Syphilis Surge—Are We Neglecting Other Infectious Diseases?

During times of an outbreak and especially during a pandemic, all resources get thrown at responding to the issue. It’s natural though, to throw every resource—all but the kitchen sink—at an outbreak or emergent situation. The challenge then becomes, avoiding neglect of all the other health issues we’re facing. This isn’t the first time though, that we’ve seen other diseases surge as a result of all efforts focused on one and the impact to a health care and public health infrastructure. In response to the 2014-2016 Ebola virus outbreak in West Africa, there was a significant 

 services that exacerbated malaria, HIV/AIDS, and tuberculosis.

Now, as we near a year and a half of COVID-19, we’re starting to see impacts to 

. Syphilis is 1 that has been starting to rear its head. 2000 numbers left us with promise of near eradication, but since 2015, cases have risen by 74%. This trend though has been worrying public health officials more as congenital syphilis rates soared from 2012 to 2019.

In Fresno, congenital syphilis spiked 900% in 2018. Erica Pan, MD, MPH, 

It’s been a really long, hard year responding to this pandemic, but people have really acknowledged and realized the impact of divesting in public health infrastructure. I hope that a lot of the resources that we hope to bring to bear in the longer term after this pandemic will benefit STDs as well.” This serves as a critical reminder that in the midst of a pandemic, we need to be able to step back to see the full health care picture.

J&J Vaccine Pause Shouldn’t Instill Fear

This week was busy with the news of the single-dose Johnson & Johnson (J&J) vaccine and requested pause on distribution to investigate 6 blood clotting cases. Instantaneously, the news took off and began to instill fears about the safety of the vaccine. First, this recommended pause is an indicator of a vaccine safety system via the Food and Drug Administration(FDA) and the Centers for Disease Control and Prevention (CDC) is working. This surveillance and transparency are vital for vaccine safety and overall public trust in vaccination efforts. As virologist Angela Rasmussen, PhD, noted: “Approximately 1.5 million doses of the Johnson & Johnson vaccine have been administered to women under the age of 50, so if the risk is high only for that group, the incidence is around 1 in 250,000. Pregnancy, using hormonal contraceptives, and smoking all are associated with a much higher risk of this form of blood clotting than even crude estimates of the vaccine-related risk for clotting. The odds of having a blood clotting disorder as a result of having Covid-19 is much higher, affecting as many as 

. This means that if you received this vaccine and you are under 50, the odds are in your favor.”

The next Advisory Committee on Immunization Practices (ACIP) 

 to review data will be on Friday, April 23, which will be a likely deciding session for future recommendations and distribution. During this time though, it’s important to continue discuss vaccine safety, efficacy, and how the regulatory process is built around ensuring transparency and safety for individuals.

Articles

The number of syphilis cases in 2000 raised hopes that it could be eradicated, but since 2015 cases have risen 74%. 

Hot Topics in Infection Prevention: Syphilis Surges, While J&J Vaccine on Pause

Imagine technology that could decontaminate N95 respirators for up to 25 times? Christina Yen, MD, an infectious disease specialist at Beth Israel Deaconess Medical Center didn’t need to imagine the technology, just a new way to put it to use. “This isn’t new technology,” Yen tells 

. “But it’s not really been studied in N95 respirators.” Yen’s talking about vaporous hydrogen peroxide or VHP, which hospitals have been using for years to decontaminate various areas. How would the process work with N95 respirators? Great, as Yen demonstrated in a presentation today at the annual conference for the Society for Healthcare Epidemiology of America (SHEA). VHP can decontaminate an N95 up to 25 times. Yen and her co-authors found that “in fact, it was safe, and it did not compromise the way the respirator fits or the way it feels to the face. It works the way it should.”

What did your study entail and what did you find out?

Sure, of course. Our study at the BIDMC in Boston, Massachusetts, tried to answer the question of how many times can we safely reprocess N95 respirators using a technology called vaporous hydrogen peroxide or VHP. It sounds very scary. But VHP is actually something that hospitals have been using for decades now to clean things like ambulances and rooms. This isn’t new technology. But it’s not really been studied in N95 respirators. We wanted 

to see if by reprocessing these respirators using this technology, we would be able to retain the fit of the respirator on your face, the way it sealed and the way it worked. And so that’s what we were hoping to find as we reprocess the N95s up to 25 times and we found that, in fact, it was safe, and it did not compromise the way the respirator fits or the way it feels to the face. It works the way it should.

It does seem to buck tradition or convention. And I think that for a lot of us, especially myself, when I first took on this project, I was not sure what we were going to find. But I think what was pleasant to discover was that there actually was a body of evidence that was slowly being built, even before the pandemic, trying to answer this question. Actually, there was a 

 that was conducted by the FDA [Food and Drug Administration] in 2016, looking at exactly this technology—N95 respirators—to see how many times they could be processed in a safe manner. And so, although it was one study, I think in light of the fact that it was of interest, and because more programs outside of our own program were also doing it, we were developing a body of literature as the months went on during the initial pandemic that was demonstrating over and over that this was, I think, actually not only safe, but probably doable for many of us. I learned a lot in the process, and I read a lot, too.

Do you think this sort of decontamination will become part of infection control protocols or will we go back to the old standards?

I think so long as our supply is able to meet demand, we will likely return to the older or the original standards. And I think that is still reasonable. We do want to ensure that we have an adequate supply of N95 respirators going forward for all of our health care workers. But as you mentioned, I think it is worth noting and retaining this information that we’ve learned because this won’t be the last pandemic and there will certainly be more outbreaks in the future. We in infection control notice. Realizing that we have taken something we’ve learned, something from this experience—as awful as it has been—that will protect health care workers and the patients they care for going in the future. It does need to be retained and we should be able to use this technology and use these strategies when we need to again, when the time comes. There is plenty of hydrogen peroxide to go around. Generally, how it works is that there is actually a machine that is generating or actually converting liquid hydrogen peroxide, which I think a lot of us are familiar with. We have it at home to get out stains or you see it sometimes in the hospitals. It actually converts the hydrogen peroxide from liquid to a gas. And in a contained room where the machine is located and where your respirators are located, that gas actually penetrates the surface of the N95 respirators further in. That actually disrupts the cells and the other viruses and other bacteria, things you don’t want in your respirators. It breaks up the cell walls and deactivates bone. And the best part is—and I think this is something that makes VHP very attractive to many of us—is that once it does its job, hydrogen peroxide breaks up into water and oxygen. All you have to do is ensure that your room is well-ventilated and you blow out your oxygen and water vapor. You really don’t have any dangerous visual things or chemicals on your respirators when they’re done. So long as it’s properly ventilated.

