Coronavirus update blog

This is my update of my April 14 coronavirus blog and podcast. 

INTRO

A lot has changed, as you probably are all aware, and in the meantime some of the things that I wrote and talked about back then, I think have held up pretty well. But there are some corrections and some additions and some subtleties that have emerged and some of these will be of interest to my patients with chronic fatigue syndrome, with immune activation, Epstein-Barr virus and other types of problems that may put them in harm’s way.

I know we lived a charmed life here so far in Australia and probably mainly because of closing our borders early and reasonable “social distancing”. But eventually we do need to face this virus – it is highly transmissible, it’s not going away, and while we have made it through the first wave, we are all sitting breathless here in late May 2020, just waiting. 

I think it’s reasonable to prepare ourselves for what is likely to be a second wave that is likely to challenge us a somewhat with increased numbers of people infected. The big issue is probably going to be when we open our borders again to travellers from overseas and get back into global economy. 

I think between now and the end of this year we will be tested. The virus is still present, community transmission is low at the moment, but I think we can learn some of the lessons from the countries that have had large numbers of people with COVID-19, here and maybe America and China, Italy – there are many many countries that have got now good experience and rampant experimentation going on when it comes to the kind of things that can be done.

So first of all let me go through a few of the corrections or modifications I would make to my previous blog regarding our chronic fatigue syndrome sufferers and their risks of corona virus infection.

TRANSMISSION - DROPLETS, AEROSOLS AND SURFACES

One important correction to make is that I said at the time that droplets seem to be the major mode of transmission that droplet transmission which falls away fairly quickly with him 1.5 m from a person speaking or coughing, and the surfaces people touch with their hands and then touch their face afterwards, was probably the major mode of transmission.

Now as of May 25th, the thinking is that aerosols, which were not considered to be a problem, are as big an issue as droplets, and may be even bigger than fomites.In other words the surfaces that the virus collects on – the handles, the doors the other surfaces – is probably a much smaller component than had been originally thought.

“What’s the difference between an aerosol and a droplet”, you ask. Aerosols are ultrafine particles that are not droplets. They are effectively virus that can come out of the breath with no observable droplet size and that can become airborne and stay so for a long period of time.

Now why is this important? Well it primarily becomes important when people are cooped up together in enclosed spaces, say schoolrooms or workplaces, especially open-plan workplaces, restaurants, bars and the like. The droplet size may mean that we can avoid the droplet contact which falls off within the 1 1/2 m BUT the aerosols can remain airborne for 45 minutes or longer have not had much attention paid to them. 

Some of the work from overseas is identified that on the airflow of air-conditioners from one corner to another corner of a room, that has been transmission over a distance of many metres occur primarily when people are infected in the same room as people who are uninfected for fairly long periods of time.

What can we do about that? Well, probably not all that much.We just need to be aware that there is an air transmission beyond droplet transmission. If you think of an aerosol as the finest of fine sprays invisible to the eye under any circumstances, and if you think of droplets as the fairly microscopic droplets but still sometimes visible droplets that you sometimes see, from a person’s mouth when they cough or speak loudly or shout out. Droplets stop way quickly but the aerosols do not. 

So we need to rethink distancing in that light. If you’re going for a restaurant, for example, try not to be in the airflow of the air-conditioning – don’t have the air-conditioning washing from one area of a restaurant past other tables and in your direction. If you can feel that air flow, that’s possibly not the best place to be sitting. You need to watch out. 

In other areas projection of voice, say in pubs where there is cheering (should the football ever come back on) and those kind of circumstances, we have to think bigger. Not just the droplet distance from another person that social distancing (which actually is in social its physical distancing) has us consider, but we also have to think how long I am in this room with other people. Others may be expressing the virus into the air, so if I am going to be here for, say, half an hour or an hour, in that time I’m more dependent upon the airflow around the room and the number of other people there who can plausibly be infected. 

Currently, the expert opinion is aerosol is probably around about 40% of transmission, droplets about 40% of transmission. That leaves the surfaces probably 20% or maybe even as little as 10% of transmission. So that was my mistake, before the data were sufficient. I thought it was mainly droplets and surfaces. I think now it is reasonable to say that the aerosols and droplets – the time you spend in a room with other people who may be infected, and your proximity to people – may be more important touching contaminated surfaces. 

