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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 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.

 

Hospital waiting times

When we hear statistics about hospital waiting times, what does that mean? When does the clock start ticking?  The NHS website says it is from the date of the initial referral, but the following case history casts doubt on that.

  • Week 0. GP appointment. Referred to hospital for surgery.
  • Had to wait 3 weeks before it was even possible to make an appointment
  • Week 3. Offered appointment in week 10.
  • Week 10. Appointment cancelled at short notice. Offered appointment in week 14.
  • Week 14. Surgery outpatient clinic.
  • Week 18. Pre-op appointment. Referred to cardiology (low heart rate, ?unsuitable for general anaesthetic)
  • Week 19. Cardiology clinic
  • Week 20. Surgery clinic confirms different operation with local anaesthetic. Told operation would have to be before January (the “breach date”).

This implies that they have re-started the clock at this point, when a further 18 weeks would take it to the middle of January. But this is 38 weeks from the initial referral. It may be that NHS rules do allow re-starting the clock in certain circumstances, which would not ne totally unreasonable, but it does mean that there could be a substantial level of undisclosed waiting.