LPRC - CrimeScience Episode 53 – The Facts About COVID-19 From an Infectious Disease Expert ft. Dr. Frederick Southwick (University of Florida)

Episode Date: May 27, 2020

The COVID-19 pandemic has drastically affected the retail industry globally, resulting in a permanent change to the landscape. As of now, stores are facing unprecedented issues as they start to reopen their locations. With misinformation spreading along with the virus, it can be difficult to determine the best practices to keep both employees and customers safe. To help combat this ambiguity, Dr. Read Hayes, Research Scientist at the University of Florida, Director of the Loss Prevention Research Council (LPRC), and host of CrimeScience, sat down remotely for a conversation with Dr. Frederick Southwick, Professor of Medicine and former Chief of Infectious Diseases at the University of Florida. As an expert in the field and a professional with hands-on, clinical experience helping patients with COVID-19, Dr. Southwick aims to clear up any misconceptions and help retailers adapt to the new normal. The post CrimeScience Episode 53 – The Facts About COVID-19 From an Infectious Disease Expert ft. Dr. Frederick Southwick (University of Florida) appeared first on Loss Prevention Research Council.

Hi, everyone. Welcome to Crime Science. In this podcast, we aim to explore the science of crime and the practical application of the science for loss prevention and asset protection practitioners, as well as other professionals. Co-host Dr. Reid Hayes of the Loss Prevention Research Council and Tom Meehan of ControlTech discuss a wide range of topics with industry experts, thought leaders, solution providers, and many more. We would like to thank Bosch for making this episode possible. Take advantage of the advanced video capabilities offered by Bosch to help reduce your shrink risk. Integrate video recordings with point of sale data for visual verification of transactions and exception reporting. Use video analytics for immediate notification of important AP related events and leverage analytics metadata for fast forensic searches for evidence and to improve merchandising and operations. Learn more about extending your video system beyond simple surveillance in zones one through four of LPRC's zones of influence by visiting Bosch online at boschsecurity.com. Welcome everybody to another episode of Crime

Science the Podcast. We're coming to you from Gainesville, Florida. As you all know, I'm faculty at the University of Florida as a criminologist, but today I'm going to be talking with Dr. Fred Southwick, who is a medical doctor, a physician, an infectious disease physician, and who's got extensive training and experience and even recent clinical experience with COVID-19, but with infectious disease and with emerging pathogens. So we think it's very timely, beyond timely right now to go through this. So welcome Dr. Southwick to Crime Science Podcast. Thank you. So we'll dive into this. We've talked before a little bit, we've been exchanging some

notes here and there. So we've got an outline and again, the logic for us here today, hopefully, is to flow through. But tell me a little bit about your background, your experience, your training, and how that's prepared you for now and what we need to talk about today. Well, I was very fortunate. I went to, I think, a superb medical school, Columbia College of Physicians and Surgeons, Superb Medical School of Columbia College of Physicians and Surgeons, which really emphasized the importance of listening to the patient. And critical thinking was a very important component of my education. And then I fell in love with infectious diseases. And after training in internal medicine at Boston City Hospital and Massachusetts General Hospital, I did my infectious disease training at Mass General. And a huge number of very interesting cases from all over the world, because that was a major referral center. So I really got a very in-depth training in infectious diseases. And then

subsequently was on the faculty at Harvard and then went to the University of Pennsylvania. And finally, in 1991, I was asked to be the chief of infectious disease at the University of Florida. So I came down to Gainesville and never wanted to leave. And then about seven years ago, a number of us felt that we needed an institute that could focus on emerging pathogens because we were very concerned about these new bacteria and viruses that were showing up because of the change in climate, because of the extensive travel, and because we were actually,

of the extensive travel and because we were actually, many people were coming in contact with nature and wildlife in a way they had not before. And those are all conditions that increase the likelihood of new types of human infections. So I did research in the emerging pathogen institute really studying uh bioterrorism in particular anthrax as well as the food uh contaminant organism listeria monocytogenes and uh then what's uh i decided in 2010 that i wanted to retool because I wanted to learn more about quality and safety and also systems of health care. And so I spent a year at Harvard Business School as Advanced Leadership Initiative Fellow and retooled and have been working in the field of quality and safety through the hospital's division since 2011. And the interesting thing is this infection, COVID-19, actually brings together the concepts of emerging pathogens and infection control and also highlights deficiencies in our systems for public health and for health care.

So I would have to say it was a perfect storm for me, and that brought all the training and all of my experience together in one disease. Now, fascinating and relevant. And a couple of things, as you know, many of our listeners are members of the LPRC, And a couple of things is, as you know, many of our listeners are members of the LPRC, are, you know, the major supermarket chains, the mass merchants, the Walmarts and Targets of the world. And even we've got the dollar stores and the convenience and fuel stores. So a lot of processed, but a lot of fresh food and consumables moving through the system all the time. So everything you just mentioned is very critical and important, not just now, but over time and through their daily business. So what I wanted to do was kind of go through a little bit of a flow here and talk about

really quickly, you mentioned the Emerging Pathogens Institute at the University of Florida. Just a brief description. What's the mission, the objectives, and who all is involved in the institute? Well, an institute is an organization or organizational structure that brings together individuals from various colleges. So what we've brought together is, for instance, geography, the veterinary school, the medical school, IFAS, the agriculture school, all under one umbrella, all focusing on how new organisms can spread and infect humans and get into our food supply, into our water supply, and into our environment in various ways through various animals. And the other area that's big is insects. And there are a number of people that are experts in insects that are also involved in the Emerging Pathogen Institute.