TRANSMISSION - THE ASYMPTOMATIC PERIOD

What is also now a lot clearer than it was a month ago is that the asymptomatic period can be truly asymptomatic and prolonged, that people can be contagious at a time when they experience no symptoms. The asymptomatic transmission is just a real bother, as it means that we are never fully sure about when the virus is under control, and we are never fully sure about who may or may not be carrying the virus now in Australia. 

We’ve about half a million tests done around the country now. It’s not a high proportion of the population, but for pretty well anyone who is symptomatic with a temperature, a cough, muscle aches and pains and fatigue, they are tested. But we are seeing that the three days asymptomatic period is a time of transmission, and other people may have already caught the virus by the time the person who is infected even knows they’re infected. 

FACE MASKS

This brings me also to the area that I addressed previously – face masks.  I heard one of the podcasts in the US saying,  “you know, the reason that Australia has escaped this virus is that you don’t see a face without a mask on in Sydney”. I looked around and in fact it’s obvious that that’s not the truth. There is a tiny minority of people, and there has been all the way through, who are wearing face masks. Maybe at the peak there was 5%, maybe even up to 10% for a week there. Generally Australians are unmasked even in areas of enclosed spaces. Is this good? Is this bad? Well depends on the numbers in the population who could be infected, and in Australia it seems that right now our numbers are low and the sensible advice is not to wear face masks. 

Face masks protect other people from your SARS-CoV-2 to some extent. Probably. But they do not really protect you from the coronavirus of other people. And that’s the anomaly. When numbers are low (and we think that the caseload is very low in Australia), the masks are of very limited value. The idea of hand washing, personal hygiene and distancing are good. Those type of actions reduce the transmission. 

Right now it seems the best advice to allow for normal social interaction and to allow your phone to recognise your face when you open it, you don’t need to wear a mask right now. But if the numbers of COVID-19 infections rise, I’m pretty sure that the Australian advice will be to adopt face masks, because once case numbers rise the potential benefits also rise. With tens of thousands of Aussies infected, you do get increasing benefit from lower transmission because the masks are in place.

There was one study which in fact found that masks accumulate the virus on the outside surface, and that all the benefit of masks is lost if you touch the outside of the mask. Now I watch mask-wearers everywhere, and most are forever adjusting and touching their masks, and that is not the way to go if the accumulation of virus should you be shedding is on the outside of the mask. Perpetually adjusting the mask may increase the risk of you are having it having the virus on your hands.They may give a false sense of security as well. So just keep your eyes open for the advice on masks. It’s not clear right at the moment and there are downsides. 

People’s facial expression is blocked by masks – that’s what masks do! There is great value in the expression of other people’s faces. The sense of empathy, and the ability to know if there was a smile behind a comment to understand and interpret other people in a country like Australia. I think that we are very very dependent on that here. There are many other countries where masking has become habitual and high proportions of the population wear them. They may have learned how to counter the inability to determine the meaning in another person’s face and expression. One’s face is like the emoji that goes with speaking of words. So we keep our energies unmasked at the moment here, but with an eye to the future.

TESTING

I want to deal also with COVID-19 testing, because people feel that if we all got tested, all this would be okay. Testing is just testing! I’ve been doing PCR and antibody testing on bacteria and viruses like Epstein-Barr virus for my patients for decades now. I have done many thousands of antibody tests, many hundreds of PCR tests, and I’ll tell you the interpretation of the test results needs a lot more care, experience and depth of knowledge than is currently evident. The idea that if you test, trace and isolate (which is termed TETRIS) that everything will be okay. Untrue.

A major problem is that we still to this day have no “gold standard” for SARS-CoV-2, as no test that has 100% or anything even close to 100% for sensitivity or specificity exists. Nothing even close to 100% for what we call “positive predictive value” or “negative predictive value”.  Worse than that, there is no way of determining what you would compare the current dozens and dozens of tests to!

There are two main types of tests that we should never conflate, termed the PCR test and the antibody test. The PCR test measures viral RNA, and a sample is swabbed from deep in the nose or the back of the throat (or maybe soon saliva with the new tests). We get the strands of RNA which are the signature of the SARS-CoV-2 virus, and therefore say “this person actually now at this moment is suffering COVID-19”. 

The problem with the PCR test is that we don’t know the sensitivity and specificity and we have these anomalous findings of people being positive and negative then positive again. Or in the worst case of the cruise ships that have come to Sydney where the initial tests are negative, but the person already has the symptoms, and subsequently the tests become positive.

