This Week in Virology
Host: Vincent Racaniello
Guest: Daniel Griffin
Aired 18 October 2020
Vincent Racaniello: This Week in Virology, the podcast about viruses, the kind that make you sick.
VR: From MicrobeTV, this is TWiV, This Week in Virology, Episode 673, recorded on October 16th 2020. I’m Vincent Racaniello, and you’re listening to the podcast all about viruses. Joining me today from New York, Daniel Griffin.
Daniel Griffin: Hello, everyone.
VR: Boy, the weeks go by, don’t they, Daniel?
DG: It’s actually amazing. It’s amazing how quickly you and I – I sign off with you and then boom, it seems like there’s so much that immediately happens and we’re back here again.
VR: Looks to me, Daniel, that case numbers are going up not only in the U.S., but globally.
DG: I was joking with the people in the ICU today that the Europeans are trying to beat us, apparently they’ve got – We’re not going to let the French do it this time, nor the Italians. No, it’s really unfortunate. It’s a pit in my stomach when I hear the numbers and then I actually see them first-hand. We have well over 100 admissions at the Northwell hospitals now. The numbers are rising. They’re rising in Europe, they’re slightly ahead of us as they were the last time, but we were the ones who were on our way up. Everyone else was getting it under control, but now they’re just like us. They’re having that same trajectory and they’re even a little ahead of us.
VR: Do you think it’s a combination of back to school, cooler weather, and complacency as far as face masking and distancing is involved?
DG: I think these are interesting comments. When we talk about back to school – My wife brings this up quite a bit. The schools themselves have tried to do certain things along the lines of separating the desks and masks and so I don’t know how much transmission necessarily goes on within the school. When you have returned to school, it sends a message to the community and I’m going to share one of these stories, but they start having birthday parties, they start having get-togethers. “Oh let’s get everyone in the class together.” Then those extra-curricular activities that really are triggered by the message that, to be honest, that the schools are sending, that’s where we’re seeing the cases.
We’ll discuss a couple of cases we dealt with this week where birthday parties, weddings, all these gatherings. Yes, I do think it’s the school reopenings. They talk about, “We’re not having transmission within our walls so we don’t need to test.” That’s, I think, irresponsible. You’re part of a community, schools. [chuckles] Just because it doesn’t happen within your walls, the fact that that sets up a societal expectation, a societal view of what’s permissible because this signal that they’re getting. Then you look around, people are done with the virus, the virus isn’t done with us.
People are relaxing, they’re not wearing masks. They’re getting together and having dinner with people they haven’t seen in a while. This is a problem. My wife was just telling me close friends of ours that we haven’t spent a lot of time with recently, were just about to have drinks tonight but then they found out that those people they’re about to have drinks with apparently are PCR positive. It’s just – Yes.
VR: Let’s get right into your COVID-19 report.
DG: Let me start with my quotation. “In a dark place we find ourselves, and a little more knowledge lights our way.” This is Yoda, I don’t know if people have ever watched Star Wars or heard – It’s a George Lucas film. It was popular. I like to feel like this is a place where people can come and as dark as it gets at times, as dark as I feel it’s becoming as we see these rising numbers, hopefully this is a place where we can share a bit of the knowledge and also hopefully I can give that optimistic spin that we are learning things. We are moving forward.
Let me start with our patient updates, people always like to hear a little bit about that. This will be the good, the bad, and I’m going to leave out the ugly. The good news, a lady who contracted COVID from her daughter is waiting to go home. She made it through. She had her first PCR negative today, and then hopefully tomorrow after 9:00am comes, one of the hospitals I’m working with. She’s like, “She’s negative.” I’m like, “No, no we need a second,” [chuckles] because she’s going to go to a Skilled Rehabilitation Center, and we’re really careful to protect those individuals. She needs a second. It needs to be a little more than 24 hours apart.