So we have a large building that has laboratories that will manage BSL-3. that will manage BSL-3, that is organisms that are quite dangerous and could, if an investigator were to contract them, could be very serious infection. And so it's a very careful isolation technique with high flow air and micron filters to filter out the pathogens. So it's a physical plant that's brought together large numbers of people from different disciplines, all focusing on new and emerging pathogens. And it just really, I appreciate that. It makes so much sense that our IFAS, which is part of our College of Agriculture, would be involved because of the zoonotic, as you mentioned, animal to animal, but animal to human spread, I guess, as well. Yes.

And then geography. And our listeners know we're working with the Department of Geography on crime mapping. So we're looking at the contagion or the spread of crime events in that way. Is there something, I know there's a team over there in groups that are working on mapping the the space and time and and travel of these infectious diseases any more illumination there yes we uh we have a group of uh modelers uh who are are really experts at looking at the infectiousness of COVID-19, the R sub zero, and looking, trying to assess human behavior and emotion studies to actually come up with predictions as what will happen depending on what actions are taken by our government and by the world in general

as to how this will spread. There's one particular expert, Ira Longino, who is well known in WHO as well as throughout the United States, who is helping us model what will happen with COVID-19. And I believe I've heard him on NPR and other sources recently for the reasons you just mentioned, just a ton of expertise in this area. So let's talk about this virus, if we could, this SARS-CoV-2 coronavirus, novel virus, we hear all these terms. Could you talk to us, doctor, describe a little bit about the virus itself? Sure. Yeah. Coronaviruses have been around forever and they infect the entire animal kingdom. And fortunately, there hadn't been too many severe coronaviruses to infect humans.

In fact, before 2003, the four major coronaviruses were all caused really the common cold. They could not be differentiated clinically from a rhinovirus, which is the other major cold virus. And one third of all our colds are due to those coronaviruses. But then in 2003, it was in China, the Guangdong province, in a live animal market, the first SARS virus, which was a more pathogenic, that is, it caused more serious disease in humans, showed its ugly face. And it spread to and actually infected about 8,000 people before infection control was able to actually stop it. And since 2004, there have been no cases of SARS. Now, then in 2013, a second coronavirus that was very pathogenic called MERS developed in the Mideast and probably is related to camels is where it spread from.

And that one is still ongoing, but it seems to be not as infectious. It doesn't spread from person to person very well, so it's been quite contained, although it's very, very deadly. It's got a 30% mortality rate. The SARS had about a 10% mortality rate, the original SARS. And then in 2019, it's quite clear from the sequencing that a bat virus had mutated. And one of the problems with it, this is an RNA virus, and RNA viruses are known to reproduce their RNA inaccurately. In other words, they make mutations all the time and it turns out in the bat these mutations are high the highest rate of mutation occurs in bats and so this one mutated

a the spike protein and that what the coronavirus gets its name from the word crown or coronation. And so the coronavirus has these little spikes that sort of make it appear like a crown. And the spikes are made of this S protein. And the mutation that occurred caused the virus to bind with very high affinity to human receptors, the ACE2 receptor. The ACE2 receptor happens to be on cells that line the respiratory tract, the upper respiratory tract, the lower respiratory tract, and even into the air sacs or the alveoli. And so what's happened is this virus spread very, very quickly. spread very, very quickly. And it became clear as we've studied it that for every one person, if one person is infected on average, they infect 2.2 to 2.5 other individuals. So that's a fairly high R sub zero. For instance, influenza is probably about 1.2. The one that's most infectious is measles, which has a R sub zero of 10. In other words, one person with measles can affect 10 people.

But the problem with the SARS-CoV-2, and when you looked at the sequence, it was closest to SARS, it was closer to SARS than to MERS. And that's how it got the name SARS-CoV-2. When you look at its ability to cause a disease, it's very effective. And what it does is it first enters the upper respiratory tract. It stays there for about two days. Then it spreads down into your bronchi, into your lower respiratory tract, and then into the lungs and into the little air sacs called alveoli. When it gets into the alveoli, it causes inflammation that causes the alveoli to fill up with fluid. And when they fill up with fluid, they can no longer exchange air. And this causes hypoxia or low oxygen levels. Your oxygen in your blood goes down because you can't get the oxygen

from your lungs to your arterioles. And the primary manifestation of this disease is severe hypoxia or low oxygen levels in the arterial blood. So a fantastic description. And you and I talked a little while ago about your experience now clinically with some COVID patients. How is that reinforcing that overall description? What are you seeing and how is that presenting in a way that we can understand it a little bit better? Yes. What usually happens is you breathe in or get on your face, your eyes, the virions, the viral particles from somebody else's droplets as they cough or speak to you. And then they quietly grow in the upper respiratory tract where you do not have symptoms. So in the early phase, there are very few symptoms.

However, when you look at the viral counts, if someone sneezes or coughs, the viral counts are very high. And it turns out in the first five days, the incubation period is about two to five days and can be as long as 14 days. But it's in that early period before you have symptoms or during the early symptoms that you're most infectious. And it's in that first five-day period that most people spread it to others. And so that's the window. Then what happens when it gets down because of the irritation of the bronchi, you get a cough. And it's usually a dry cough.

And it's a persistent cough. And you develop fever. This virus really stimulates the immune system. And that's probably why it causes so much inflammation in the alveoli. So fever is to be expected. A dry cough is almost always present, probably in about 75%. And then other symptoms, severe fatigue, and then muscle aches, and then you may get short of breath. And those that have more severe disease, about 50% of them present with shortness of breath. Those with mild disease, only about 15% present with shortness of breath. And the shortness of breath is because the lungs are no longer able to exchange the oxygen properly.