So these are not great tests. These are ones with poor sensitivity for when we’re testing populations, so they are really not up to scratch to give us high confidence in the results. So when we say to a person “your test is negative, you don’t have COVID-19” we can be only about 80% certain that is true. Nor can we say “you are positive and you definitely have COVID-19” because many times those tests are negative just days later and we left wondering about the accuracy and the reliability and repeatability of the tests. But the PCR test is the one you do when you suspect you have active COVID-19.  If you have the cough and the temperature and sore throat and breathlessness that are indicative of SARS-CoV-2 infection, then this test is about as good as it gets. 

If you detect the viral particles in the RNA then you probably do have COVID-19. If you don’t detect them, you can’t be that sure that you don’t have it, but at least the best guess is you’re not currently infected. So we will have to wait a little bit on better technology. The bottom line is you cannot rely on the PCR test! It’s a good approximation and it’s good enough when the numbers are low in the population. It allows us to get it right most of the time. 

The other test is entirely different. It is called an antibody test. It tells you whether you have had a SARS-CoV-2 infection in the past. There is some confusion about whether the best immunoglobulins (antibodies) to test are the IgG and IgM, or the IgG and IgA.  For most of the respiratory and mucus membrane viruses, the IgA a is the antibody which is the first sign of active membrane infection. When infections make it into the bloodstream, we expect a different antibody called IgM to be the first responder. SARS-CoV-2 is an encapsulated RNA virus with a surface  infection, so we expect it’s IgA that may give an early sign.

Most of the early “quick and dirty” antibody tests are for IgG and IgM. IgG is thought to be the antibody that indicates that you have fought and won your battle against COVID-19, and that when you have those antibodies you cannot infect anyone else you cannot yourself be infected. It’s like the magic armour that we believe is protective against both transmission and re-infection. We don’t know that yet, though! 

The IgG we are measuring are very very specific antibodies that develop in response to infection, but it doesn’t mean they neutralise the infection, nor does it mean that they prevent infection. They are just antibodies that are formed as the body tries to work out “how do I deal with this bug?”. An infected person usually produces dozens of different antibodies to the SARS-CoV-2, mainly to the spike proteins (that are so photogenic and you’ve seen a million times). These antibodies converge over time to better quality antibodies as B lymphocytes and Helper T cells get together in the lymph nodes and focus on the virus. Those spike proteins are thought to be the target of our immune system, and it is thought that if we can just get a vaccine with an antigen that induces antibodies that attack that spike protein, that all will be well. 

However as of 25th of May, there are cases of people who have developed spike protein antibodies who become reinfected, and there are infected and recovered people who have developed no spike protein antibodies. So what we don’t know at the moment is whether SARS-CoV-2  induces an antibody response in humans which is either neutralising or protective. 

VACCINES

That is research that is going to have to be done as the vaccines are being invented, and as the different trials of vaccines are done. We have no prior evidence apart from two vaccines that were made for the original SARS virus, where there was very very moderate protective activity in one of them, and reasonable activity in the other. 

The problem was they never completed the full safety and efficacy trials, and we never got a chance to use it because the infection disappeared before we had a chance to do so. So be careful when you get a blood test done. It is likely to be the antibody test  What we discover over the next say 3 to 6 months will give us an idea about what type of antibodies truly are protective, and those will be the type of antibodies that any successful vaccine is going to try to induce the body to produce. 

I have a concern about this. Everyone is very enthusiastic about developing the RNA vaccines, in other words, injecting something into the muscle that induces your body’s own cells to start to use viral RNA to produce viral proteins, to produce something that signals the immune system. But in doing this, we are pushing viral RNA through ribosomes of our own cells, hijacking it somewhat to produce a foreign protein. That foreign protein in a vaccine is meant to induce the body to produce the antibodies that would then protect you against SARS-CoV-2.  Many chronic fatigue syndrome patients, and especially the who have the more autoimmune-type problems where the immune system has gone off script somewhat, is not only attacking infections but is attacking the host with lupus or thyroiditis of polycystic ovarian syndrome or vasculitis. 