What would a decontamination room look like? Would the masks be laid out on tables side by side? I imagine that you wouldn’t want to stack them.

Correct. You definitely don’t want to stack them. You want to make sure that every respirator is getting its own space so that the hydrogen peroxide gas can settle and get into the respirator. As you mentioned, it depends on the location. Every institution did it a little bit differently. Many folks who did do it liked to opt for shelfs. What you can imagine is there is a room with either shelfs, or some people like lines to hang respirators on. That way each respirator gets space and has enough area for the VHP to circulate. And so, depending on how much space you have in your room, and how much room you have on your shelves or your lines, you can fill it up with many respirators.

Do we have enough N95 respirators on hand so we don’t need to do VHP decontamination right now?

At this time, at least at my institution, we are no longer requiring or needing it because our supplies now are adequate. We’re able to supply folks with respirators, be they N95 or others as people need. I think, ultimately—and I can’t speak for other institutions or the states—but I think many institutions have not necessarily decided to continue using it because supplies have become more available. And I think for that reason, many institutions, such as ours, have considered or are thinking about at this time stopping VHP usage for now. But as you’ve mentioned, and as we’ve talked about, who knows when the next surge will come, the next pandemic will come with the next outbreak. So potentially, in the future, there will be a time and place again.

Which department of the hospital would actually do this?

That’s a great question. And I think the takeaway lesson for me, at least, and I think also for our community, was that it is a team effort. And I think it is reflected in the background of the authors and the contributors for our study. It was not just infection preventionists. It was environmental safety It was health care epidemiologists. So many people from so many different backgrounds with so many different skillsets made this possible. I think if I were to say anything, it would be that collaboration, which we have learned is essential for success this year, it will continue being essential going forward. And so, for any infection preventionists who are thinking about or are reviewing the need for VHP sometime in the future, just know that those colleagues that we’ve relied on this time around are going to be there and are going to be your partners in the VHP process.

You were part of a study team and a study team has a very methodical way of doing things. But in the real world, if someone isn’t told that they’re in charge of something, wouldn’t that make it a bit haphazard?

I think that the folks at our institution who will be choosing or picking VHP…this speaks for general hospitals. They will probably be in the setting where an incident command structure will be in place. There will be a structure and an order to who will be taking points, and which partners will be involved in setting up a process like this. This is definitely not an isolated process, no matter how big or small your hospital is. No matter how many hospitals.

Is there anything I neglected to ask you about this, Doctor Yen, that you think is pertinent and that my audience should know about?

I think one thing that I would love to let folks know is that amongst the many methods that we all explore, for N95 respirator use and reuse, this was but one. And I think it’s important to also note in our study that while we did do multiple cycles, that the FDA emergency use authorization for VHP did change from the time in which our study was started to the current day. So as a people, the current recommendations on the FDA emergency use authorization for VHP, if you were to use it, now it’s set at five cycles. At the time when we did it, back in August and July, it was at 20 or 25 cycles. So, it is a little different now and always remember to check your EUA first before you pursue or before you jump onto one of these technologies.

This interview has been edited for clarity and length.

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Christina Yen, MD: “For any infection preventionists who are thinking about or are reviewing the need for VHP sometime in the future, just know that those colleagues that we’ve relied on this time around are going to be there and are going to be your partners in the VHP process.”

N95 Decontamination Process Allows 25 Reusages

’s wide-ranging coverage of the infection prevention and control world. Everything from interviews with known opinion leaders, to the news that infection preventionists and other health care professionals can use on their jobs.

Face Shields Called Flawed Protection Against Pathogens

Surgical masks offer better protection against aerosolized particles than face shields or even better than face shields and surgical masks used together, study finds.

APIC Answers CDC’s Call to Take on Racism in Health Care

“APIC will be focused on conducting research on how health equity and health disparities should be addressed in the field of infection prevention and control including designing interventions…”

If COVID Could Talk … But It Does, at the Cellular Level

Joachim L. Schultze, MD: “We decided that the knowledge that we have in immunology, as well as in genomics and single-cell technology, should be used to understand this new disease.”

Infection Control Certification: What Are You Waiting For?

Stand with the 7000 other infection preventionists who decided it’s important to be certified. It isn’t easy, but the satisfaction of this achievement far outweighs the preparation needed to pass.

Hot Water Might Disinfect Sinks Better Than Chlorine

Emilie Bédard, PhD: “We worked in collaboration with infection prevention, environmental services…. We had a multi-disciplinary team to make sure that we would look at all aspects of this approach.”

Take 5 minutes to catch up on Infection Control Today®’s highlights for the week ending April 17.

Weekly Rounds with Infection Control Today

COVID-19 generated, continues to generate, and will always generate studies. But as infection preventionists (IPs) and other health care professionals and researchers know too well, there were infection prevention and control challenges long before COVID-19, such as health care-acquired infections (HAIs). HAIs—which are generally bacterial or fungi—continued during COVID-19 and, in fact, some seemed to take advantage of all the attention being paid to COVID-19, such as the deadly 

. Also, there’s concern that COVID-19 itself can become 

As with the case with almost every health care discussion during the last year and a half, COVID-19’s presence could not be ignored at this week’s annual Society for Healthcare Epidemiology of America (SHEA). But there were other matters on the agenda, as well.

