fresh and different, and not the ogre he was painted out to be. In 2019. JC’s TV performance seemed, to me, to lack that degree of freshness and excitement; he seemed much too cautious.  However, it has to be said that he leaves the Party in a much better shape than it was. In this constituency (High Peak) membership has soared, and very many of the new members were out on the streets campaigning – which has helped a lot in sealing any initial differences between the new members and the ‘old guard’ – one of whom commented to me that it was great to have a team of people to help him when he previously had to do it all on his own.

5. Where do we go from here? It would be a serious mistake to shift away from a radical agenda to something more ‘centrist’. Although it is of course important to gain power, it is essential to do something with that power, otherwise it is pointless. And the aim should be to achieve changes that are essentially irreversible. The Attlee administration achieved this with the establishment of the NHS (the Tories are still only nibbling at the edges), although many of their other changes were subsequently reversed., as were most of the radical measures of the Wilson years.  The Blair governments (for all their faults) did achieve that with the Nation Minimum wage. But for an extensive and long-lasting shift in the power balance in the UK we have to look at the Thatcher years – de-industrialisation, sale of Council houses, anti-Trade Union legislation – all of these changed the nature of British society in a way that we are still struggling to cope with. So I hope that Jeremy Corbyn’s successor will be elected in a comradely manner, and that s/he will carry on the good work of developing a radical, socialist agenda – and that the Parliamentary Labour Party (and other major figures in the Labour movement) will pull together to re-establish Labour as a dominant force in the country.

Changing cheque signatories

How to change cheque signatories (or not) – a diary

Back in May, I became Treasurer of the Glossop Labour Club. There were other changes to the Committee as well, so we needed to add 3 new signatories to our bank account (and take off 3 as well). No problem, I thought; just pop into the bank and get a form. But it wasn’t that easy. They told me it was all done electronically now, so I had to ring their Business Team to get an electronic form.

21 May. I rang them, and they sent me an email with a PDF attached, into which we had to insert signatures (as a jpg), and attach PDF copies of photo ID (passport or driving licence) and proof of address. Taking a photo of my signature was a pain, but eventually I got something I thought was OK.  I then needed to pass it on to the others to do the same. But neither of them could get the form to work. So they passed all the details to me and I finished filling in the forms. That all took about a month.

I also got them to send me a form to apply for online banking, which was simpler – just print it out and fill it in, then return it by post, which I did on 19 June.

28 June.  What do I do with the signature forms now? There was a button marked Submit. But all that did was create a gmail account that I didn’t want. So I rang them again. “Oh” they said, sounding surprised. “Well, then email it to us.” “But you haven’t given an email address.” So they gave me one, and I emailed it to them.

At the same time, I asked about the online banking form. It had been received, but they couldn’t process it because I wasn’t a recognised signatory.

9 July. As I hadn’t heard anything, I rang them again. “You sent an e-mail? We get so many e-mails we don’t bother to read them. You had better print it off and post it.”

16 July. Still no news, so I rang them again. “We received it yesterday. Ring again in a week’s time,” (Their website says it usually takes a few days).

24 July. “We’re still working on it, Ring again next week.”

30 July. One of the signatures is unclear. So I did some electronic enhancement on it, and sent it back by post.

7 August. We received a letter saying the other two signatures are unclear. They provided a piece of paper for us to sign and return by post, which we did.

9 September. No news, so I asked at the local branch if the new signatories were now OK, which they weren’t. So I rang them again. The problem now was that the Chairman, who signed the form to say that we had passed the appropriate resolutions wasn’t a recognised signatory (he’s one of the ones being added) so he had to go into a bank branch to verify his identity.

3 October. So that’s where we are now. I’ve been Treasurer for coming up to 4 months and I still can’t sign cheques. I wonder if we will get this finished before the next AGM when we might have to start all over again. And online banking is still a dream – that process can’t start until the signatories have been changed. I hope that doesn’t take as long.

An update:

11 October. I rang the Business team: ther’s a bit of a delay. Call back next week.

21 October. The business team have not heard from the local branch about our Chairman’s identification.

November. Our Chairman confirms that he has presented his documentation to the Branch. So I checked with the Branch – they say they have no way of passing the information to the Business Team.

10 December. I rang the Business Team again (Every time I do this, I get a recorded message saying they are having a higher than normal number of calls!). He said that there seem to be no further deficiencies, and he is trying to get ‘them’ to activate it.

17 December. I asked at the Branch, and they said it had not yet been done. So I am still waiting.

Further update, January 2020.