This concerns me because what we are going to be inducing in a whole broad population (and you can believe it will be the whole population when the vaccine comes out. I’d be surprised if it’s not made mandatory even if we don’t know the full long-term consequences). What bothers me about it is that when you induce normal body cells of the person to start to produce foreign proteins, there is high potential for an autoimmune response which will attack what it sees as infected cells. I don’t want to be a naysayer here, but when you are looking at a whole new vaccine technology and saying “hey why don’t we hijack the person’s own cells, their normal everyday cells, to start producing this viral protein”, and those viral proteins get taken to the surface of the cell, there is potential for mischief for the people who already have autoimmune processes going on. Some already have that tendency to not be able to clear an infection, but to simply retain the fight for long periods of time. I worry.

I’m not arguing that we shouldn’t move that way, but we going to have to be very very careful of the vaccines which have whole new technologies and whole new potential not for short-term adverse effects but for 10 years 20 years down-the-line effects which could make for a very interesting time for inflammatory and autoimmune conditions. 

CO-INFECTION

There is evidence that part of the trick of the SARS-CoV-2 is that it may awaken and work with other infections, For a simple coronavirus there are a lot of complications that look like some other type of infection. There is an emerging view that it’s not really the coronavirus the causes that second week, or phase 2, of the infection, where person fights the virus well in the first week and then a “cytokine storm” happens for no apparent reason in the second week. At the time of that cytokine storm, the viral titres are dropping. This is important for my chronic fatigue syndrome patients, especially the ones who have the persistent relapsing or chronic Epstein-Barr virus. A study in China (a preprint, not so far peer reviewed) showed that almost half of 67 COVID-19 patients had reactivated their Epstein-Barr virus, with IgM and early antigen antibodies positive. The likelihood is that the SARS-CoV-2 brought back to activity an old herpesvirus, the Epstein-Barr virus. 

Now we know that happens frequently enough with shingles, a reactivation of a chickenpox virus, but this was quite impressive. 50% of people IgM positive in the roughly 25 to 52 years age group is a very high proportion of active Epstein-Barr virus. Higher than the proportion I see in my own practice with chronic fatigue syndrome. What this suggests is that coinfection, maybe with EBV,  Chlamydia pneumoniae, Mycoplasma pneumoniae or other dormant intracellular pathogens that can persist for long periods of time are potential targets. 

What the SARS-CoV-2 may be doing is lighting small fires along the upper respiratory tract and lungs, and maybe in the gut and elsewhere, attracting immune cells to the site. If another infection, say an Epstein-Barr or a chlamydia or rickettsia or mycoplasma, gets awakened in that fire, the flareup in the second week could well be not the coronavirus but a secondary infection. And it’s that secondary infection that could bring about the cytokine storm that everyone’s talking about. 

Now my chronic fatigue syndrome patients know about cytokine storms. Most of them, when immunology is involved, have been through repeated crashes with past uncontrolled enemies. The one I’m interested in mostly is Epstein-Barr but other herpesviruses and persistent bacterial pathogens are frequently reported in CFS. So there is the potential that the SARS-CoV-2 acts like a firebug that sets off little fires and provides an opportunity for other organisms to mobilise, especially in the elderly and others with chronic health problems.

This may explain some of the issues that we see with intravascular clotting, pneumonia, generalised prolonged fatigue and more. Even the recently reported problem of teenage kids developing a Kawasaki-like syndrome that has more of an autoimmune look. 

So what concerns me is that those suffering chronic fatigue syndrome where there is evidence of persistent infection with EBV, CMV, varicella, chlamydia, mycoplasma and those with vector-borne diseases such as Ross River virus, Q-fever, Babesia, Bartonella, Anaplasma and Lyme-like illness, may be at increased risk of pathogen exacerbation after COVID-19.

There are lots of bugs around that, when you are reasonably healthy, can be under control, but barely under control. That that’s a position for many chronic fatiguers, that all you need is just some little firebug to light the fire again, and those opportunists kick on. That’s why I’m advising all my patients with chronic fatigue syndrome be very careful to avoid COVID-19 until we know a lot more about this. Until we know how it ignites other battles, we need to be ultra cautious and keep out of harm’s way. 

PREDISPOSITIONS

For many patients I have seen have inherited predispositions to persistent infections. Many of my patients will know this because I have a high proportion the people with specific types of immune susceptibilities. One of them is called mannose-binding lectin deficiency, or MBL deficiency. MBL deficiency is an innate immune response deficiency that leaves the gate open for infections to persist, and this draws in large numbers of neutrophils, depleting the neutrophils in peripheral blood.

Infections can get quite dramatic in people who suffer MBL deficiency. You may not be able to do much about it, but this impairment of the innate immune response may contribute to that secondary cytokine kick. I’m not saying we know this yet – we have no studies as yet. MBL deficiency may even turn out to be protective as it is against noroviruses. But until we know, I’d assume it would be more likely harmful.