For instance, Bhagy Navalkele, MD, an assistant professor at the University of Mississippi Medical Center who specializes in infectious diseases, 

 about how quick response helped to contain an outbreak of human parainfluenza type 3 (HPIV3) at the medical center’s neonatal intensive care unit (NICU). That outbreak occurred in 2019, but the lessons that IPs at the medical center learned were utilized during the COVID-19 pandemic, Navalkele says.

“One of the most important kind of learning points have been that you have to be quick,” Navalkele tells 

. “You can’t wait anytime you hear that there is a trend in number of infections going up. You have to immediately inform leadership about it, you have to immediately inform the necessary unit or staff members about it. You have to immediately determine what interventions need to take place so that there is this does not occur again. All these kinds of interventions were applied during the pandemic, as well.”

The lessons infection preventionists at the University of Mississippi Medical Center learned from an outbreak of respiratory illness at the facility’s NICU in 2019, were later used to help deal with the COVID-19 pandemic.

Lessons Learned Pre-COVID-19 Used During Pandemic

Ultraviolet C devices (UVC-D) used after standard cleaning procedures in hospitals can dramatically reduce pathogens in microscopic samples, or colony forming units (CUFs), according to a study unveiled this week at the annual conference of the Society for Healthcare Epidemiology of America (SHEA). The study, presented by Gabriele Messina, PhD, a professor of public health at the University of Siena in Italy, concludes that UVC-D can cut CFUs by 97.3%. In an interview with 

, Messina talks about how UVC-D could be used in the real world. For instance, his study states that “in some situations, UVC light was sufficient to reduce CFU to zero, even without chemical and mechanical cleaning. However, we do not recommend this approach, considering correct to apply UVC light disinfection only after sanitization procedures since it does not remove dirt.”

Which begs the question: Doesn’t this add another step to the cleaning and disinfecting process for environmental services (EVS) teams that may already feel that they have enough on their plate?

Messina contends that it all depends on how the technology is used. He says that the cost can be “balanced” for the “structure who wants to adopt it, but also it can be very effective in reducing the possibility of cross contamination in the environment, including, of course, hospitals.”

In addition, Messina says that UVC-D does not add that much more time to the cleaning process. “Three or six minutes, on average, it's not a big issue,” he tells 

. “It’s something that you can insert into a protocol.”

There’s also the matter that UVC-D cannot be applied while there are patients or unprotected health care personnel in the room. And proper training will be a must. “You can have very good devices, but if you don’t have a well-trained health professional, the user is not going to be very effective.”

Ultraviolet light should be used in concert with traditional cleaning and disinfection procedures utilized by environmental services teams, study’s author maintains.

Looking to Fit Ultraviolet Disinfection into Hospital Systems

Electronic medical records (EMRs) operate along the lines of most data-crunching technology: It’s only as effective as the data it’s given to crunch. One of the many jobs of infection preventionists (IPs) involves surveillance to prevent health care-acquired infections (HAIs) or to control them—i.e. eliminate them—once they appear. A study by investigators with Piedmont Healthcare in Atlanta (among the 5 largest health care systems in Georgia) underscores just how important a role EMRs can play in combating HAIs. The study was presented yesterday at the over the annual conference of the Society for Healthcare Epidemiology of America (SHEA). The challenges of controlling HAIs in the maelstrom of a worldwide pandemic that requires a proportionate response by health care systems can’t be overstated.

Infection preventionists (IPs) at the health system, which comprises 11 separate hospitals, were able—with the help of the system’s business intelligence (BI) department—to refine software that allowed the information collected about HAIs to be easily integrated into EMRs. This was a case in which COVID-19 was definitely the mother of invention.

“We actually put it into place during COVID,” Meri Pearson, MPH, CIC, Piedmont’s infection surveillance manager tells 

. “We were creating this dashboard for COVID. And that’s when we determined that there are these new functionalities within this software that would make our vision possible. So, if it wasn’t for COVID, we might have not even thought to do this, honestly. But because we were so resource strapped, we were trying to work smarter and not harder by using technology.”

As the study notes, before COVID-19 the infection prevention team performed HAI surveillance “through a home-grown system that didn’t interface with their EMR” by entering information gained on rounds into a spreadsheet. However, this meant that only 1 person could enter data at a time.

“Due to the necessity of increasing efficiently in the current pandemic, the IP team proposed using technology to automate our HAI drill down process,” the study states. The IP and BI teams wanted to see if the HAI data in the infection surveillance system could be registered in interactive data software that the health care facility uses in other HAI prevention dashboards.

“The existing spreadsheet was reviewed to select variables essential for HAI drill downs and where the data existed in the EMR,” the study states. “The BI team worked to find the correct data tables within the EMR so that the data could automatically refresh daily in the data visualization software.”

The BI team could identify HAI variables that had once been entered manually within the EMRs. “This automation of drill downs allows for quick analysis of trends and areas for opportunity to prevent future HAI,” the study states. It concluded that “this utilization of technology can be applied to other health care facilities who have similar software systems to streamline IP workflows. The automation of quickly and efficiently recognizing areas for opportunity will give more time for the IPs to be rounding preventing HAI.”

Piedmont got much better at tracking and treating HAIs, but that can create other problems, Pearson tells 

. “When you start to look for something, of course, you’re going to find more and that’s exactly what we found with our situation when we got this more robust surveillance system,” says Piedmont. “We had to explain to our physicians and surgeons that you aren’t doing worse per se than you were before. We were just not detecting this patient harm, because we were just looking at cultures.”

Hospital officials reminded doctors that according to the National Healthcare Safety Network (NHSN)—a division , culture-based surveillance systems miss between 50% and 60% of surgical site infections.

“We did write an SBR [situation-background-assessment-recommendation] to the NHSN to request that they revise how they risk stratify facilities, because that’s not currently in their NHSN patient safety annual surveys,” Pearson tells 

. “We really want to make sure that we’re being compared fairly against other hospitals across the nation who have other enhanced software systems like this, because that’s not currently being done.”

