|Posted on 23 March, 2022 at 2:50||comments (4)|
In the year 400 AD the Emperor Constantine and two patriarchs (Eusebius and Macarius) found what they said was Calvary, where Jesus Christ was crucified and entombed at the site of a Roman temple to Jupiter and Venus. They pulled down the temple and built a church. In 613 AD the church burned down while the Sassanids occupied Jerusalem but 20 years later the Emperor Heraclius re-built it. Although the Muslims didn’t pull it down when they took Jerusalem afterwards, it was...Read Full Post »
|Posted on 19 March, 2021 at 3:00||comments (85)|
Fishing in Scotland
Salmond fishing in Scotland presents no difficulties for anyone in the know and at the right time can be highly satisfying. We all understand how a salmond will go for a bright and flashy lure dropped in upstream and floating down in the roiling current of the Scottish National rivers. But salmonds are slippery and they can jump. It’s well known in Scotland that a ‘jumping fish is nay a takking fish’ and no one c...Read Full Post »
|Posted on 12 March, 2021 at 8:35||comments (1)|
I’m a bit puzzled. I read and heard about the laudable Reclaim our Streets campaign. What is being said suggests that London’s streets are less safe than previously, and that there is a lot more sexual harassment of women nowadays.
At the age of 70, I look back at what I’ve witnessed in the past and I don’t think things are less safe. They never were in my day either.
I recall that at the age of 13 ...Read Full Post »
|Posted on 21 May, 2020 at 4:05||comments (222)|
I wrote in a previous post about Koch’s postulates. To recap, whether you get an infection or not, depends on 3 things:
1. Host vulnerability – if you are immunocompromised (for example)
2. Virulence of the organism – if you get Ebola as opposed to a mild cold
3. Dose of organism – if you have a huge dose of an innocuous infective organism you are more likely to become ill than if it is only 1 bacterium or virus.
With the Corona virus we know that certain individuals are more prone to both catch the disease and to die from it. We do know that people of BAME groups are more likely to be affected and so are front line NHS workers. There is much consternation over this, but applying the above, there may be some answers. It is improbable that it is postulate 1 or 2 above that results in the increased incidence and death rate, although clearly older individuals are more likely to die if they get the respiratory distress and since they have more ACE 2 receptors, they will get a bigger viral load.
Since front line workers are not only more likely to get the virus and more likely to die from it, it seems logical to assume that the problem is dose of virus. They are exposed to far more virus than the average person out for a walk 2 meters away. The droplets hang around in the air in a still atmosphere for hours so exposure to that environment makes it more likely that the dose of virus is high where the PPE mask (for example) didn’t fit properly or the virus gets in through the eyes under the visor.
The much-maligned Marseilles study showed that in people who were mildly infected, they cleared the virus quickly and it was assumed to be the drugs responsible. I make no judgement on that, but I suspect the real significance was that the ones who went on to develop the late respiratory distress syndrome probably had such large doses of virus that they overloaded their immune system and developed the auto-immune ARDS.
There are numerous studies which show that using acoustic rhinometry, the size of the nasal cavity varies with ethnicity and that Caucasians have smaller nasal cavities than other racial groups. Asian people are in-between in nasal cavity size. The proportionate difference is very similar to the racial differential mortality with Covid-19. I think this may be important because in a large nasal cavity, the infection will cause a greater viral load, leading to a greater likelihood of the late development of the respiratory distress and organ failure.
All this leads me to conclude that the size of the viral load is the important factor in the development of the severe acute respiratory distress. The people with mild illness had a smaller dose and cleared the virus quicker.
Just sayin’ is all.
|Posted on 16 April, 2020 at 18:49||comments (0)|
I may seem like a bitter old git, but I have serious reservations about all the praise for NHS workers. I see how people are clapping and join them unreservedly in praising how front-line NHS workers are going to work every day facing fears and genuinely risking their lives to save patients in the present Covid-19 crisis. It is what the NHS and the wonderful people in it signed up for, are committed to, and execute with kindness and empathy.