I’m not trying to be a scaremonger, but I do know that the innate immune deficiency of mannose-binding lectin deficiency can make life very very difficult.

The other one is a better-known one which is the Lewis non-secretor (an FUT2 gene homozygous variant). While this has consequences as far as B12 requirements go, it is associated with a loss of a glycoprotein that is normally in human mucus.  The gene codes for an anti-adhesion glycan which prevents persistence of viruses, bacteria and pathogens of all types. Without it our “teflon coating” of mucus membranes is impaired.

Non-secretors (with the phenotype  Le(a+b-)) are at a disadvantage because they cannot easily wash the virus off. They lack protection factors in the mucus for a respiratory virus like SARS-CoV-2 on the respiratory membrane. 

Lewis non-secretors are around 30% to 35% of my practice. Mannose-binding lectin deficiency is again about 35% in my practice. The background population levels are about 15% to 20% in Australia, while severe MBL deficiency is under 10%. So this kind of predisposition to infection may put my CFS patients at a disadvantage if you are infected with SARS-CoV-2. 

LOSS OF SENSE OF SMELL

One item that I just love and has been reported in major journals recently is the loss of olfaction in COVID-19 patients. Those who suffer a loss of their sense of smell and sense of taste (which really probably is a sense of smell). Many of you probably remember I wrote an e-book (which has had over 600,000 downloads!) titled Killing Us Softly . I relate the story of the olfactory bulb and the fact that the olfactory nerves are card-carrying brain cells. They are not neurones in the normal sense, not like the optic nerve and other nerves with synapses. Olfactory neurones poke through the top part of the nose and our brain cells dribble down to sample the world outside. 

Those cells are exquisitely sensitive to volatile chemicals, to finding food, to pheromones for mating, to avoiding danger and so much more. There are many things that those brain cells do when they’re out there, but it seems they get infected by SARS-CoV-2, and often in the early stages. This has now been reported repeatedly as people lose their sense of smell and it may be a predictor those people who really struggle with the second week of that infection. 

It is thought that that loss of smell may be predictive of something, and now there have been papers reporting this. How good is this JAMA recommendation for recovery from the loss, and suppressing the inflammation by administration of high-dose omega-3 orally and vitamin A as a nasal spray! The omega-3 dose is not given, but in principle, high dose in the 6 to 10 g per day range is sensible. I have not used vitamin A nasal spray, but the studies done to date use 10,000 IU per day.

I’m certainly going to call some of my compounding pharmacists. If a nasal spray is able to be partially protective of the respiratory tract with vitamin A, there are good principles for thinking that they can do some good not just for olfactory sense of smell and taste but also possibly for the risk factors of viral progression and accelerating neuronal replication of the olfactory bulb.

CLOTTING

Sicker patients tend to be those with clotting disorders, and lots of COVID-19 sufferers who go on in that second week to develop those cytokine storms have clotting issues, with pulmonary embolism, strokes and other disorders of the clotting. Even heart problems are probably related to clotting defects, and so there is again thought that we may be able to do something to protect ourselves ahead of time by at least maintaining good Omega-3 intake through fish and free range meat. You need the eicosapentaenoic acid and docosahexaenoic acid (EPA and DHA) are probably good ways of preventing the aggregation of clots and stopping some of the clotting.

Also, either aspirin or something with high salicylate content from our foods may help. This is one of those periods where people get a sense of just what the difference between organic food in non-organic food. When we use pesticides the natural salicylate content of the plants goes down because they don’t need to protect themselves. Just wasted energy. With good organic food, the plant insect protection system relies on salicylate, so the salicylate component of those foods is much higher. Now it’s bad luck for people who maybe have a bit of salicylate sensitivity (there is a well-known hospital in Sydney which believes that it’s the only disease in the world). 

For the vast majority of us, organic fruit and vegetables in season as a means of keeping clotting under control is a really good trade, and if you can’t then probably a low-dose aspirin each day as prevention. We need to work on reducing clotting before infection, it seems. 

Much of the world is now talking about or what other straightforward things you can do nutritionally, whether by foods or supplements, and I think the general support for vitamin D and vitamin A is clear. Australia is going into winter right at this time, and plenty of people who have chronic fatigue syndrome have been at home all the time recently. Vitamin D levels are usually low and vitamin A levels are generally low in my CFS patients.