The infection prevention and business intelligence teams at Piedmont Healthcare put their heads together to streamline the process of tracking health care-acquired infections.

Integrate HAI Tracking with Electronic Medical Records

The often deadly and contagious pathogens lurking in sinks and drains in hospitals may soon find themselves in hot water if the research being conducted by Emilie Bédard, PhD, keeps coming up with findings unveiled yesterday at the the annual conference of the Society for Healthcare Epidemiology of America (SHEA). Bédard is an assistant professor in the department of civil, geological and mining engineering at Polytechnique Montréal. Her study compares the tradition disinfectant for hospital sinks—chlorine—against very hot water. She found that the hot water (about 90°C) was anywhere from 100 to 1000 times more effective in getting rid of pathogens than chlorine. Bédard, who ran her tests at the MontrealChildren’s Hospital, explains to 

 how the hot water method can be used in the real world.

Would you explain how you conducted your study and what you found?

Yes, it would be my pleasure to do that. So maybe just on how this study came about. We had some suspicions of sink drains being the source of pathogens in an intensive care unit. So, as you said in the introduction, we went with the common solution. We put chlorine in the sink drains, thinking we would reduce the load of bacteria that’s present in the drain. Although we had a doubt, so we measured it. We measured the bacteria two days after and seven days after disinfection, and we realized that less than a week after the disinfection, we were back to initial concentration of bacteria in the drain. We went back to the drawing board looked at other options and found an interesting study where they had installed a valve drain on the drainpipe to make sure that the disinfecting solution could stay longer in contact with the 

surfaces of the drainpipe. And in parallel, we had also observed in another study that in sinks where hot water had higher temperatures at the faucet, we had less contamination within the drain. We decided to combine those two ideas and to go with an approach where we would pour hot water in the drainpipes with a valve so that we could ensure that the hot water would stay in contact with the surface of the pipe drain and maintain a better disinfection capacity. And so, in parallel to that we thought maybe that’s why chlorine didn’t work. As we poured it down the drain, it just went through and didn’t have enough contact time with the surface. We repeated the experiment with chlorine as well. We would pour chlorine into the drainpipe. But this time close the valve to make sure it would stay there for the duration which was 30 minutes for both the hot water and chlorine.

And how hot did the hot water have to be?

The hot water was initially close to boiling points. It was around 95 degrees Celsius. So that’s the initial temperature when we poured it down the drain. And then after a half hour, there was some heat loss through the pipe. We were down to about 60 degrees Celsius after a half hour.

Who at the hospital coordinated this with you? What departments did you work with?

We worked in collaboration with infection prevention, environmental services, and the pediatric unit; so intensive care unit. We had a multi-disciplinary team to make sure that we would look at all aspects of this approach. And it’s interesting that you mentioned that, because we also have the team that looks after the infrastructure—so the hot water system. And after a few weeks of conducting the study, we noticed that it was not working as well as the previous weeks after our disinfection with hot water. And the water in the drain was at lower temperature after half an hour. And as we brought it back to the team, we realized that there was some construction going on in the surrounding area with fans that have been installed which was cooling down the drain. The reason why I mentioned that is the temperature that you maintain within the drain for half an hour is important. If you go to lower temperatures, then it’s not as effective.

And you got some pretty amazing results in terms of how much how much better the hot water worked compared to chlorine.

Yes, it was 100 to 1000 times higher reduction [of the bacterial load] with hot water compared to chlorine in the study that we conducted. And yes, so that was working better.

Not really, because…. In drains there is a thick, what we call a biofilm. A thick structure of bacteria and organic polymers that forms on the surface. And when you put chlorine and the chlorine needs doesn’t reach the bottom of this thick layer of bacteria, and organic matter. With the hot water, what happens especially because we were working with metal pipes, the temperature is really high, and it’s going to help disintegrate this biofilm that’s present on the surfaces of their pipes.

And it seems like a fairly inexpensive method.

Hot water is pretty cheap. Chlorine will react with the organic matter that’s present in the drain. And there will be some odors and some fumes that will be in the surrounding environment so that the advantage of the hot water is you don’t get that exposure with the hot water.

And in further research will you look at how this could actually be applied to the real world? Will there be stations set up in hospitals where any health care provider can get the hot water? Would it be done in a systematic way? I think you said that it would have to be done weekly?

What we’ve done with the preliminary results … we did a weekly disinfection. Now we’re working on how to optimize. Could we do it less frequently and have the same kind of results? Could we play on the time of contact? We went with a half hour disinfection. Could we do 20 minutes, and we’d have the same results? We’re looking at that. And we also need to think that you don’t necessarily want everybody and anybody to be able to do it because you need to activate or close down the drain valves. And if that’s done and not reopened, you can have some issues with water overflowing from the drain. You would want to integrate it into a cleaning routine or a routine where there’s a dedicated or identified staff that would take care of that, for example.

Do you think that the plastic pipes could handle it?

Well, actually what I do at home…. I have some problems with drainpipes that tend to block now and then. And when that happens, I put it to the hotter temperature—the hot water directly from the faucet into the drain—and I let it flow until I get a better drainage in my sink. And that works. And I have plastic pipes at home. I think that that’s why we need to work on the optimization of this approach. There might be other ways to do it without necessarily having to pour boiling water down the drain. But we need to experiment with that.

I know that in many hospitals, infection preventionists oversee environmental service teams, or at least the two departments work very closely together. I’m sure they’ll be interested in your study. Is there anything I forgot to ask you that you think might be pertinent and that they should know about?

I guess the last thing I maybe want to add is that you know it might look like more work or additional work. That’s why we’re trying to work on this to see how it can be part of their cleaning routine of a room, for example. Or try to integrate it so that it doesn’t add additional work. And that in the end it has a positive impact because we reduce the risk of infection from the sink drains to the patient or through the staff using the sink.