It's interesting, though, that patients don't feel short of breath until they are very, very seriously ill in most cases. And when you check their oxygen levels for oxygen saturation, it should be 95%, 96%. They're down at 83% and 82%, 85% at the point when they first get symptoms. And this was very surprising because usually when you have any form of pneumonia, you get short of breath far before this development, before you get that hypoxia. And it turns out that the lung compliance, the elasticity of lungs in this particular disease doesn't interfere with elasticity of the lungs early on. And that's one of the major

ways you feel short of breath. The other thing it doesn't do, it doesn't interfere with ventilation so that your carbon dioxide levels do not go up. And that is the other major driver of the sense of shortness of breath. So it really sneaks up on patients. And at the point they get short of breath, they need, most of the time they do need hospitalization. And then what happens is you give them supplemental oxygen and it doesn't, they can't, they initially it works, but as the fluid fills up more and more

then you are forced to intubate them and put a breathing tube down and use a ventilator in order to get enough air in to maintain their oxygen levels and that is the primary cause of death is irreversible hypoxia and inability to ventilate the lungs and get oxygen into the arteries. And as a consequence, patient goes into shock and then dies. Interesting in that way. And I want to ask you quickly about this, you know, the proning studies that are starting to come in evidently around that procedure as well. What is your take on that where the person's face? Yeah, well, what happens is when you lie on your back, and most people when they're on a ventilator lying on their back, it turns out the largest

area of your lungs are in the back in your back area. The lung is smaller is not as long in the front. The diaphragm, it angles down in your back. So when you're lying in your back, you collapse a lot of the alveoli and lung tissue that's in your back area. And therefore, when you've got all this fluid, you want to maximize the healthy alveoli. And a lot of them get compressed by lying in your back. If you lie in your stomach, the smaller part of your lung is compressed and your back, the back region of your lung, the posterior area of the lungs are able to ventilate more effectively.

And we, I have had a patient, actually both patients that were in the ICU, both required proning when they were were in the ICU, both required proning. When they were lying in their back, their oxygen levels were about PO2s of 60. And normal, you would expect a PO2 to be 100 or even higher, 200 with oxygen. Their PO2s were in the 70s. When they lay on their stomach with the same amount or giving the same oxygen supplementation, they would go up to 150 to 200. So it really can make a dramatic difference in the ability

to exchange oxygen. And that's why they do this proning. Thank you. So one thing you and I talked about previously too, was infectious dose and viral load. You told me that was very significant, the amount of virus that is initially onboarded. Yes. We're seeing that some of the most serious cases are in healthcare workers. And when you look at what happened, they were involved in intubations or where they put the tube into the lung or some other respiratory procedure that produced large amounts of virus in the air. We call it aerosolizing. And droplets are large, much greater than 10 microns. They usually drop to the ground and are not directly inhaled most of the time. Well, aerosol are less than 10 microns in diameter and they float in the

air. And therefore you can breathe those in and they can actually go down into the bronchi, into the alveoli, into the lungs very, very quickly, causing much more serious disease. And the larger the amount of the number of viruses that you inhale or get into your posterior pharynx, the more severe the infection is. If you have a tiny exposure, your immune system could actually prevent that from spreading. As you get more and more virus, it overwhelms the immune system, and that's how the virus really takes off. system. And that's how the virus really takes off. So I tell all our healthcare providers that it's very important that they wear the protective gear and the protective masks. And even if they get a few virions, they will only get mild disease. They won't get severe disease. But if they're not being cautious and they're not using their masks, they are at risk of getting a large exposure. And this is true for the public as well.

So if you don't wear a mask and you happen to come in contact with someone who sneezes, you could get a large dose and you could become very seriously ill and need to be placed in the ICU and be on ventilatory support. The other thing I can tell you is from watching these patients, the usual duration of ventilatory support is somewhere between six and 12 days. So you're on a ventilator for a very prolonged time compared to other diseases, infectious diseases that I've encountered. And the course of this illness, patients are usually sick. Even after they get off the ventilator, they feel weak and tired for at least a month. So when you get this infection,

it really wipes you out. So we're hearing a lot about people that are asymptomatic or very mild. And the infectious dose, the dose, the viral load, sounds very critical there, the dose that we onboard right then or over some period of time maybe. But can you describe, if you would, doctor, a little bit about the immune system, the innate and the adaptive immune responses that we all have and what role that plays in whether we get infected or our response to the infection? Well, we don't know. I can say that one of the things we're

seeing is that young people under the age of 10 hardly get any symptoms. Under age 30, no one has died or very one or two people have died, very rare, and they have underlying diseases. So it seems that young people probably, it's really not sure. One of the questions is this ACE2 receptor, whether you get older, you get more ACE2 receptors and therefore the more the virus attaches to people that are older. We don't really understand the differences, but we do know as you get older, your cell media immunity does go down a bit. And that's your lymphocytes and your macrophages may not be as powerful. And that may be part of it.

The other thing we do know for sure is that diseases like diabetes, chronic lung disease, cardiac disease, and hypertension all seem to make it more difficult for individuals to fight off the infection, and they tend to get more severe disease. And then antibodies play somewhat of a role. They're important probably in preventing the virus from attaching to cells because the antibodies usually are directed against the spike protein. Those seem to be the most protective. So if the antibody binds to that spike protein, then it can't bind to a cell and get into a cell. So that's probably how the antibodies work and are protective.