I can’t believ it! It’s been done! I can now sign cheques – after over 7 months trying.

Now to try to get them to allow us online banking.

 

An excellent day !?

I left the house at about 8.20, caught the train into Manchester. So far, so good.

But, just after we left Flowery Field, the train ground to a stop. And stayed there. The very helpful guard explained that there was a problem with the overhead power lines, and we were likely to be there for some time. After about an hour (!), he told us that we would have to do a ‘controlled evacuation’ and walk back to Flowery Field station where a bus would take us into Manchester.

So we did that. But there was no bus. We were told to walk to Hyde North station, which was only a few minutes away, and get another train from there. He didn’t say it was a few minutes by car, and about 15 minutes on foot.

When we eventually got to Hyde North, a train did arrive, but then it sat there to wait for everyone else. We finally got to Piccadilly about 11.30. I decided I had done enough walking and would catch the free bus, but that didn’t turn up for about 15 minutes. Then at the junction with King Street, there was a lorry blocking the road. We sat there for a while and then were told to get off and walk. (Ironically, it was  Kingspan lorry!)

So I eventually arrived about 12.15 – nearly 4 hours for a journey that normally takes about 1.5 hours door to door. I then checked in, and was told that by that time they had sorted out all the jury panels that were needed that day, so I could go home again!

Fortunately the journey home was uneventful and I got back at about 1.45 having spent 5.5 hours achieving nothing (apart from experiencing a controlled evacuation and finding out where Hyde North station is.)

Vaccination

Despite the clear success of vaccination in the control of a number of infectious diseases, there are still far too many people who decline vaccination, for themselves or for their children. Why is this, and why does it matter?

The reasons fo declining vaccination, ignoring inertia, are i) doubts over the effectiveness of vaccines and ii) concerns about safety. The first point is totally unfounded. Smallpox was completely eliminated, in large part due to the success of the vaccine. Polio has been almost eliminated – and could be by now if the few countries where it still exists were not so resistant to use of the vaccine. Diphtheria, tetanus, – the list goes on.  All the vaccines in current use have been shown to be effective (leaving aside the use of BCG for control of TB, which is a complicated question).

That brings us to the safety issue, and especially the MMR (measles, mumps, rubella) vaccine. In 1998, Andrew Wakefield and colleagues published a paper describing a study of 12 children with autism and chronic intestinal disorders. An incidental finding was that most of these children had received MMR. Although the paper actually states that they did not prove an association between autism and MMR, it was widely believed that they had. This erroneous belief still persists, despite numerous large and well-conducted studies that have failed to find any association whatever, and despite the fact that the Wakefield paper has now been withdrawn. To a large extent, the misplaced belief is fuelled by the fact that the age at which the MMR vaccine is given is the age at which signs of autism often first appear – so it is inevitable that in some cases autism will show up soon after the vaccine is administrered.

A very similar situation arose in the 1970s with the whooping cough (pertusssi) vaccine, where some children showed neurological problems after having the vaccine. This wasn’t anything to do with the vaccine – it’s just that some children do have these symptoms at about that age. But the unjustified fear of the vaccine led to a decline in its uptake, with the consequence that in the winter of 1978-79 there wee 100,000 cases in the UK, with many deaths and even more neurological problems.

Finally, does it matter if some people refuse the vaccine? Isn’t it a matter of personal choice, to accept the risk of getting the disease? The answer lies in the question of how can we protect those who cannot be vaccinated – especially very young children who are too young to be immunised (because their immune system is not fully devloped)?

Spread of a disease depends on an infected person coming into contact with others who are susceptible to the disease. If you can reduce the proportion who are susceptible to a low enough level, then the disease will not spread. This is known as herd immunity. For smallpox, it was quite easy – only about 75% needed to be vaccinated to stamp out the disease completely. Measles is much more infectious, and the critical level is much higher – about 95%. Failure to achieve that level means epidemics will occur – and they are occurring. So those people who refuse vaccination are not only putting their own children at risk, but they are putting others at risk, including all those babies who cannot be immunised.

For a more complete coverage, read my book Understanding Microbes

 

“Taking back control”

When Brexiteers talk about ‘taking back control’, they often mean specifically regaining the ability to make our own trade deals. (There are other issues, but trade deals are often mentioned, and this is the main reason for the obdurate refusal to consider a customs union which would be the obvious solution to many of the Brexit problems). Superficially, making our own trade deals might sound like not such a bad idea (apart from the level of bureaucracy involved, duplicating what the EU already does). And indeed if it was just a question of setting import/export tariffs, there would be little reason to be concerned about it.