I’ve been a consultant neurosurgeon for 34 years in the NHS and have had the privilege of working beside the finest nurses, porters and ground staff any system could offer. Many of them worked without demur despite poor conditions, under staffing and poor remuneration. The nurses on my neurosurgical ward never went home at the end of their shift on time because they had to make sure that in the presence of staff shortages (always there) the patients would be OK. I loved those people for their kindness, care and empathy. About time you appreciated them too.
But… And there is always a but…
Think about it. Those people you are all praising, and admiring have been doing that job for a long time. What have successive governments done to them? Yes, not just Tories but Labour Governments also?
Margaret Thatcher wanted to dis-empower doctors and abolish ‘shroud waving’ because she and her Government were underfunding the NHS and under-paying the hard-working staff – doctors, nurses, porters and cleaners. She put doctors into management to divide and rule – setting doctor against doctor to make them blame each other instead of the niggardly governments. There was a review body which did what the Government wanted and never paid anyone in the NHS even at the level of inflation.
Next came successive Labour and Conservative Governments who engaged in and encouraged ‘doctor bashing’ – vilifying doctors generally. The press joined in and the politicians tried their best to redress the balance between the public view of doctors compared to the public view of politicians.
NHS workers – all of us- felt undervalued and underpaid. Morale was rock-bottom and descending.
Suddenly – Covid-19!
Yes, you are going to die without our glorious NHS. Well, buddy, let me tell you the NHS was always bloody glorious!
Not only are we there for you now, we always were, despite what the politicians did to us. They tried to damage our status (nurses and doctors). They cheated us over pensions. They underpaid us.
And Now? Wonderful NHS – saving lives – we are so grateful!
You for real?
We have one of the lowest per capita rate of cost for health care in Europe. We have had desperately insufficient ITU beds in the country for years. Patients died for the lack of them and no one cared. We cajoled, we urged, and we begged for more ITU beds and were laughed at. No one cared and people died unnecessarily.
Perhaps now, even Boris Johnson realizes what the NHS is. It is a wonderful institution and the people working in it do so and give everything they have, even their lives for others without complaint (or remuneration).
Shouldn’t you be paying them for what they do? Shouldn’t they have a right to a decent wage and a feeling of security?
Keep clapping and wafting your virus at the people round you.
It wont pay anyone’s mortgage.
|Posted on 7 April, 2020 at 8:26||comments (69)|
Virology half-understood, pseudoscience and and maybe a little hope:
Coronaviruses are interesting. They have the biggest genome of any RNA viruses in their nucleocapsid (the envelope with the RNA in). There are three proteins – S- or spike protein which makes up the spikey part on the outside, M protein which makes up the outer membrane and N protein which encloses the nucleocapsid inside.
The virus spreads in two ways. It can force replication of its own RNA and the new virus particles exit the cell emerging into the extracellular space to infect other cells. The other way it moves to new cells is by syncytial spread – moving through cell membranes into adjacent cells. The ‘clever’ part about that is that it can spread along a mucosal (lining membrane) surface without ever being exposed to the extracellular environment where antibodies (IgG and IgM) can neutralise it, or extracellular toxins (like drugs) can affect it.
The virus has an affinity for a particular site on human cell membranes called angiotensin converting enzyme-2 or ACE-2 receptors. That receptor is common and present on many cells in the body. The purpose of ACE is to increase levels of angiotensin which is important in the renin/angiotensin mechanism (which keeps your blood pressure up). This renin angiotensin pathway raises blood pressure by causing vasoconstriction. Inhibitors of ACE can occupy these receptors on cells and work by causing smooth muscle relaxation and lowering of blood pressure.
The Coronavirus spike protein latches onto that receptor site and changes shape to allow passage of the nucleocapsid into the cytoplasm of the infected cell, where is latches onto the Golgi apparatus and creates replicas of its own RNA. Unfortunately giving ACE inhibitors doesn’t prevent viral attachment because the spike protein can change the morphology of the receptor site to adapt.
Potentially the only way to affect the virus is during replication or to block the exiting particles.