That’s great, but then I had another patient and this was, as mentioned, the party. Her 10-year-old grandson was having a birthday party, because it’s all good, we’re back at school. She went to that birthday party. No one wore masks. He’s 10-years-old. None of the kids were wearing masks. None of the grown-ups were wearing masks. A couple days later, I want everyone to think about the timing. So the birthday party is on Sunday, about three days later she sees her primary doc who says, “You went to a party. Let’s get a test.”
The test is negative, we can wipe our brow, we missed that bullet. Four days later, she starts feeling sick. How can that happen? As we know, a negative test predicts the future now. She was still in the [chuckles] incubation period. Then she has her positive test and I’m now taking care of her in the hospital. She’s a woman in her 80s and we’ll see how she does.
VR: This could be a superspreader event. She’s not going to be the only one infected.
DG: Yes, that’s why we worry and we just had another nice birthday party here in my local area, and this was older brother had a fever, so they sent off one of these PCRs, it didn’t go through our system so, apparently, there was a several day delay. The test was done on Thursday, they got the results Sunday afternoon about an hour after the younger brother’s 20-child birthday party. [chuckles] It rained, unfortunately it rained and so that child then actually was then tested. Turns out the younger brother also is positive, and he just had a birthday party.
Since it rained, the 20 other children, all the parents, everyone crowded inside the house for that birthday party. You cringe and I cringe too. I think there’s a couple lessons here. One is, I know it’s raining, I know it’s a birthday party, but tragedy when this grandmother is now in the hospital. Just think about all those kids and all the parents and the people that they might get exposed to. That’s our updates on some patients, but now let’s hit some news. I don’t know if anyone heard, but the President is now not infectious and he is immune. [crosstalk]
VR: I was going to ask you about that, Daniel. [chuckles]
DG: Let’s just hit both topics. Let’s talk about infectious, and you’re going to enjoy this. There were a couple things that came out that were the basis for the President is not infectious, and they told us there’s several reasons why people believe that’s true. I’m going to weigh in on that here. One was, they said, “Oh, it’s more than 10 days into the course of his illness.” We now know that he was sick for a little longer than we were initially led to believe.
We were also told that he had two negative rapid antigen tests using the BD Veritor System. Just to give people a sense, the rapid antigen tests turn positive when an RNA copy is 50,000. RNA copy number is 50,000 or higher. That’s going to be about or equivalent to a CT Value of 30. We were told he seemed to have a level below that. We were also told that this was consistent with his RNA, PCR, CT Value. This is what I’m going to say was somewhat entertaining. I was actually having a discussion with Apoorva Mandavilli, she’s one of the New York Times reporters, journalists. Actually quite a bit of a star. She was the 2019 winner of the Victor Cohn Prize for Excellence in Medical Science Reporting.
VR: I sent her your way, Daniel.
DG: Oh, okay, great. [chuckles] Actually and thank you. It was very entertaining to talk to her. I’m talking to her, she published an article back in August, “Your Coronavirus Test Is Positive. Maybe It Shouldn’t Be.” I’m having this conversation with her about this issue and I say, they told us that the CT value is consistent with him being non-infectious. I said, “But we haven’t been told the CT value, and I would love to know the CT value.” She says, “Oh, you know, I know the CT value. I just got off the phone with Anthony Fauci, and he told me.” [chuckles] I was like, “Okay, I would love to know what that was.” She shared it with me and apparently, the CT value was 34.3.
Two things, one is, Anthony Fauci can actually get those CT values, unlike me. If you look at a CT value of 34.3, that really means you have an RNA copy number of less than 4,000. On the TWiV, when Anthony Fauci was on, and he was asked this question, he said, “Anyone below 35, or I should say a number higher than 35, a CT value showing an RNA copy number of less than that, they’re not infectious. 34.3, that’s – we’re rounding up a little, but it’s true.”
I would say that when you look at the combination of a negative antigen test, so less than 50,000, a CT value on your PCR of 34.3, that’s down at about 3,000, I’m going to say. The fact that they tried to do the viral culture, and couldn’t do it. They did it in the BSL-3, and anyone who works in the BSL-3 knows what they’re doing, and these are well-trained individuals. I think everything put together, it’s reasonable to agree that he has passed that infectious zone. Actually, hopefully, it’s a learning experience for people. They’re going to hopefully start sharing these CT values so we can do similar things.