Emilie Bédard, PhD:  “We worked in collaboration with infection prevention, environmental services…. We had a multi-disciplinary team to make sure that we would look at all aspects of this approach.”

Wearing a surgical mask along with a face shield affords health care professionals only statistically insignificant better protection against aerosolized particles than wearing a surgical mask alone, according a 

“Surgical masks alone provided good protection, surpassing the protection provided by face shields alone,” write investigators with the Detroit Medical Center. “Both used together provided the best protection, although the combined protection was similar to surgical masks use alone.”

 and experts are in agreement that infection preventionists and health care professionals need to wear masks; preferably N95 respirators but even surgical masks—the masks used in this 

 study—will offer better protection than just face shields alone, or the combination of face shields and surgical masks.

As the study explains: “Small respiratory particles from a patient coughing can remain airborne and spread widely through a room, leaving health care workers and others vulnerable to becoming infected through inhalation, especially if in the room for an extended period of time. The rate of airflow in a room will also affect how far droplets can travel.”

As the study states, other research also questions just how much protection a face shield affords. An 

 noted: “Face shields aren’t perfect…. The absence of a good seal around the face could allow aerosol penetration. Also, they might cause fogging or glare.” However, as also noted in that article, face shields were one of the means to alleviate the drastic shortage of face masks in the United States at the beginning of the pandemic.

 study simulated what would happen if a sick person and someone not infected were to have a conversation in a room.

 an aerosol generating system was made using a bacterial suspension in a nebulizer attached to an oxygen cylinder,” the study states. “A fan connected to the nebulizer created aerosols. Transmitted aerosols were detected using blood agar plates at 0.1524 and 1.8288 meters from source, simulating exposed person. The study was performed under controlled conditions at room temperature in a biohazard hood with high-efficiency particulate air (HEPA) filter and UV light.”

They used various combinations: sick person without a surgical mask, with a surgical mask alone, with a face shield alone, and finally with both a surgical mask and a face shield. The simulated well person would do the same and just what the two “people” wore at any one time were investigated. For instance, in one simulation, the sick person would be wearing both surgical mask and face shield while the well person would be without any facial covering. There were 17 combinations in all.

“Growth score was assigned to each scenario based on colony count on the agar plate,” the study states. “Increasing the distance between the 2 subjects decreased the colony count. Highest growth score was obtained when none of the subjects used any protective measure and the lowest growth score was achieved when both subjects used mask or mask with face shield.”

After each simulation, the air inside the room was let out through a HEPA filter for 5 minutes. “Culture plates were incubated at 35°C for 18 hours to allow the growth of bacteria and formation of visible colonies,” the study states. “The number of colonies on the culture media was used to evaluate the efficiency of mask and/or face shield wear by the sick person in reducing the transmission of aerosols. In some simulations the effect of mask and/or face shield in protecting a simulated listener in close proximity to the emission source (sick patient) was evaluated by protecting the culture plates with mask and/or face shield.”

Investigators pointed to the limitations of the study. First, there were no human subjects involved. The “listener,” a petri plate could not actually inhale. Also, the simulated speech could not take into account the different speaking patterns and volumes of different people. Also, a bacterial solution was used, not a virus.

“Recent information has indicated that SARS CoV-2 is transmitted by aerosols and droplets, and we could not simulate various droplet sizes,” the study states. “Virus quantification in this type of experiment would be very cumbersome and use of SARS CoV-2 was not possible due to safety requirements. Thus, bacteria better served the purpose of this model.”

They also note that aspects of face shields make them more user friendly than surgical masks. They are cooler and less suffocating. They offer eye protection, prevent somebody from touching their face and can prolong the use of surgical masks if both are worn together.

“Professionals working in high-risk settings with exposure to aerosols and droplets, such as dentists, would benefit from the use of face shields, or perhaps goggles, which this experiment could not simulate, as added eye protection,” the study states.

That said, though, health care professionals should not assume that face shields alone will afford enough protection.

“The mask alone provides such a significant improvement that it is difficult to tell, based on this simple simulation, whether the protection afforded by a surgical mask combined with a face shield is improved,” the study states. “Face shields might provide eye protection if when worn as a supplement to the mask, but the role of the eyes in transmission of SARS CoV-2 is not well established.”

The COVID-19 pandemic presented daunting challenges to hospital departments all too familiar with daunting challenges: neonatal intensive care units (NICUs). However, COVID-19 isn’t the only pathogen in town, as IPs and other health care professionals can attest. One of those health care professionals is Bhagy Navalkele, MD, an assistant professor at the University of Mississippi Medical Center who specializes in infectious diseases.

 Navalkele co-wrote and presented yesterday at the annual conference of the 

Society for Healthcare Epidemiology of America (SHEA)

 explains how staff at the medical center’s NICU sprang into action to contain an outbreak of human parainfluenza type 3 (HPIV3). It is a common respiratory tract illness in infants and young children.

“Early diagnosis and isolation of respiratory tract viral infections is important to prevent an outbreak,” the study states. “Successful control of outbreak in NICU requires prompt implementation of IP measures with focus on symptom screening, cohorting, and disinfection practices.”

One infant was identified as having hospital onset HPIV3 on April 30, 2019. In May 2019, 3 other infants in the NICU were diagnosed. An investigation into the outbreak began on May 3, 2019. “Enhanced infection prevention (IP) measures were immediately implemented,” the study states. “All positive cases were cohorted to a single pod of the NICU and placed in contact with droplet isolation precautions.”

that when the frontline health care professionals realized that they dealt with a cluster, they contacted the infection prevention department. “When we stepped in with our role as infection prevention specialists, we kind of make it a little bit more organized and structured,” she says. “We provide them definitions. We provide them a complete plan on all aspects which might have been missed.”

For instance, the IPs established a symptom screening system for all babies in the NICU, as well as all staff going in and out of the department. “All those added measures—and data mining when the outbreak ends—is performed by infection prevention.”

But the precautions didn’t end there. Other departments got involved.