Chloroquine affects the developing malaria parasite by blocking one locus on the protein necessary for it to exit the red blood cell it infects. Since Coronaviruses have a large complex RNA chain and require certain proteins to burst out of the host cell there must be some logic in using Chloroquine to damage those proteins.
Similarly, bacteriostatic antibiotics (Doxycycline, Azithromycin) inhibit protein manufacture by acting on a different locus on mycoplasma proteins (the antibiotics of choice for Chlamydia) and prevent the infected cell from letting out the infecting organism.
So, my feeling is to treat the infection as early as possible with those two drugs, so the extent of the infection is reduced and hopefully the second phase of the illness won’t occur. This is unproven but there was one small study, poorly controlled and much criticized which did show that patients on these two drugs did better than patients who did not take them, albeit in a different hospital but otherwise age and illness matched.
I think that if/when I get this virus, I want early treatment with those 2 drugs!
|Posted on 31 March, 2020 at 3:50||comments (88)|
I realise most of it isn’t rocket science, but as a neurosurgeon, I’m used to looking at figures of outcomes and mortality. I’m puzzled.
In January last year the winter mortality in the UK was just about 1500 deaths per day. The daily death rate fell to around 1200 by 31 March 2019. The cause of the excess deaths (1500 – 1200 = 300) was due to an increase in respiratory infections, mainly in the elderly.
I have not seen the current daily death rates for this year, but it remains unclear to me whether the figures given out for Covid-19 are to be included in the normal daily death rate or whether they are on top of the known seasonal excess winter death rates. It is puzzling because I have a suspicion that a proportion of the people dying from Covid-19 would have died from another respiratory illness (influenza, bronchopneumonia) in any case. The only way to know would be to look at the effect that Covid-19 has had on those figures. The Office of National Statistics indicates that in the week beginning 13/3/20 11,019 deaths were registered. The comparable average figure during the previous 5 years was 11,205. There is no significant difference between the two as far as I can see but maybe I’m missing something.
You might be thinking that Covid-19 figures have not been taken into account yet, but when you think about it, the figures we have are related to the testing statistics – number of cases = number of positive tests in people admitted to hospital because they have become seriously ill.
The figures bandied about indicate around 200 deaths per day at present. If the mortality from this virus is 1-3% (we’ll call it 2%), then the over all incidence in the general population is probably around 10,000 ((200 x 100)/2). This makes little sense when others suggest up to 50% of the population may have been exposed to the virus.
The fact is we have no idea how many people are or have been infected, because only a selected group have been tested and all it tells you is the number of hospital admissions who actually have the virus in their nose/throat.
Once the antibody test is available things will become much clearer. We will have a better understanding of who has been exposed and who is probably immune.
I guess in a round about way, all I’m saying is the information given out generally is confusing and there just isn’t enough data about the general population’s exposure to predict anything.
There is an article in The Spectator which is interesting:
It makes the point that many deaths due to Covid-19 may simply be an incidental cause of death in people who would have died of another virus in any case. I sincerely hope it’s true.
|Posted on 29 March, 2020 at 5:54||comments (0)|
So, we’ve hit the 1K mark for deaths. The PM says it’s going to get worse. We know this already. If we all behave and don’t touch anyone else, we may keep the deaths to a minimum but not before the death rate peaks.
Seems to me there is some pretty flawed thinking about who is at risk. Front-line NHS workers I suspect are among those who are most exposed to the Covid-19 virus. The Government is wanting to test them because… because what?
The average doctor in ITU whether he has PPE or not, may or may not have the virus at any one point in time. If he tests negative, he might become positive later today or tomorrow or the day after. Testing him now tells you nothing.
A front-line nurse in ITU may test positive – she drops out for 2 weeks.
On her return we cannot know whether she is still infectious unless she is tested again.
It represents the pitfall of epidemiological statistical thinking. It doesn’t matter how many people have the virus what matters to the NHS staff is if they have had the virus or not. Once you have established who is immune, you have a workforce who can rest assured they are much less likely to get the illness again.