Excellent. I appreciate it. So you've gone through, we've touched on a lot of what the symptoms are and even a little bit about why you might experience or we might experience that. a little bit about why you might experience or we might experience that the the some of the cells are irritated or the um the lung components are irritated that's what's generating the cough and things like that that's very very helpful um i wanted to kind of go into now um what are some of the implications here and and you and i've talked about now under what the retail chains in this case and restaurants and others are trying to do, government offices, universities, everybody is a try and reestablish some sense of normality in public function. So we talked about a logical flow. We understand now a little more and more about what the virus is, what is this, how is it possibly being spread, and how does it affect us individually and as a group in public health. Now, what are the

implications here? And so we want to talk about reducing the likelihood of an individual becoming infected, and that individual infecting others seems to be the bottom line, what are things that we can do in that area to reduce that infection likelihood? Yeah. One other key point that I don't know if I emphasized, that there are a very significant number of individuals who have no symptoms or minimal symptoms. number of individuals who have no symptoms or minimal symptoms. And the younger you are, the more likely you are to be an asymptomatic carrier. The estimates are anywhere from 20 to 60% are asymptomatic carriers, depending on the study. So the worry is someone could innocently

come to work and feel just fine. And they're talking to you and they're spreading the virus to you. And why then you would get very, very sick. What we found actually in Seattle area, Washington State, what happened is it was probably in that area in subclinical disease. In other words, maybe it was mimicking a cold or a regular rhinovirus, or the patients didn't have symptoms at all, but someone with the virus went into a nursing home. And the elderly are much more likely to get sick. And that's when the elderly started getting really sick.

It became very clear that the virus was in the area. And they were very much like a canary in the coal mine. So this worry about asymptomatic carriers makes it very, very difficult. Now, so how can we prevent asymptomatic people from coming to work and infecting others? And I don't have a really good answer right now. One of the possibilities is, well, you would have to do a PCR test of the nasopharynx and prove that they weren't carriers. and prove that they weren't carriers. Now, the problem with that test is it has, and it's not really clear if it's a sampling issue or what point in the illness you catch it,

but when you suddenly discover someone has COVID-19, it turns out that you missed 30% of the cases with the first PCR. So it's only got a sensitivity of about 70%, maybe 80%. Now, if you do two tests, you're likely to exclude most people. Now, so that's the PCR that tells you whether you're carrying the virus right now. The second test is an antibody test. And what happens when you get the virus, and it turns out that it appears that by 14 days, virtually 100% of individuals will have significant IgG levels against the virus. levels against the virus. And that test, now there are at least two really good ELISA tests, one by Abbott and one by Roche. And both those have sensitivities of probably 98% to 99%.

And much better than the PCR. But the problem is in the first 14 days, you won't necessarily detect. It takes 14 days to go up. But after 14 days, it's very sensitive. And also, both tests claim a high specificity, somewhere in the order of 99 to 100% specific, because the epitopes they use, the antigen they use to measure the antibody is actually the single amino acids that were mutated and the spike protein that caused it to be so infectious to humans. So these amino acids are unique to this virus. No other virus has them. And that's why they've been able to get such high, what we call high specificity, high accuracy of the test. would be if someone has a positive antibody test and they haven't been exposed in three or four weeks, they're probably safe. Or maybe you've got to do one PCR to prove, or maybe you've got a positive test and you wait 14 days and then they would no longer be infectious. The experience is that most people carry the virus, live virus, for a maximum of 14 days.

Unfortunately, there's some that go on beyond that. So then the other question is, and this is all hypothetical at this point. I don't think anybody has the two answers because we're still studying it. But then the question comes up, well, this virus does stimulate the immune system. It is very immunogenic. Do asymptomatic carriers actually have a low-grade fever? It's very possible. This is the problem. I actually have an electronic thermometer called Kensa that communicates with my smartphone and then sends my temperature to a central bank. And I'm trying to help do fever weather maps throughout the United States, and I'm contributing to Florida's weather map. United States and I'm contributing to Florida's weather map. But my wife and I both took our temperatures. And every day I take it at 9 a.m. and my temperature is Fahrenheit 97.4 Fahrenheit consistently. My wife's temperature, on the other hand, is 98.3 consistently. So what we do when we define fever, we say anything over 100.4 degrees Fahrenheit

or 37 degrees centigrade is a fever. Now, if I had a 99, I would not be declared as having fever, but that would be a very significant rise in my temperature indicating and there's a potential indicator that I was carrying the COVID-19 that I had COVID-19. So one of the things that I think and this has not been explored is if every employee followed their temperature every single day and determined what their natural set point was and it varies from 97.5 up to about 99 in some people. And if you, if you, then you do your, your regular temperature is always, it will always be the same at the same time of day. If it goes up above that degree, then you, you, you shouldn't come into work. So I think that is another possibility that I think employees

could think about. And another thought, and one of the big problems with any epidemic is where does our right to privacy begin and end? And when does the right and safety of the community trump that right to privacy? I tend to swing on the side of the community. And I am willing to share my privacy for the good of others. But not everyone is. Theoretically, what could happen is everybody could have an electronic thermometer that communicated to a central database for your work. And you could keep a graph of everybody's temperatures. And when the graph went up, then that person, you would, maybe then you would do a PCR for them.