However, I suspect what they have in mind is considerably more than that – something more like TTIP. A deal, in other words, that would not just cover tariffs, but would also open all aspects of our economy to multinational corporations. This would include our education and health services. We have already seen the corrosive effect of private companies in these areas, but at least at present the government has the power to decide whether or not to grant contracts to such companies.  So we could be prohibited from any attempt to bring back services such as water supply, or the railways, into public ownership. Although it could be argued that EU regulations already impose such conditions, that is limited in many ways, and at least EU regulations are governed by a semblance of democratic control.

Furthermore, such a deal would impose severe limitations on the extent to which our government could restrict the activities of those companies – such as environmental regulations. We might end up being forced to accept fracking, for example. Any attempt to do so would result in the companies taking their case to a quasi-judicial ‘court’ (of members selected by the companies themselves). This is not fanciful scaremongering – we have already seen other countries being fined millions of dollars under similar deals.

And we would not able to back out of such an arrangement. Is this ‘taking back control? We would be permanently putting ourselves into the hands of the multinationals.

TB and Badgers

 

Some background

Tuberculosis (TB) in people is typically caused by a bacterium called Mycobacterium tuberculosis (MTB). This is, more or less specifically, a human pathogen and so you catch the disease from someone who has TB, and not from infected animals. The most common form of the disease affects your lungs, and so you pass it on by coughing, or indeed by anything that generates aerosols including talking and breathing. When you breathe in the contaminated air, the bacteria settle in your lungs. A curious feature of TB is that most (about 90%) of people who are infected never show any signs of the disease (and are not infectious). About 5% will develop symptoms within 12 months of being infected, and the remaining 5% will develop symptoms at some time during their lives, maybe 50 years later. This reactivation of an earlier infection generally reflects a decline in the effectiveness of your immune system as you grow older.

Until the middle of the twentieth century, there was another form of TB in the UK, caused by a very closely related bacterium called Mycobacterium bovis (MB). Unlike MTB, MB is a very versatile bacterium that is capable of infecting probably all mammals. The main way in which people were infected was by drinking contaminated milk. By this route, instead of the bacteria going for the lungs, they move to the lymph nodes that monitor material draining from the throat (neck lymph nodes) or digestive tract (abdominal lymph nodes). These sites of infection tend not to shed material into the environment, so people with this form of the disease are much less likely to be infectious.

This form of the disease in humans was virtually eliminated by two measures: tuberculin testing of cattle, and pasteurisation of milk. Tuberculin testing involves making an extract of killed mycobacteria and injecting a small amount into the skin of a cow. If the cow is infected, it will react – shown by a swelling at the site of injection, That cow is then killed (and the farmer is compensated). This is coupled with restrictions on the movement of cattle until the entire herd is declared free of the disease. Pasteurisation involves heating the milk to a specific temperature, which kills the mycobacteria (and incidentally some other significant pathogens), while producing minimal changes in the quality of the milk. For a while, consumers had a choice of tuberculin tested (TT) milk, pasteurised milk, or ‘ordinary’ milk. Nowadays, all milk in the shops is both TT and pasteurised.

There is also a potential risk from eating undercooked meat from an infected cow. While the tuberculin testing of cattle should ideally prevent this, to make sure none get through, vets at the abattoir inspect the carcasses to make sure they do not have any signs of TB.

So what’s the problem?

Since the existing control measures mean that the risk of human infection with MB is very low, why is there so much fuss about it? This comes mainly from the cost, to the government (and therefore to us as taxpayers) and to the farmers, costs arising from the testing of cattle and the killing of infected cattle. Although farmers are compensated for the cattle destroyed, this does not necessarily reflect the disruption to their business, let alone the loss of morale from the possible destruction of a herd that may have been built up over a period of many years. Understandably, the farmers argue strongly for the government to take radical action to tackle the sources of infection.

How do cows catch TB?

A rational strategy for controlling any infectious disease depends to a large extent on understanding the route of infection – i.e., how the disease spreads. The assumption behind the culling of badgers is that badgers are the source of infection. Is that true? It is undeniable that badgers can be infected with TB, but whether, and to what extent, they pass it on to cows is unproven. In a well-run farm, direct contact between cows and badgers is likely to be uncommon, hence direct transmission is unlikely. The main exception to this is if badgers can get access to cattle sheds, but this can be prevented.

Another possibility is that the cows eat grass that has been contaminated by badgers. e.g. by urine or faeces. However badgers use regular latrine areas, and these are likely to be avoided by cattle. So there are unsolved questions about the possible route of transmission from badgers.