“Dedicated staffing and equipment were assigned,” the study states. “Environmental cleaning and disinfection with hospital-approved disinfectant wipes was performed daily. Visitors were restricted in the NICU. All employees entering NICU underwent daily symptom screening for respiratory tract illness. All NICU babies were screened daily for respiratory tract illness with prompt isolation and RPP testing on positive screen.”

The multidisciplinary team included NICU nurses, physicians, nurse practitioners and, perhaps most important of all, environmental services (EVS) personnel. “We met with the environmental services staff, and we explained to them that this is a critical situation in the neonatal ICU. And this cannot spread more.”

EVS came through. “They helped us with cleaning, the disinfection,” Navalkele tells 

. “Clearing was occurring very meticulously, almost every few hours. All the surfaces were getting cleaned and the equipment was getting cleaned.”

The hospital’s laboratory also needed to get involved. “Lab was notified. We said, ‘Hey, we’re going to test all these babies for parainfluenza type 3 so that we can identify it immediately. They made sure that they had an adequate supply of testing kits. And they helped us transport those specimens to the health department” as well as the Centers for Disease Control and Prevention (CDC).

The CDC tested the HPIV3 positive test specimens using whole genome testing. In this way, investigators confirmed 7 cases of hospital onset HPIV3; 6 from the NICU and 1 from the newborn nursery. Investigators determined that the case in the newborn nursery was unrelated to the NICU cases; that the nursery baby had been infected by a sick visitor. Five of the NICU infants had lower respiratory tract illnesses, and 1 had an upper respiratory tract illness.

“Average time from admission to diagnosis was 71 days (range: 24 -112 days). None had severe illnesses requiring intubation and all had full recovery,” the study states. “No CO HPIV3 cases were reported from NICU during the investigation. Maximum likelihood phylogenetic tree of HPIV3 WGS (figure 1) showed that sequences from the 6 HO cases clustered together separately from the 3 CO controls suggesting single source of transmission and 3 CO cases were not related to the HO cases or source of the outbreak.”

Navalkele B. Successful control of human parainfluenza Type 3 outbreak in Level IV Neonatal Intensive Care Unit. Abstract presented at: Annual Conference of the Society for Healthcare Epidemiology of America; April 14, 2021. Remote.

The multidisciplinary team included NICU nurses, physicians, nurse practitioners and, perhaps most important of all, environmental services personnel. “We met with the environmental services staff, and we explained to them that this is a critical situation in the neonatal ICU. And this cannot spread more.”

Quick Action Keeps NICU Respiratory Illness in Check

What goes on on the cellular level when it comes to COVID-19? To find out, 

 reached across the Atlantic Ocean to the University of Bonn in Germany. Joachim L. Schultze, MD, is a professor of genomics and immunoregulation at the Life & Medical Sciences Institute at that university. Schultze is also the coordinator of the German COVID-19 OMICS Initiative, which seeks to integrate biological and science data with social sciences and the humanities. Schultz’s research focuses on understanding the range of severity of COVID-19 symptoms through an analysis of single cells. His latest research appears to indicate that proteins such as TLR3 and IFN I and II may be useful indicators of disease severity and/or an area to explore for possible therapies. His research also seems to indicate that the heterogeneity of COVID-19 may have to do with three factors: the host, the environment, and the virus itself. Schultze seems to have ruled out the virus. In a wide-ranging discussion with 

, Schultze also discusses the significance of neutrophils in immune response to COVID-19, the immune system’s role in COVID-19 long-haulers, and how the single-cell analysis that can be useful in the diagnose and treatment of COVID-19, can also be used to diagnose, treat, and potentially prevent other kinds of bacterial, viral, and fungal infections.

 Your research focuses on understanding the range of severity of COVID-19 symptoms through an analysis of single cells. So, in layman’s terms, could you explain to this beat reporter where your research has led you?

When the first wave hit Germany, we basically decided that the knowledge that we have in immunology, as well as in genomics and single-cell technology, we should basically use to understand this new disease, which is basically due to the SARS-CoV-2 infection. And at that time, there were some early reports on classical techniques used in the clinics, looking at blood samples that the immune systems seem to be awkward. And depending on how severe the disease was, it seemed to be different kinds of things. It looked very heterogeneous. And that’s why we thought that modern technologies, single-cell technologies, that allow us to dissect the immune system cell by cell would basically help us to understand this heterogeneity. We teamed up with clinicians and other partners and university hospitals in Germany, but also Europe, to get a sufficient number of patient samples that we could analyze the immune cells. We mainly focused many studies on the blood compartment. But with some colleagues, we also looked into the lung. And I had a couple of questions. The first one is, what is the dynamics of the disease over time when the symptoms started, what is the difference in the immune response when you have mild symptoms versus severe symptoms, and maybe also find early signs that tells us that people are at risk. And we wanted to know whether there are certain aspects concerning the two different arms of the immune system. Is there something happening in the innate immune system versus the adaptive immune system that would be associated with severe disease. And that’s what the starting point was. And that’s when we basically looked at many, many patients then by these modern single-cell technologies.

You published your findings. Which journal did you publish in?