The woman that I’m now requiring to have two completely negative PCRs. It might be fine to say two negative PCRs but we’re going to shift that cut-off to 34 cycles, something like that.
VR: Okay, but Daniel, is he immune?
DG: That is the second and that is actually the most interesting. Again, thank you for sending Apoorva my way because she knew stuff that actually takes me about a day to get. Let’s go here. A couple of issues. First, just thinking this through, considering the President got Remdesivir. He got the two monoclonal antibodies, which if people want to learn more about the Regeneron products, listen to the most recent TWiV where this is really discussed in depth.
He gets Remdesivir, monoclonal antibodies, and then he gets steroids. His response to the natural infection was blunted, so he did. Then, Apoorva tells me, because she’s all-knowing, apparently, when he got the Regeneron product, he had none of his own antibodies at that time, so he was serology – They really gave him these products before he had a chance to start mounting his own antibody response.
He may not develop his own robust natural response to the infection, which in a sense is good, because a lot of the problems we run into with COVID-19 is not the virus, it’s the immune response. They’ve blunted that, meaning, he probably is not immune. Now, the antibodies he got, they have a certain half-life. While they’re at a high level, and I think Apoorva did a good job of pointing out like, well, 10% of all the immunoglobulin in his body are these monoclonals. He is temporarily probably protected, but these have a half-life.
The half-life ranges from, again, Apoorva knew the half-life of all the antibodies, and I’ve been working with Lily a little bit, and it took me a day to find out the half-life of their different monoclonals. Anywhere between 20 and 27 days for the different monoclonals that are being studied by the different companies. 20 days from now, he’s at half that level, another 20 days, he’s down to a quarter. Each 20 days, he’s dropping his level of immunity, unlike a natural infection, which we think may give you immunity for longer than these 20-day drop cycles.
VR: Okay, so he’s not immune.
DG: [chuckles] He is not immune. He is temporarily protected, it seems, from the antibodies he got, but we may have actually prevented him from developing natural immunity.
VR: Daniel, maybe he got a vaccine.
DG: [laughs] Of this, I don’t think we have any knowledge.
VR: He did get things that a few others are getting, so who knows.
DG: That’s true, but that also brings us to the other interesting topic that was discussed most recently on TWiV, is, “Even if you get a natural infection and it’s not blunted, can you get reinfected?” If you get reinfected, is that second infection mild or perhaps worse than the first infection? Lancet Infectious Diseases just published, “Genomic evidence for reinfection with SARS-CoV-2,” case study. Actually, I got an email from a buddy of mine, Bill Tams, who’s a retired physician over in England that actually worked in Bududa in Uganda. Apparently, this got people in the UK talking about this issue too.
The first infection, this case was documented with a positive PCR, April 18th, but then a second test on June 5th, with a genetically different variant was documented. This was 48 days later. I did the math here. I looked at a calendar, something like that. The first infection was mild, but the second infection was severe. I think it was Kathy who pointed out, of the four documented infections so far, half of them were worse the second time. Our statisticians will kill me if I say 50% were worse the second time, but I’m not extrapolating.
VR: Those are not numbers you want to hang your hat on, right?
DG: Yes, an ‘n’ of four, and I’m going to predict the future. This is a little bit – Is the President immune? Am I going to hang my hat on that? Should he stop wearing a mask and not worry about it? Do people around him don’t have to wear a mask anymore because now he’s immune? No, continue to take the virus seriously. Let’s see what else I have to say here. There was another sobering report. This was from the Netherlands, which was, at this point, it’s not peer-reviewed, but it was, “Reinfection of SARS-CoV-2 in an immunocompromised patient,” a case report.
Here, the woman was reinfected, actually, she died the second time, which is worse than what happened the first time. This was 59 days after the first infection, she did have underlying issues. She had Waldenstrom’s, which is an issue with B cells, so she wasn’t a completely healthy person. [crosstalk]
VR: That would be a good candidate for monoclonal therapy, right?