And then if they were positive, obviously they wouldn't come into work. That's another way to do this. So I think there's a lot of creativity and exactly where the ELISA is going to fall into this, the immunoglobulin test. I don't know. But the other key thing, I think, and until we work all this out and can be assured that someone that walks in is not an asymptomatic carrier, it's probably the best course of action is for everyone to wear a mask. If you wear a mask, then if you're infected, you won't spread it to others. And if you're not infected and you're wearing a mask, that further protects you. So that by everybody having a mask, the likelihood

of anybody spreading it to others is dramatically reduced. And if they were to spread it, the severity of the illness would be very mild. The other element that I think employers have to take into consideration is the age and underlying diseases of your employees. If they have a lot of underlying disease, they're at a much greater risk of dying and severe disease. If they are over the age of 60, they've got an increased risk of severity and increased risk of death. So, you know, how maybe they are in a more protected environment. Maybe you encourage them to do more. If their particular task can be done virtually, perhaps they should be doing the virtual task while the younger employees

can afford to be at work. And if they were to get an infection, it probably would be relatively mild. This is a debate that I think is going to come up in the universities. The University of Florida, most of the students are under 30. There are virtually no risk of serious illness. But the professors, many of them are over 50 and 60, they're at risk. So how do you prevent the students from infecting the professors? And these are some of the challenges that we all have to deal with. And as we get more information about how to use the ELISA, as we get more information on how to use temperature, body temperature to decide these things,

I think we're going to have better and better and finer and finer guidelines. And I think we all can help contribute to that information. That's incredible insight. And again, helping us all make sense and start to formulate plans, or at least the outline for a plan. And, you know, I put in my notes too about DARPA that I've had some affiliation with through engineering faculty, but the Defense Advanced Research Project Agency, but some of the work that they are funding and doing with Duke and Mount Sinai and Princeton and so on, but that they've now got tests that are under approval through the review process right now that's supposed to detect it within 24 hours, that there's some initial, I guess, some sort

of immune response before the person starts becoming infectious or at the very, very, very beginning. Any thoughts on something like that that could supplement the PCR or eventually replace if this, in fact, bears out? Yeah. Well, this kind of work has been done since the anthrax episode in 9-11. anthrax episode in 9-11. A number of investigators are trying to look at what the cytokine profile, what happens is when the cytokines go up, you'll see an increase in message RNA, because you have to synthesize that cytokine. And so you can, you can use the PCR to actually quantitate the messages for these various cytokines. And that's a surrogate marker for the actual cytokine levels.

And that would occur before they would actually produce the cytokines. So say that COVID-19 gets into your body, a macrophage detects it, and then it begins to produce these cytokines that stimulate lymphocytes and the immune system to rev up. And if you could pick up that message from the RNA early on in those macrophages, you could actually decide that the infection was starting before it became symptomatic at all. So yes, that definitely could work. And that work has been ongoing for at least a decade. Yeah. Excellent. Because I understand part of that

program, as you mentioned, doctor, is this digit program, which includes gene editing. And eventually, you should detect over 1,000 viral strains and even the origin of some of the strains of the targets, I guess. But we don't know. Is that a week away or is that 10 years away or somewhere in routine, I guess? I don't know. I that that research, it's been on. It's surprising that it hasn't come to fruition because this has been gone. That kind of work has been going on since 2001. So I don't know. The fact that it's taking so long is a little worrisome.

Yes. It's still not ready for prime time after all these years. Yes. It's still not ready for prime time after all these years. There you go. That's well said. And, you know, another angle we saw was development of masks that a person could put on to protect them, but also would sense and I guess do something as part of a testing protocol. You know, we were on our team talking about, well, I guess it would be a smiley or a sad face that would present on the front, but that would render that eventually. But again, are these things, is there reality here? And if so, what's the timeline look like? Yeah. With regards to masks, the other thing I would like to point out is that there's a really nice study in nature medicine that looked at how well a cloth mask actually prevented the droplets and variants from getting out, getting through the mask versus the paper, the disposable surgical masks. And they are virtually equivalent. So one of the problems you get into is supplies and cloth masks. Everybody is making cloth masks and you can buy those through Amazon Marketplace.

There are local people everywhere sewing masks. And it turns out if you have a triple ply cloth and you put a paper dish towel in and there's a little pocket for many of them, that is really just as good as any commercial mask. And they're actually a lot more comfortable. And the other thing is you can wash them and use them over, which I also think is a real plus. So the protective gear is not necessarily expensive, and it can be reusable. And one of the interesting things in Asia, they've been using cloth masks for the last decade. Ever since SARS-1, all of Asia has been concerned and they've been wearing masks in public ever since that time. So that is a tradition there. In fact, I purchased some cloth masks from South Korea. And speaking of that, they had a little, they have different

funny symbols on the front. There's one with a mouth with a zipper on it. You know, so they've actually been used to that. And I think in our own society that this is going to become the norm. It should become the norm. And then we will not have all these devastating infections. That's interesting. Our team's working with Qualtrics and other online systems to do research as we speak on two angles. on two angles. One, you can imagine it's providing cover for criminal offenders,

which is a big part of what we deal with, armed robbers that take advantage of the business or the customers. And so what are other things we could do with AI to maybe recognize or just eyewitness to recognize offenders and deny that anonymity for them? But the other side is the intimidation that, you know, in Asia, as you mentioned,

it's probably more acceptable and it will be here. What's the transition? Should public supermarkets wear green masks and they're less intimidating, but just as protective for the wearer and talk about, we've been looking at FDA's got this CTAP, you know, Coronavirus Treatment Acceleration Program. You know, they're reporting over 70 active therapeutic agent trials underway and other 211 development programs and other things. But what should we look for and look at with some of the therapeutics that people are trying to make available? Yeah, this is a major area of development. And one of the problems is, as I told you, Richard, I'm an associate editor of the Journal of Infectious Diseases. And it turns out when it comes to evaluating reports of various

therapies, that has been invaluable. What happened is there is an online service which allows all potential reports of therapies to be downloaded, even if they haven't been yet peer reviewed or submitted to a journal. And it's called MedRx. And it's actually sponsored by Yale University and the British Medical Journal. And I checked it a week ago. There are on COVID-19 right now, there are 2,300 articles and most of them are related to therapy. And it turns out that particularly the some of the articles on hydroxychloroquine were extremely biased and terribly designed, and the analysis was flawed.