This why testing for the antigen isn’t much help unless you keep testing the same individuals. We have moved beyond the stage of contact tracing to try to confine the disease. We are now on damage limitation to limit the spread and the pressure on our 8000 ITU beds with ventilators.
Antibody testing may well be helpful but that is in any case, not completely reliable, since serum titres of the antibody are highest around 2 weeks after infection. So, if you return to work after a week’s isolation it is probably better to do the antibody test a week later – after the horse has bolted.
The WHO say test, test, test, but the timing is important and much depends on what stage we are at in the epidemic. For us now in the damage limitation phase, antibody testing is probably the most important.
There is a lot we still don’t know about this virus. From one description I read by someone who had the virus badly and survived, there is a an ‘allergic’ response after the initial temperature/cough phase and it is this which causes the severe form which starts days after the initial symptoms.
To quote a character in Full Metal Jacket: ‘It’s a big s**t sandwich and we all just gotta take a bite’.
I hope that no one who reads this gets the damn illness.
Stay home, stay safe.
|Posted on 20 March, 2020 at 11:04||comments (0)|
It has come to my attention…
That’s the way all unpleasant missives begin, after all, isn’t it?
Look people, there seem to be a lot of you who still don’t understand what we are facing here. If the epidemic peaks badly like in Italy, the mortality will quadruple. All the intensive care facilities will be taken up (average stay is about 8 days in ITU). Infected people will not get treatment and more and more will die.
We bandy figures around like 1% mortality but in Italy, the mortality over all is over 8% because as facilities get used up there are more people dying at home without ventilatory support.
On the patient info website (https://patient.info/news-and-features/covid-19-coronavirus-myths-debunked) is a list of misconceptions and myths which are listed to be dismissed. My take on it is:
1. The virus does not respect any national boundaries. You are as vulnerable as anyone else whether you are an Eskimo in an igloo or Pygmy in Africa
2. A hot bath makes no difference to the infection
3. Antibiotics don’t work
4. A vaccine will take about 6 months to be tested and used, even if it is possible to develop one
5. There are no effective drugs
6. Paper face masks will not help. The air and droplets you exhale come downwards and at the sides, even over the top of the mask. The paper will only protect the person you are talking to and surgical masks only work for a few hours – after that they are useless.
7. Washing your hands with soap is very effective. This is because it denatures the fatty molecules that the virus contains (lipoproteinolytic).
If all that is true you may feel it is hopeless. It isn’t. Our Government’s current strategy will probably work if people cooperate.
1. Reduce social contact with others – the less you go out, the less you are in contact with places and things used by many people, the less likely you are to contract the disease.
2. Avoid pubs, clubs, sporting fixtures and anywhere where there are crowds.
3. Don’t go to any social gatherings.
4. Don’t hold meetings at work – use teleconferencing and video conferencing.
5. Don’t touch other people and don’t shake hands or give a reassuring peck on the cheek.
6. Don’t stand close to people when you speak to them – space, space, space.
7. Clean the things you use most often – your phone, keyboard and mouse, car keys, doorbell, door handles etc. using anti-septic wipes or fluid.
So, what happens then? Even if we are all going to get this virus, we won’t all get it at the same time and we can benefit from there being sufficient ITU facilities when we do, so we won’t just die at home waiting for a bed in hospital.
When will it be over? New cases will probably have reduced to reasonable levels by autumn, but we might then see an upward surge as people start to relax.
I read somewhere that no country has an exit strategy. This may be true, but if a vaccine appears we may yet terminate this disease. So, fingers crossed. I think most of the world’s virologists will be working on it. For once there may be global co-operation.
I hope so.
For all our sakes.
And it isn’t just because I miss going to the pub.
|Posted on 19 March, 2020 at 7:09||comments (2)|
A nineteenth century traveler called Charles Kinglake published his travelogue of a journey across the Mediterranean and Middle east (Eothen). I had to study it for ‘O’ levels. At the time I couldn’t understand why there were frequent references to plague and weird superstitions about things like: if you have a cold you can’t catch plague. He thought he was lucky to get a bad head-cold on his journey. Maybe I understand him a little better now.