DG: Perfect candidate. With Waldenstrom’s, we actually use a therapy that depletes the B cells. Here’s someone who doesn’t have the ability to make her own antibodies, perfect candidate to be given the passive immunization or the passive vaccination, however, we want to word that. I’m thinking we should word it immunization because we have anti-vaxxers, but we don’t have anyone who’s anti-immunization.
VR: All right, good.
DG: Let’s see. The next thing I’m going to talk about is just to give people a sense of – A lot of people are talking about, well, you know what, it looks worse in the U.S. because we’re testing so much. That’s why it looks like we have so many cases. There’s one thing that testing doesn’t really get rid of or make happen and that’s mortality. There was a research letter published in JAMA, “COVID-19 and Excess All-Cause Mortality in the U.S. and 18 Comparison Countries.”
Early on, in the start of the pandemic, there was a pretty high mortality, really, everywhere. A lot of people got it under control. They do COVID-19 deaths per 100,000. On the start of the pandemic, we had 60 per 100,000, Belgium was struggling with 86.8, the UK at 62.6. Since May 10, once we started to get things and then they even go out to since June 7th, what has the rate been per 100,000 and who are the outliers? The U.S. is at 27.2 per 100,000, Sweden is 10.3, where Italy is down at 3, France is down at 3.2.
Since we’ve known that this is going on, there’s been a high mortality hike, and this is not testing, testing doesn’t make people die of COVID-19. Testing, actually, I’m going to argue, is going to keep people from dying from COVID-19. There was a bit of a shout out for this calculator that we developed that actually people can go to Parasites Without Borders to the COVID-19 update part of our webpage, and actually they can go and they can look at how you can use different testing strategies to prevent infections. We finally got our paper out there and yes, I did. It’s on a preprint server. I was involved in the discussion, but it was not really ideal at the end but I went along with it.
Identifying optimal COVID-19 testing strategies for schools and businesses, balancing testing frequency, individual test technology and cost. Michael Mina’s website, rapidtests.org, has a link to it as well. Hopefully, we’re giving people information to help guide them so they can use testing to prevent infections, prevent deaths. An update on treatments. A couple of things came out. We got finally the final report for, “Remdesivir for Treatment of COVID-19.” This was published in The New England Journal of Medicine. We really saw very similar results compared to the preliminary report, but now we have follow-up out to 29 days.
There was a statistically-significant shortening of hospital stay. A trend towards lower mortality, but not reaching statistical significance despite enrolling over a thousand patients and follow-up. It’s open access so people who are not driving or maybe can put this later to do. Go ahead and take a look at the article and look closely at figure two and three. Just figuring out who are candidates for Remdesivir, who gets the benefit? It appears that the therapy is most helpful for patients under the age of 40. Interesting, right? Patients with less than 10 days of symptoms prior to receiving drug. That goes along with our phases that we’ve discussed. Patients receiving oxygen.
It really doesn’t look helpful if you wait until someone is sick enough to be on a mechanical ventilator. Again, that’s a timing issue. Most of those people are past the 10 days later stage. You’ve missed your viral window. More evidence that understanding the disease and phases is critical. “Effect of Hydroxychloroquine in Hospitalized Patients With COVID-19,” in the same New England Journal of Medicine. We finally get the data. We get to see the final HCQ data from the recovery trial. Now they’ve looked at almost 5,000 patients. Just to sum it up, no benefit was seen. Actually, there was a trend toward a higher risk of death within 28 days in the HCQ group.
Mortality was about 2% higher. P-value didn’t reach statistical significance 0.15. Then they went through looking at all kinds of subgroups and consistent results seen in all pre-specified subgroups. The results suggest that patients in the HCQ group were less likely to be discharged from the hospital alive within 28 days. Among the patients who did undergo mechanical ventilation, those in the HCQ group had a higher frequency of either ending up on a vent or dying. Just some really solid, large, prospective data to say, “Please don’t give our patients HCQ.”