And so hydroxychloroquine was suggested was a miracle drug, and that was picked up in the popular press as well, when in reality, when you looked at the studies, the popular press as well, when in reality, when you looked at the studies, there was virtually no evidence that they were a benefit. And so what's happened, the Infectious Disease Society of America actually reviewed all the therapies, and they used a system that allows very accurate assessment of the evidence called GRADE, G-R-A-D-E. And it looks at bias. It looks at the design of the experiment. It looks at the interpretation of the experiment. And then it concludes, what's the level of evidence that this particular therapy will be a benefit? Well, when they did that with hydroxychloroquine studies, they concluded that

the likelihood that this drug would be a benefit was very low. And that's true of also been true of all the antiretroviral, all the HIV drugs that have been tried. the evidence is very low that they're ever going to be a benefit. The drug that is now looking to be potentially a benefit is remdesivir. Remdesivir is actually an RNA analog that actually gets into the RNA chain and terminates it because it can't be, you can't add to it after it goes on. So it's a chain terminator. And it's been, it was shown to be of some benefit in animal studies with other coronaviruses. And the preliminary study, there's only one good study where any of the data has been released, and that was from the NIH. And they found that it shortened hospitalization by three to four days. Very significant.

And it almost showed a statistically significant reduction in mortality. It went from 11%, I believe, to 6%. But the p-value was 0.056. In order to say it's statistically significant, it's got to be less than 0.05. In other words, only a 5% chance that it's not a benefit. So remdesivir, I think, is promising. There are some preliminary studies on convalescent plasma. That is patients that have had the disease, documented to have the disease, and then they do an ELISA test and show the elevation and immunoglobulins. And it's been discovered that peak value for IgG is usually at about 24 to 28 days is when you'll get your peak titer. So patients that have had the disease that are no longer infectious have a positive IgG

at about 28 days, they're actually harvesting their plasma and giving it to patients. And and giving it to patients. And again, there are no controlled trials yet, but there are anecdotal cases. There are six cases of which four dramatically improved. And I personally have taken care of two very, very sick patients who we gave a convalescent plasma. And in both cases, day two, their lymphocyte counts, which had been very, very low, and the lymphocytes are very important for fighting the virus, more than doubled after this. And both patients have turned around. One is now off the respirator and the other is about to be weaned. So, you know, a series of two, but I'm hoping that there will be a you know, a series of two, but I'm hoping that there will be a randomized controlled trial for convalescent plasma because I do think it's probably a benefit. So far, those are the only

two. There have been studies of monoclonal antibodies directed against cytokines because when the patient gets very, very ill, the amount of cytokine release is huge. This leads to a sepsis-like syndrome. The patient goes into shock, has high fevers. There's a acute phase marker called C-reactive protein that just goes off the map. Other indicators of inflammation go way, way up. And that's when these patients get very, very sick. And the hope is that some of these monoclonals, in particular one against IL-6, may be a benefit. However, we've actually been doing, there was a randomized clinical control trial, a UF, and the preliminary data did not, for milder disease, did not look promising. It's possibly helpful in more severe disease, but that study is still ongoing. So at this point, the IL-6 inhibitors are a possible benefit, but it's not proven.

So that's basically it for therapies at this juncture. And so the primary care is supportive care, giving the patient time to fight the virus themselves and to recover their ability to exchange oxygen. And that could usually will take being on a respirator for seven to 10 days for those that are severely ill. So all very helpful as we build our case here now. Vaccines, I think for just if we just spend one, you know, one to two minutes, we understand there are different types of vaccines, all different approaches. There could be anywhere from 50 to 150 or more at various development levels, and who knows. But any discussion around vaccines, what that might look like? we have right now is in Florida, the number of individuals who have been infected and have

immunity is estimated to be 2.5%. So that means a huge naive population that so the if the virus gets out again, it spreads like wildfire, and we're going to have to do shelter in place. And that's why we need to use the mask. That's why we need to stay six feet apart. That's why we shouldn't be in any crowds at all. And we have to use these methods because we don't have a vaccine. If we had a vaccine, then we would generate protective antibodies and we could stop all these methods that were required. So a vaccine is critical for changing how we deal with our lives and the social distancing. We can only go back to normal after a vaccine. Now, the vaccines that, the primary vaccines, in my understanding, are directed against the specific amino acids in the S protein that are responsible for causing the high affinity binding to our respiratory epithelial cells, the ACE2 receptors. receptors. And I understand the one from Oxford is looking very promising and actually was protective in primates, which is very encouraging. And they moved on to the trials. The problem is trials take a long time. And there is a worry that if you get sometimes what can happen with an antibody is it can have the opposite effect.