It seems to me that even when confronted by facts and scientific truths we still cling to foolish superstitions in the hope that hope will save us. It won’t. Get used to disappointment folks. In the current pandemic, we should all accept the few facts that are available:
1. The virus spreads like any upper respiratory tract virus – droplets that emanate from your mouth and physical contact of virus particles on hands with your eyes, nose or mouth. When you cough, micro-droplets of moisture emanate from your mouth. In a still atmosphere, they have a range of up to 2 meters. Sneezing is even more powerful. Speaking results in droplet spread as well but not as distant as coughing or sneezing. So – keep your distance from others – it’s not offensive to do so, only sensible. Don’t shake hands. No peck on the cheek. Wash your hands every time you come home. Wipe all communal surfaces with an ant-septic agent – that means door handles and your computer mouse and keyboard. Do it frequently or at the very least when anyone else has used them. Wipe your smartphone, door keys and car keys. If you go shopping, wipe the handle of the supermarket trolley before you start pushing it round and when you go to your car, sanitize your hands before you get in. Wipe the car door handle, steering wheel and gear stick with an antiseptic wipe before you set off.
2. Whether or not you get an infection depends on three things (Koch’s postulates):
a. Host susceptibility and resistance
b. Virulence of the organism
c. Dose of the infecting organism.
You need to think about this because the people most at risk are those who fit the above criteria. Living with and being in intimate contact with someone who has the virus means that you have a pretty good chance of catching it and your outlook isn’t good if you have an illness that compromises your immune system. Stay away from old and sick people – if you care about them.
3. As far as I can see reading stuff, 75% of people will get a ‘flu-like illness. 15% will be seriously ill and between 1% and 2% will die of respiratory or multi-organ failure. Mortality is highest in old people especially those who have an underlying illness. Over the age of 80 the mortality may be as high as 20%. So why are younger people less affected? I have a feeling it’s partly because they are never still – they are fitter to start with i.e. they have a better respiratory reserve. They also have a higher metabolic rate and burn off calories faster. That readiness of the body to raise core temperatures from metabolism may be a reason for their relative resistance. Most respiratory viruses take hold best at slightly below core body temperature – that’s why they get into you through the upper airways, since your nasal temperature is a little below core temperature. The cell turnover of the ciliated mucous membranes in the airways is probably better in younger people too, so recovery may also be better in young people. We can’t get younger, but maybe we should all exercise more on a regular basis to try to increase over all fitness and metabolic rate. OK that isn’t fact but there is some logic in there somehow.
4. If you have had the virus and no longer have symptoms, you probably won’t get it again for a long time – like resistance to influenza. That doesn’t mean the virus won’t mutate and change its characteristics in the future, just that this virus will gradually peter out with time. But… and there is always a ‘but’. It is known that as a virus passes from person to person, it attenuates, that is, it gets weaker. A new infection is very virulent but by the time that virus has infected a number of individuals, it produces less of an illness – the later in the epidemic you get the virus, the more likely it is that it won’t make you as ill as it made the first person with it.
5. Herd immunity is necessary. It’s all about who’s got it and who hasn’t. If you are in a room with ten people who are not resistant and one of them has the virus, potentially they all get infected. If you are in a room with nine immune people and one person is infected, the odds are you won’t be infected. If you then look at a population of people, eventually as immunity increases, the virus can’t reach enough people to continue in a big way. The immune people form a kind of resistance wall, since they can’t pass on the virus to you if they don’t have it.
6. Dog shit. Yes, that’s it! The way to think about contagion is, in your mind, to picture the virus as dog shit. Each time you touch something potentially infected, think how it would be if you could actually see and smell it. You would never put your hand in dog poo and then touch your face or shake hands or fail to wash your hands (regularly). If you want to avoid this virus, think dog shit.
7. The probability is that we will all be exposed to this virus. Once you accept that it is easier to come to terms with the future. Some of us will die – hope it’s not me and I hope it’s not you.
There’s more but I’m getting bored.