We had several papers that we have published in the meantime. Our first study was published in 

 last summer where we actually focused on the innate immune system, particularly the so-called myeloid cells. These are mainly monocytes and granulocytes in blood because we had the idea already there were some clinical observations that neutrophils were 

very high and lymphocytes were very low, so we get lymphopenia. And they basically built also a ratio saying that if the ratio is toward neutrophils that you have a severe course. And so, what we did try to answer is, is what kind of neutrophils are these? It’s very interesting because many labs in the world are using peripheral blood mononuclear cells when they look at blood. And usually, what you then do is you delete also the granulocytes because by this way of isolating the cells from the blood of patients, you’re losing the granulocytes. And we had the idea that based on the clinical observations that it would be a good idea to look at the granulocytes as well. And so, we used technologies that allowed us to do that. For example, for the single-cell RNA sequencing technology, we knew that a technology based on arrays and the one we used was the Becton Dickinson Rhapsody technology. But the cells are very nicely kept in this system so that we could capture also their information. And that was very good because over time we could see that in these patients with severe COVID-19 we had not only more of these granulocytes, but we had also some that changed their program completely. An interesting point is except for the absolute experts in neutrophil biology, not so much was known about single-cell RNA sequencing of the cells because many people always said these cells are not transcriptionally active anymore. And so, they are not so interesting. But we found even in healthy people that there are different subtypes of neutrophils on a transcription level. And in COVID, they changed completely. We found suddenly cells that were very inflammatory. But later during the disease, they would look more like cells that can suppress other cells, so kind of suppressive functionalities. And they could only be uncovered by these high resolution, single-cell technologies. Otherwise, we would not have seen that. And we not only did that in one cohort. We actually did that in two cohorts in one study. We had validation within our own project from the beginning. And I think that was one of the strong points early on in the COVID pandemic that also convinced the editors at 

 that we had really nicely validated. Many studies at that time had looked at a few patients only at one cohort, and that is sometimes prone to bias because you just take the samples that you get from the patients you have and then you cannot generalize it. We basically circumvented that by having two cohorts, finding the same in these two.

You mentioned that severe COVID-19 … what are some of the practical applications of your research? Will this help physicians in the future or near future be able to determine who might be more susceptible to severe COVID-19?

Yes. We also complemented the studies in the meantime with technologies that are more clinically feasible. So now, we know from our single-cell studies which cell types are changed and the granulocytes have played an enormously important role. But you can also do blood testing, for example, on transcriptome level on old blood, and we did this as well and then could correlate that directly. And what we can see in these studies is that you also see this granulocyte signatures in the blood. And what we found out, that there is a molecular phenotypes. So, you're not having one kind of COVID, but we found molecularly in the immune system, in the peripheral blood, that there's at least five subtypes of this disease. And what you then can do, is you can do, for example, drug prediction. So that’s what we did on these. We basically say, which drugs are known based on previous work where people had screened drugs for changes these drugs can do in transcriptomes, which of the transcriptome changes that we see in COVID could be returned back to normal by these drugs that have been tested. And what we predicted early on is that a subgroup of patients with severe disease would benefit from steroids. We knew that last Easter already, so a time when people really were searching heavily for treatments. And what was interesting to see then when clinical colleagues, particularly also in the UK, started these large trials also looking for drugs that could be used and they treated patients in a large trial with corticosteroids. Their finding was that none of the mild symptom patients benefited from corticosteroids really and the subgroup of patients with severe COVID. And that’s exactly what we predicted from these kinds of studies. We wouldn’t have said already because of the molecular phenotypes that it’s not all severe patients but only a subgroup and the clinical observations are in accordance. So now, we have to bring this together. I think it’s a good example of taking these high resolution, high throughput technologies identifying molecular phenotypes, and then tailoring better potential treatments. What we want to do in the future with precision medicine. In a way, I think, all of these findings will help us in the long run to find better drugs and better treatments for these patients.

What do you think may be the immune system’s role in these occurrences of long haul COVID-19?

The concept of long COVID is also to really understand that this is a heterogeneous syndrome. It’s just basically in the beginning saying that there are people that have long-term effects, but we now already know that there are different reasons for that, because you have those that had a very strong and severe disease and then take extremely long to basically get back to normal. So, that’s one basically big group of patients with long COVID. There’s another one where you had mild symptoms and then maybe even no symptoms for a while, and then symptoms come back like fatigue, and so on, and there’s mixed versions of this. So, there might be a heterogeneous picture. And again, in this situation, we think that all of those have to do with changes and reprogramming of the immune system both in the adaptive immune system as well as in the innate arm. So, I know that worldwide studies are ongoing to better understand what happens there and what are the changes that we seek to find, again, potential therapeutic or even preventative strategies for those that might have a mild COVID and might be prone to get these fatigue life syndrome diseases. If we understand what the role of the immune system in these patients is, I think we can very much help them to reduce their symptoms. I’m pretty sure that the immune system plays an enormous role.

Did it challenge you a lot that this is so new, that COVID was so new, never seen before? And even as you just talked about looking at long-haulers, I mean, it hasn't been around that long. We don’t really know how long long-haulers can suffer from the after-effects of getting COVID, right?

But what I’ve found interesting despite the fact that it was not organized worldwide in a completely organized fashion, I have to say that science has done an enormous job in the last 14, 15 months, and the technologies that we have at hand and that can be applied to patients these days allowed us to answer things much faster. And so, combined with the communication that we have in science worldwide, you could basically team up in larger groups. That’s what we did in Germany, for example, with this German COVID-19 OMICS Initiative where we have more than a hundred labs and more than 45 institutions now and that worked together on things. That’s the good side of things that when this happens you suddenly can answer questions much more quickly because we have experts for everything in the team and you can organize yourself better. We have basically protocols across different hospitals and can deal with patients in a similar fashion. And with the long COVID, they started already in the first wave. And now, since we have 14 months into this, if you started from day one to think about potential long-term effects, then you can actually design your observational studies along this way and that happened. And if you share that information that you’re doing it with your colleagues, others can do the same. And then, of course, we have enough numbers of patients that we can really identify what’s happening there. So, that’s the good side. Unfortunately, it didn’t happen everywhere. So, I think there’s still space for improvement, but bottom line is I think we never learned so fast with a new disease compared to COVID.

I think you mentioned machine learning, and that might be a little bit off topic, but has that played any part in your research and what is it actually?