It can create so severe inflammation that the vaccine will actually exacerbate the disease and make it worse. And that's happened with dengue. The vaccines for dengue have not worked because they've actually potentiated the immune response in such a way that it makes the patients ill, more ill, sicker. So, you know, we don't know yet whether any of these vaccines will do that. And that's one of the keys before we can release a vaccine, we have to be sure it's not going to do harm, that it is going to be. And then the second thing is, not going to do harm, that it is going to be. And then the second thing is, was there that, does it generate high enough titers, that is levels of immunoglobulin high enough that they'll be protective? Will there, you have to, often you give these protein vaccines an adjuvant. It's

something that further stimulates the immune system. And there are all kinds of different adjuvants, different oils and other preparations that help encourage the immune system to direct antibodies and cell-made immunity toward the vaccine. There are many, there are all kinds of trials that need to be done to decide which adjuvant's best. So, you know, a year is the minimum I can imagine. And I think 18 months is more realistic. So don't count on a vaccine right away. All right. So let's now go to and we'll finish up here with, from listening to you, we're talking about reducing human-to-human exposure. And that means, are there ways that we can better screen staff, delivery, or maintenance people into these more confined spaces, whether it's a store or a restaurant or an elevator or an office?

store or a restaurant or an elevator or an office, and then reducing then those that are in there. We don't know they're sick or they've gotten past the screen for whatever reason. Of course, we're not talking about screening shoppers in, for instance, in the first place. So now how to reduce airborne exposure. And you've talked about that separation, that distancing, just so we're not literally hosing the person down, exposing them in that way. We've talked a little bit about, you've mentioned before, you didn't use this term, but what you're aiming your mouth at, and again, it's not a rifle shot, it's more maybe more of a shotgun blast. But if you're talking to somebody and you're maintaining a distance, should you also aim your mouths in different directions and stand at right angles or obliquely?

Does that make sense as well? Yeah, that would. If you if you look at there are there everybody's doing these photographs of people sneezing and droplets and showing how, you know, using special lighting, showing these massive droplets shooting straight out of your mouth. So whatever direction you're facing is where those droplets will go. So theoretically, if you were to face a different direction, the predominance, most of the droplets would not go toward that person. I personally like the idea of the masks more because you they would still have eye-to-eye contact if you're talking to someone you're not even looking in their eyes uh you know i i don't know i think that's a little difficult and maybe uh virtual would be better i mean theoretically you could be talking uh someone could be in the same office and you could talk to them through your iPad

and they could actually hear you. And then you could see them, their eyes and their expressions more clearly without having to get too close to them. So I don't know. I think there's the best approach here will take time. And, you know, it would be nice to look, you know, it is safer to look away from somebody, but, you know, it's not a good communication style. No, it comes off as a little strange, but I think like with our research team, we're getting back in the labs and reestablishing our capability to support on all these things that are happening. And as you can imagine, crime hasn't gone away, and the offenders are adapting as do viruses. So what we're doing is, but what we're requiring all the above, we're wearing masks,

we're maintaining that physical distance, and then we're also standing at oblique angles. So yeah, it's got to look bizarre to somebody in the, that came through a time machine, but, uh, but we're trying to use all of the tactics that you're talking about and training us on. So. I know one of the things, you know, I, uh, in 2010, I spent a year at Harvard business school in this fellowship and I was so impressed with the business people. They are so good

interpersonally. And they look you in the eyes and they're close to you and they show great interest. And the irony is those very skills that make for highly successful business people are very dangerous during this epidemic. Yeah. How do you de-emphasize that closeness, that handshaking, that putting your hand on the shoulder, that squaring up, you know? Yeah. Look, I mean, that's what you were taught. That's what you're taught. Absolutely.

And you can see their success through your career as you develop those interpersonal skills. You can tell people, you know, and that's what you teach them, right? Exactly. That's what you're supposed to do normally yeah and like my dad and all they were trained to go in there get the facts and get do your diagnostics and get out of there but yeah physicians are notorious for just give me the facts that's right give me the facts don't fly airplanes and whatever all right don't be ahead of an

investment group i think the next part you've talked about, while probably the evidence just seems to support that mostly the virus is spread through the air, but also through surfaces. Can you spend a minute on surfaces and maybe what we can do to better clean horizontal and vertical surfaces? We got a lot of buttons and cash registers and shelves and packaging and things that are going on in the retail environment. Right. Yeah, this is very important. The good news about the coronavirus is it's very susceptible to any, virtually most, probably all commercial cleaning solutions. It's not a very hardy, it doesn't stand up to

soap at all. It's a pretty fragile. And so if you wash with soap and water, it's for 20 seconds, it will be completely eliminated. And alcohol solutions over, I think it's 60% kill it on the spot. And any of the other Lysol and other cleaning solutions also will kill it. So frequent wiping down will get rid of the problem is when you cough or talk, droplets do land on surfaces. And we know this particular virus can survive up to three days on stainless steel and hard plastic on cardboard about 24 hours on other surfaces for shorter periods of time so like the nice thing is if you use a cleaning solution you eradicate it completely now what has to happen is you have to touch that surface and then you have to touch your mouth

your nose or your eyes to actually get it to uh actually infect you infect you how much that's happening i really don't have good studies to to prove how often this is happening compared to droplets i think drop you know droplets where you're coughing and it's landing on your facial area. I think that coughing is the higher likelihood in most cases, but I think it's very important to clean all surfaces. Well, we've learned from you that it's not just that there's a dose, but the more significant the dose, and that's through proximity, it sounds like, and duration and things like that. And then how sick the patient, how much they're projecting and so on.

So those are good things. And I know that in our lab, we've got UVA and B lights that we're working on to help deter intravenous drug abuse in the restaurants because of certain problems there. But we don't have the C yet, but we're getting that from another source to, is that affected? Now, we'll be working with engineers and those over in medicine to look at UVC, but they even have a passive infrared little sensor. So if now a person comes up, because you don't want to expose a human's eyes and so on to uvc evidently so that it would go off though so you might have that sort of thing over shopping carts or over certain areas that may be useful but would switch off when a human comes nearby so um they're looking at gas or you know ways they can spray or put fumes because all this packaging's around.

And the retail stores, as you know, people return not just consumable items, but products. And so now you've got employees that are going to have to handle those products and packages and things. So we need science and understanding the transfer of the virus, but also better and better evidence around what we do about it.