I am not sure if that’s because of poor nutrition or a failure of the enzymes that normally convert beta-carotene to vitamin A. Those two fat-soluble nutrients would seem to be a very low risk way of a good investment in prevention of infection of the type that we see with SARS-CoV-2 and may be a way of preventing low-dose viral exposure from turning into something which is COVID-19. 

MANAGING IMMUNOLOGY

One final thing for today is that we are now all more aware that the immune system is not one thing. It is complex. It’s not good or bad, not high or low. The best immune systems are the most adaptive immune systems. It is not the strongest or the most aggressive nor the least aggressive. What you want is high responsiveness and variability to circumstances. 

The reason I’m raising this is people say “how do I boost my immunity” and there is a concept that if I boost my immunity I won’t get the virus. But we do know that in the second week of the infection that so-called boosted immunity can be a little time bomb waiting to go off and become too aggressive. Because many of the symptoms of severe COVID-19 are complications involving pneumonia, the cardiovascular system and clotting in the arteries and veins around the body. So we don’t want an aggressive immune system and we don’t want a passive immune system. We want an ideally balanced immune system which can be managed by doing things like exercise and movement. 

One of the downsides of people being stuck in their homes for so long is that many forgot to exercise, and when they are not exercising and not moving they don’t give the signal to the brain that health is around. You’ve gotta move your body for your brain to get any signal that you are healthy. You get deconditioning of heart muscles you get deconditioning of skeletal muscle and it can happen fairly quickly. The body in effect is a saying, “okay let’s shut everything down, hunker down and get through this tough period, and we’ll come out the other side smelling like roses”. 

So the message is not that you need aggressive immune response in the early stages. It’s probably better to have the immune system on its toes looking for the viruses. Good vitamin D, good vitamin A, good zinc makes for a body which can respond quickly and effectively to any challenge with viral particles that land on your respiratory tract. You want an immune system which is quick and efficient and eliminates the virus. What you then want to be careful about is that you don’t then find you’ve recovered through the first week well, and then the overaggressive inflammation starts. So it is probably not a brilliant idea to keep the immune system overactive. It is probably better for it to be balanced in settling down in the second week.

I wish I was a herbalist. I plan one day to do herbalism, but the idea of using plants to modulate an immune system from high to low and low to high, to have it adapt is much more appealing in these circumstances.We have drugs that provoke aggressive immunity and we have ones that can almost turn off immune responses. Taking control of every last aspect of every individual with SARS-CoV-2 is beyond what we know. We just don’t know individualised medicine to that level, so there is a value to going back to diet. 

If you have your gut immunology right, and if you’ve got nothing on the gastrointestinal tract like allergies or lipopolysaccharides pouring through an abnormally leaky gut wall, you’re less likely to provoke those very aggressive responses at the end. Now again – PAY ATTENTION – no proof of that yet!

What we do know is that plenty of oldies who are healthy make this make this virus go away and they recover very very well, and plenty of people with chronic infectious and inflammatory and heart disease, diabetes, lung disease don’t make it through whatsoever. But what I what I am promoting is that there is an issue of being able to exercise, of eating healthily with lots and lots of cellulose foods that will help the gut function very well. Maybe even a time for using probiotics and anti-inflammatory probiotics (like Saccharomyces boulardii) along the way.

What I’m focusing on is if you have CFS and you’ve got underlying EBV, chlamydia, mycoplasma, and if you’ve got autoimmune problems, then your risk will be minimised if you pay attention to diet, movement and lifestyle. Get out for some sunlight or take your vitamin D, take your vitamin A, maybe a little bit of zinc and that that would give you your best chance of working through SARS-CoV-2 should you become infected. It may even in the long-term reduce the incidence of the infection and especially symptomatic infection

SIGN OFF

So that’s that’s about it guys. That’s what I have gathered since the last blog.

I know there’s a lot in this. This is a Dragon voice recognition of my podcast which I did first this time. Should you find (sometimes absurd/ hilarious) bloopers, please let me know by email.  If you find it useful pass this link around to others. Just acknowledge that it’s my work originally. There are no restrictions on the dissemination of information, certainly not in this time!

I wish you all good health and I wish you all the ability to survive and thrive in this time of COVID-19. I’ll see you again soon. I am Dr Mark Donohoe from Mosman Integrative Medicine and thanks for taking the time to read this.