All right. Vaccines, and I’m actually going to talk about active and passive vaccines here. The J&J vaccine trial was paused and most of us are saying this is a good thing and everyone says, “What are you talking about?” It just basically shows that things are being done properly, things are being done safely. This is the biggest of all the vaccine trials. We still don’t have any information on specifically what illness was detected in the one individual, but the fact that it’s not just pushing through, we’re waiting to find out what the story is there.
I think it’s encouraging to know that this commitment to safety is there so that when the vaccines are released, we’re going to have safe, effective vaccines, we’re not going to have something rushed to market. The second is the Eli Lilly trial that was paused. This I think is interesting. There are several Eli Lilly trials being done and these are the monoclonal antibody trials. This is giving someone the antibodies and there is again a timing issue here. In the animal study that was discussed in the most recent TWiV, you try to give these antibodies as early as possible in the human trials, which are being done. We try to give them within three days of a positive PCR.
Actually, Steve Catani and I were involved talking to Regeneron as early as April about, “Let’s not use these in hospitalized patients on ventilators. It makes no sense. Let’s get these done in the outpatient setting.” There was the situation where they were still running a trial giving the monoclonal antibodies to hospitalized patients on ventilators, severe disease. That was paused. I think they should just pause it from a philosophical understanding of disease point. Not an issue.
VR: What day of disease did the President receive his monoclonals? Do we know now?
DG: During the clock, we think it was day six.
VR: Okay. That’s early enough. He had just had some breathing difficulties, so still early enough to catch the viral phase, right?
DG: Yes. It’s early enough and actually the Regeneron data that was shared at the shareholders meeting, [chuckles] one day it’ll end up in – If you basically look at people who have yet to mount their own antibody response who are within 10 days, these are the people that do well. He was, we think, day six, is what we’re getting a sense. We think day six. We think prior to him making his own antibodies. Yes, the timing was ideal. We think if you can get it in in the right window, you’re going to maybe 70%, 80% of the time keep people from progressing.
I think that’s optimistic and positive things. Then understanding the tail of COVID-19. Brain fog was getting a little bit more press recently. It was interesting that actually we’re publicizing an article that had been published before. This was an article, “Post-discharge persistent symptoms and health-related quality of life after hospitalization for COVID-19.” This was published in the Journal of Infection. In here, they looked at over 100 patients. Followed them out for 100-plus days. 34% were reporting loss of memory. 28% were reporting issues with concentration.
Interesting also, they looked at whether or not you were in the ICU or just general medical ward. No difference. It looks like this is really a COVID-19 complication. I’m going to just finish there. I think we kept this on target and within our 30 minute, what I try to go for. Before we do some emails, I want to thank everyone who’s been going to Parasites Without Borders and helping support our MicrobeTV fundraiser these two months. That’s been tremendous. I try to do a lot to create content. MicrobeTV has really been a wonderful platform for getting us this information out to everyone. Thank you to everyone supporting us and thank you to Vincent and the team.
VR: Thank you and thank all the donors. It’s great. All right, we have a couple of emails. My friend Cliff, he’s a college friend of mine who I’ve kept in touch with. He writes a blurb today in my local paper suggests that according to CDC guidelines, persons with severe cases of COVID-19 ought to isolate for 20 days. Over the past few podcasts, Daniel Griffin suggests, as I recall, that SARS-CoV-2 positive patients are recommended to isolate for 10 days from the first positive test and hospitalized patients require two PCR negative tests before release. Would it be possible to ask him to clarify? Like many people, I don’t know what protocols are true or false.
DG: Okay, let me definitely clarify this because there are two guidelines. These are on the CDC website. These have evolved over time. People who have mild disease; these are people who never end up in the hospital, never require oxygen, people who get better on their own. There’s good data based upon viral culture data, based upon CT values that correlate with levels of virus. 10 days. Isolation for 10 days for mild outpatient.