Right. Yeah. The packaging, the question is how many, I guess if someone coughs directly on the packaging, you would have a high dose. But if they're just have a few virus virions on their hands and then they put it on, I think the number would be so low that I can't imagine that's going to be a big issue. I haven't been that paranoid about wiping every single thing that comes from commercial. I know some people are doing that, but I think that's a relatively low yield effort. And I'm not sure that spending huge amounts of time wiping down packages is the best way to spend resources. Okay. No, that's good. And that's hopeful. So we've talked a lot about mapping using the Kinsa and other technologies. I know they're mapping now. There's discussions with the EPA and

the FDA and everybody about human waste, that that may be a detection. Any way to understand, as you mentioned, or describe weather mapping and understand the patterns and movements and directions like we do with organized or semi-organized criminal groups. We're trying to get an idea of where they're hitting, what direction they're going, and how frequently. groups. We're trying to get an idea of where they're hitting, what direction they're going, how frequently, a lot of parallels. Yeah, the smartphone, I really like the, I know South Korea started to use smartphone apps, or where, you know, you declare on your phone that you have been infected, and then others, it helps them stay away from you. And I think that that, and the other thing that was what we're going to try to do is we're going to

try to identify the diagnosed, those that are infected and then do case finding to identify everybody that was in contact with them. And the smartphone would be a great way to prove who was in contact with somebody and that those two phones came close together. And that's very technologically possible and be very simple, because one of the problems is you talk to someone who's done case finding. It's very exhausting. You've got to call up all these people and ask them how close they were to the individual. And if they weren't, if they were farther than six feet, you don't worry. But if they came up close, then how long were they talking with them? All of these, this data,

and that could all be analyzed from iPhone data. So I think there's a huge, that's a huge area that has real potential. Well, that's fantastic. And obviously, the other basics in metering the amount of people in a given space. I know here in Alachua County, Florida, they're adopting some of Dade County, Florida's. But in this case, one person per 500 square feet. They do the math. They meter people in one in, one out, and things like that. So we're dealing too with now buy online and pick up in store, buy online and return in store was a

growing component of multi-channel retailing. Well, now it's exploded for obvious reasons. It may be the only way to do business right now, but of course, it's going to train people to have that. So we're working on de-conflicting two two ton automobiles from humans that are going to be moving in and out as well as the as the flow eventually starts to rise over the next months and years. So a lot to work on a lot to think about. We're putting up these sanitary stations to encourage more soap hand wash, you know, proper hand hygiene with, you know, the alcohol based as well as soap so um anything else we need to go to note to doctor as far as uh reopening uh safely reopening um and going back to work well two other things that i heard about uh actually in publics um use of plastic shields across the counters, I think, and for desks, if you have a plastic shield so that, you know, if someone's sitting in another desk, that would be a helpful barrier for droplets. And then the other thing is everybody walking in one direction in aisles. We actually are talking about this i'm talking to the performing arts center about you know how if they can still have concerts and one of the issues will be you can't have people want walking separate directions because they will face each

other for a significant period of time so you have have to have one way, everybody has to go one way. And I think those are traffic design to reduce face-to-face interactions when unintentional is another very helpful approach for preventing infection. Now, that's really interesting. And that feeds into some of the things we're doing with We Did Matterport. If you go online and look at, you can look through apartments or houses that you might be looking for in real estate websites. And of course we did, we're now able right now to walk and talk through some of the things you talked about. All right, how can we mark separation, marking in one-way aisles and accommodate this in sanitary stations or hand hygiene stations and things like that? So we're still able to conduct some of our research in that way virtually. But the shields was another one. They're coming to us asking about, wait, what should a shield, how high, how wide?

Should it be curvilinear versus straight? Those are things that are not our area of expertise, obviously. So we're going to be teaming up with colleagues like you. We're going to be teaming up with colleagues like you. There's one other concern, and that is actually the exchange rate of air in a closed space. And on average, my understanding, I was talking to an anesthesiologist about this. Usually the volume of air in a room exchanges three times an hour, which is pretty slow. What you'd like is a more rapid exchange. For instance, in ORs, they try to do a much more frequent exchange of air so that droplets, if droplets are there, they're diluted out and fed out of the room more quickly. And so another possible area for improvement is increasing

airflow in any closed space. That would be protective and reduce the likelihood of a large dose of aerosol. Fantastic. So we'll end on that note, Dr. Cuthwick. I really, really, really appreciate your time. And you can tell that your years of accumulated experience and knowledge and expertise are helping in law enforcement agencies and academics worldwide, as well as practitioners, we would call them in loss prevention or asset protection. So I want to wish you, I want to tell you thanks again. I want to wish you and your loved ones a safe and secure experience as we go through this. And if anything else comes up, you think of it, please email or call at your convenience and let's chat because you can tell that, you know, the people that we work with are really trying to do things the right way. Right. We're all in this together. And the more careful we can be and the few people that become infected, the better. And one of the big fears as a healthcare provider is we don't want, we want to keep that curve flat. We don't want a big peak because it'll

overwhelm our ability to care for patients. So we're all in this together and I want to help everyone eliminate as many infections as possible. So I thank you for allowing me to be on and share my thoughts on this issue. Fantastic. I want to thank all our listeners for joining us today on another episode of LPRC and the University of Florida's Crime Science, the podcast. We also wish you a safe and productive experience. Thank you for tuning in. Thanks for listening to the Crime Science Podcast presented by the Loss Prevention Research Council a safe and productive experience. Thank you for tuning in. is not a substitute for legal, financial, or other advice. Views expressed by guests of the Crime Science Podcast are those of the authors and do not reflect the opinions or positions of the Office of Prevention Research Council.