Machine learning means that we’re using large data. And instead of having us looking at the data in a more manual fashion or with the classical statistical approaches, there are new tools out there where we basically give a certain algorithm, certain data, and the algorithm learns structures in this data. That’s the machine learning. And then we have additional independent samples and you’re trying to find the same structure in the data and these other data. That’s what's the field of machine learning. And part of that can be done by algorithms that are now following principles of the brain, mainly with so-called deep neural networks, and that is artificial intelligence. It’s weak artificial intelligence. It’s not the kind of it can do everything. It is just specialized algorithm that can do one thing very good, namely recognizing patterns in big data. And it’s interesting, not only in immunology but mainly also for other things in fighting the pandemics, many groups around the world have tried to use AI to find patterns, whether it was x-rays or CT scans, but also behavioral patterns to see whether we can learn about this disease and its circumstances. I have to say it’s a very early field. And I’m pretty sure for the next pandemic AI will play a much more important role because here many people jumped on it. And then sometimes the studies were very small, and that’s a problem for AI because you need enormously large data to really be successful, to really have good recognition of structures and data. And so, the first wave was super enthusiastic last year. But in the meantime, we also have more critical people that looked at the results and see how valid they are. And here we have to say there’s a little bit of backlash at the moment because when the studies are too small, it’s sometimes not possible to validate that. I would say we’re in the situation that the enthusiasm is still there, but we’re now also getting more realistic. What we have done there is a little bit different. We’re working on aspects that we can generate larger data sets so that we can bring more people together. Again, the idea of teaming up, and that’s what’s going on at the moment to circumvent the problem of too small data sets in machine learning for this. And again, there you can use medical data. So, we are using transcriptomes and also x-rays to find out if the data sets are large enough that you then can use this new technology to learn more about diagnostic potential for

In your publication, you stated that the heterogeneity of COVID-19 may have to do with three factors, the host, environment and the virus itself, and you seem to have ruled out the virus. Can you elaborate a little bit on that?

That’s a good point. I mean, we’re talking worldwide about mutations right now in the virus and then the mutants that have different infectivity. For example, the binding to the receptor is now an issue. And of course, we’re also talking about the first mutants out there might also lead to more severe disease. So, that is basically development that we just saw in the last couple of weeks that were unclear last year and were actually not seen in the early mutants, like when the Wuhan original virus was exchanged by the first mutant as D614G, which basically happened last year already from February to April and May and that led to a higher infectivity because of better binding to AC2 that is known now, but there was no indication that the disease itself changed. Now, with some of the new variants of concern, particularly the B.1.1.7 first found in the UK, there is now indication that there might be not only infectivity but also more severity, and therefore, also a higher mortality rate, but we still don’t know exactly why this is the case. It could simply be that this mutant still has just more virus that the host has to cope with. So, I would say, a little bit more uncertain than a couple of weeks ago is that there is a chance that there might be a role for the virus, but the indication is not yet good enough. So, we have to have more data on that. Having said that, when you look at the epidemiology and then also the immunological findings that we have now and look at the host immune system, then we have indication that the people that are getting more severe disease are elderly and people with co-morbidities. They have an altered immune system very often. And so, I think the reasons for a different disease course is still mainly in the host. Now, while there might be an additional component now coming from viral mutants, the host still dictates mostly the severity. I think that's just as of today.

In layman’s terms, what do you mean by the host?

The host meaning that basically everybody of us has a certain status in the immune system, and depending on your comorbidities or your age, and so on, you have a different status of inflammation. You might have activation that a young person doesn’t have. That’s one thing. And of course, there’s a third component, which I forgot so far or didn’t mention yet, is there are also some people that have a genetic predisposition based on certain mutations in defense genes, for example, in the interferon system that has also been shown so that the pathways are not working as they do in the normal population. For example, there is less type I interferon response, and that might be also something that leads to a worse outcome because the system is extremely important for the defense against SARS-CoV-2. And there’s another aspect which has been shown that some other patients apparently have B cells that produce auto antibodies against neutralize interferon alpha. In some studies, it has been shown that those patients with severe disease are enriched for those that have higher numbers of these auto antibody producing cells and have high levels of these auto antibodies against interferon alpha. So, we have already some indication what mechanisms are underlying these problems of the immune system in severe COVID, but there’s more to be discovered yet.

Most of the experts seem to agree that they’re worried about the variants, but they say that the vaccines will have at least some effect against virus. Do you agree?

I’m not a vaccinologist at the moment, but I’m following this very closely because I think that’s important for everybody and also for interest for an immunologist. So, far the experiments that have been reported for the main vaccines that are on the market in the US or in Europe, in other places in the world, all of them seem to be still functional against the current variants. There is difference in strength that some of the new variants have, the immune response after the vaccine is not as strong, particularly in the neutralizing antibodies against the virus, but it’s still sufficient to ensure that you’re not getting a severe disease or even a lethal disease, so that’s reinsuring. But it also told us that mutants have to be followed and have to be monitored so that we’re not missing something that some mutations that might escape the vaccines that we have today. I also see that it’s very important, and this happens more and more, and in more and more countries, that we are sequencing viruses from patients and from infected individuals so that we have a good idea of what is currently happening across the globe concerning the mutation rate of SARS-CoV-2.

Is there something that I didn't ask you that you would like people to know?

I would say that an important aspect, what we had learned in this pandemic, is that very good science can help to answer important questions of this disease much faster than we had the chance ever before because of better communication, better connection between scientists worldwide, but also technologies and the application of new technologies like single-cell sequencing, et cetera, to patients directly. So, that is a very positive development. I think there’s two things that we have to learn more. Because we have this incredible development in science, we need to make sure that the right information is given to our decision makers, to politics, as well as to the society that they understand, and we have to educate because it’s complicated what we are finding. It was complicated to us and it’s still sometimes puzzling us. We have to better communicate. And I think, what we’re doing right now, these things have to be done so that we can show to people there’s good things happening. And if we wouldn’t do the science, we would not be able to develop these vaccines so fast, but we have to make sure that everybody understands what we’re doing and what the consequences are so that we can have decisions in society, in politics, with the decision makers that help us all to get through this much faster. And here, I think everything that we can do to even further optimize that is a good thing to do.

Joachim L. Schultze, MD:  “We decided that the knowledge that we have in immunology, as well as in genomics and single-cell technology, should be used to understand this new disease.”