There’s a second group of patients. These are patients who have severe disease. Patients who have issues with their immune system. That population you can continue to isolate a virus, continue to culture a virus. You can continue to have elevated CT values and high viral RNA levels out to 19 days, which is why we have 20 for them. There’s two different rules. 10 for your mild, 20 for your severe.
This is actually why the President’s story was a little bit of a mishmash. He had severe COVID. He ended up on oxygen. He ended up on steroids. He ended up in the hospital. He would have been 20 days if you used just a timetable approach, but if you went ahead and looked at viral RNA levels, he was below that level as an individual. Those are the two rules. 10 days for mild, 20 days. Then remember the third, the quarantine. If you’ve been exposed, there’s an incubation period. That’s 14. Isolate for the infected, quarantine for the exposed.
VR: Okay. Christine writes, “Dear TWiV and Dr. Griffin, I recently dealt with my family’s first bout of cold symptoms in a pandemic. I wanted to share the experience to get the perspective of Dr. Griffin on two key questions. Should I have sent my kids to school and how does the common cold spread so easily?” Christine is from a small town in northeastern Connecticut.
Low prevalence since March 27th cases, population 4,200. Public school is preschool through 8th grade, 400 students, open full-time, masks, partitions, distancing, windows, fans, etc. She has two children who woke up on Sunday with congestion. Pediatrician did not recommend a COVID test after describing the symptoms. Daughter recalled that a classmate had been sick, that child had a fever so the doctor recommended PCR.
Her kids got better within 48 hours, due to return to school. Nurse said they don’t need a negative COVID test. She sent her kids to school, husband stayed home with a tougher bout of the cold. My question is, “Should I have sent my kids to school without a negative COVID test? My daughter’s classmate eventually tested negative. Results took four days to come back, should I have had my kids tested and isolated as a family as we awaited results that could have taken four days? That’s the first question.”
DG: This is an excellent question. We’re going to be seeing a lot of this so, hopefully, I can give some guidance here. This is why I spend a lot of time trying to educate clinicians and why we do this first part. It is tough to make a distinction here between COVID or not. COVID tends not to present with a stuffy nose, which is interesting. What you’re describing here I think that a pediatrician could potentially make a distinction and say, “When you lose your smell with COVID, it’s not because you’re congested, it’s actually because there’s actually a direct viral impact on the cells that are involved in smelling.” Basically, the supporting cells.
It’s interesting. COVID doesn’t make you sneeze. That’s about the only thing it doesn’t make you do. It tends not to give you a stuffy nose. It sounds like the pediatrician here actually used judgment and said, “I don’t have a significance.” Not every illness in the world is COVID. It wasn’t presenting as a flu-like or viral syndrome, it was presenting like basically an upper congestive process and so I think this is reasonable. It also points out, I think, the issue, “Wouldn’t it have made everyone feel better if you had access to a rapid results?” Then you could have just had that knowledge as well.
VR: Then she wants to know how is the common cold spreading so easily through the school when they’re doing all these things? [laughs]
DG: That is an excellent question and I want to ask you that, how is that happening? I want you to think about this. One is we don’t think there’s a lot of spread going on within the walls of the school, but are your kids having play dates with other friends? Are they basically going back to the other extracurricular social interactions? We’re seeing colds. I have a patient I’m taking care of who is a long-hauler. She works at one of the retail stores in New York City.
She had a very similar presentation when she developed nasal congestion and a co-worker, and I’m just like, “If we’re being so careful, how did – ?” She got it in the workplace. How did you get the common cold in the workplace when we’re doing all this stuff to protect against COVID? Obviously the hand washing, all the other stuff, we’ve got to do it. We’ve got to keep doing all these things.
VR: Also the common cold caused by other viruses, there’s a big component of spread by fomites, hand-to-mouth contamination, hand-to-nose. Kids are really good at doing that, especially outside the school. That’s another part of it.
DG: Oh they are. [laughs] Watch a child and cringe.