Note that this is very different from the situation in New Zealand, where possums are a significant source of infection of cattle. Possums are very susceptible to TB, and they tend to die in the grazing areas. Cows being curious animals, they sniff at the possum carcass and thus become infected. New Zealand is making progress towards eliminating this by controlling the possum populations. Since the possum is not a native animal in New Zealand, there is less objection to control measures than is the case with badgers in the UK.

Will badger culling work?

If badgers really are the source of infection, then clearly something would need to be done about it. Is culling the right answer? Would it work?

To try to answer that question, a scientific study was carried out in selected areas, comparing what happened in those areas where badgers were culled with control areas where there was no culling. Although this seemed to show that in the culled areas there was some reduction in the level of TB in cattle (provided that a high enough proportion of badgers was removed), there was a rather surprising additional effect: In areas immediately adjacent to the culled areas, there was an increase in cattle TB. The likely reason for this is that the culling disrupted the normal badger population. Badgers are highly territorial, so removing badgers from one area will result in more contact between badgers in adjacent areas as they try to re-establish their territories. The conclusion is that culling could be effective, with two conditions – first, that a high proportion of badgers are removed, and secondly that the culled area should be large enough and surrounded by natural boundaries (e.g., large rivers, mountains) to prevent any mixing of badger populations in culled and non-culled areas. (The current culling programme largely fails on both counts).

What other methods are possible?

Firstly, we have to recognise that badgers are not the sole culprit. Leaving on one side the possibility that other wild mammals may be involved (remembering that MB can infect all mammals), we also have to take into account the transmission of the disease from one cow to another. Modern farming practice often involves movement of animals from one part of the country to another, with the possibility of spreading the disease. In this respect it might be significant that the increase in the number of cases of bovine TB, and the widening of their distribution, followed closely on the foot and mouth outbreak in 2001, when there was large-scale re-stocking of farms, involving moving cattle around the country.

When a case of TB is found on a farm, movement of cattle off the farm is prohibited until the herd is declared clear again. This may be inadequate in two ways – infected cattle may have  been moved before the disease was detected, and a ‘farm’ may involve widely separated pieces of land. Tighter control of these areas, and recognition by the farming industry that they have an important role in disease prevention, would help.

The second possibility that is often raised is vaccination of cattle. There is a serious problem here. If you vaccinate a cow with the existing human vaccine, BCG,  then that cow becomes a reactor – in other words it will now react with the skin test in the same way that an infected cow does. So you cannot distinguish between a vaccinated cow and one that has been infected – and since the vaccine is far from 100% effective, even a vaccinated cow can be infected. One important consequence would be that the UK would be prevented from exporting animals or meat to other countries which require all animals to be TB free.

There are two ways in which this could be overcome – either develop a better vaccine that would not interfere with the skin test, and/or develop a better testing method that could distinguish infected and vaccinated animals, (There is a need for a better test anyway). Unfortunately, promising research efforts on both fronts were terminated when the government withdrew its support.

Finally, instead of vaccinating cows, you can vaccinate badgers. This is not straightforward, as the BCG vaccine has to be given by injection. So you have to trap the badgers first, which is a skilled job. But it can be done, and is being done in some areas, by voluntary groups (the Derbyshire Wildlife Trust is involved in such a programme in Derbyshire). Ironically, the only safe and effective way of culling badgers involves trapping them first and then shooting them while they are in the cage. You may well wonder why, if they have been trapped already, they don’t vaccinate them rather than shooting them.

Three time less

I frequently get annoyed by reports in the media that one thing is, for example. three times greater than another. What does that mean? Three times what?

If it is said that John is three times older than Mary, and Mary is, say, 20, then how old is John?  If we said John is 40 years older than Mary, then we would add (20 + 40) so he would be 60. So, as three times Mary’s age (3 x 20 =60), we should add that to Mary’s age, and get 80. But I suspect that what is really meant is that John’s age is three times Mary’s, so he would be 60.

That could be regarded as mere pedantry. But things get worse if we consider less/younger/smaller etc. If “Mary is three times younger than John” what does that actually mean? Three times what? If we agree, as above, that Mary is 20 and John is 60, then 3 x Mary’s age = 60, subtract that from John’s age, and Mary is 0 years old. Even worse, 3 x John’s age = 180 and Mary is minus 160 years old!

Even the respected scientific journal Nature is not immune. I recently came across the statement that a new solar probe will reach seven times nearer to the sun than any previous probe, and I am completely at a loss as to what they actually mean.