VR: Jean writes, “Did the first patient that Dr. Griffin describe on October 8th suffer from a spontaneous retroperitoneal bleed, central access that was attempted or present that resulted in the bleed in the context of anticoagulant, spontaneous common femoral artery or vein bleeding as the culprit or something else?” I hope you understood that because I don’t. [chuckles]
DG: This is a good – that doctors, we’ll all get this and I’ll explain it to everyone else. [chuckles] This is an individual who had COVID, got admitted, got standard treatments including being put on anticoagulation, because we know that probably about one in four, something like that, depending on the study you’re looking at, can actually develop major clotting complications if you don’t do that. The bleeding here was not retroperitoneal. Retroperitoneal is behind the peritoneum, back where the kidneys are.
This bleeding was actually into the thigh. It was a spontaneous bleed into the thigh. Was it coming from the artery or the vein? Considering that she dropped her blood volume this quickly, basically her hematocrit went from 42 to 21 in a matter of hours. That would actually argue that it was an arterial bleed to be and how tense the leg got was under quite a bit of pressure. That’s what we think happened here.
The general recommendation across the board by the American Thoracic Society, by the American Society of Hematology or ASH, is to put patients on a prophylactic dose of something called low-molecular-weight heparin. The acknowledgement is there is a certain bleeding risk as we saw here, but without that intervention there’s a significant clotting risk.
VR: One more from Alan Cohen. I’m a volunteer retired ID physician working with a local university as part of a COVID-19 response team. We want to do frequent testing of competitive sports teams and students with higher exposure risks, we’re looking at Abbott IDNow, Quidel systems, and BinaxNOW. We’re trying to see which system ProHEALTH New York is using for rapid testing, and also if a concern of a false positive arises, do you repeat the same test or switch to a molecular test?
DG: We use actually a lot of different modalities for each different school, and actually it’s been nice now that we have the calculator. We’re already using that to walk institutions through the different approaches. You always need a confirmatory test because it doesn’t fly to tell people considering that the majority of positives are false positives. There are indeterminants as we like to say, that they just need to stay out of school that day and we’ll test you again tomorrow. We’re usually using the Abbott IDNow as our confirmatory testing.
Just because within 8 to 12 minutes, we’re getting a result there. We’re using a lot of different modalities upfront. If it’s going to be a once a week testing, then we’re going to be using the PCR. If we can work out a system where it’s more frequent, either daily or bi-weekly, then we’ll consider using the – we’re using the BD antigen system. The Veritor is what we’re using. If you’re going to use the antigen test, you want to do it more often than once a week. If you do it every day, that’s fantastic. If you do it bi-weekly, that’s also reasonable. You can look at your budget using the calculator. We usually are using the Abbot IDNow as the confirmatory test.
VR: If you use some other test and it’s a positive, you use Abbott IDNow to confirm it?
DG: We do, but interesting, I’ll tell you, if you went to one of our urgent cares and let’s say we only had supplies for Abbott IDNow, and this happens. If the first test came up positive, we would run a second Abbot IDNow, because the positive test, it’s not the person that makes the test positive, it’s the technology and so it’s not as though the second test. If you run a second test 15 minutes later, and the first one was positive and the next one is negative, it’s not like suddenly your level of RNA is going to drop and you’re getting a negative.
VR: If you do the second test, is it a new sample or is it the same sample?
DG: New sample. Actually, it’ll be nice someday to do a little video so people could see how this is done, but you put the Q-tip in, you roll it around, I like to do 15 seconds minimum each side. You’ve already got the machine set up and now that Q-tip is then going to go into a little area in the machine, and you move it around a little, the special swirling you do. Not too vigorous, but vigorous enough, and then there’s moving some stuff around pushing some buttons.
Each time you run it, you really want to have a fresh swab that goes straight in. They’ve done some studies, and I think this can get you into trouble, where they do the swabs and then they put them in a little envelope and then they put them on dry ice. You’re losing sensitivity when you do that. Our process has always been to basically do a fresh wet swab straight into it, you’ve got that sensitivity down to like 6,000 or less RNA copy number.
[00:39:25] [END OF AUDIO]