Author Archives: Eric

About Eric

Immunologist and Infectious Diseases Research Scientist by day, ultra runner and mountain adventurer in my spare time. Blogging about whatever comes up in life.

The COVID-19 Workplace

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This past weekend much of the State of Colorado moved from “Stay-at-Home” to “Safer-at-Home” restrictions. This is the first step to us opening up more businesses and moving slowly back towards a state of ‘new’ normal. As part of this a lot of people across the country are preparing to go back to work (or into an office/store) in some capacity in the coming weeks. Some people think this is all BS and a hoax, you can stop reading now, for those who are worried or uncertain exactly what this return to a ‘normal workplace’ might look like, I’ll try to outline a few best practices that my work has been using and also highlight what the State of Colorado has outlined for businesses that are reopening.

Governor Polis’s outlines what Safer-at-Home means for Colorado. Note that individual Counties may enact additional legislation beyond these basic measures. Here in Boulder County masks are required in public settings where you can not maintain 6ft of separation.

To start with for those that don’t know my background, I work in a vaccine and drug development laboratory. So my workplace will definitely look different than many of yours, but there are still many applicable practices that we’ve implemented that all types of work environments can utilize. Much of my experience in mitigating infectious hazards comes from years of working in Biosafety Level 3 facilities (with airborne, highly infectious, incurable pathogens). The stringent types of biosafety measures we implement in the lab aren’t applicable to daily life, except if you’re working in a healthcare setting in close contact with highly infectious patients (ping me separately if this is of interest to you). I’ll divide the topics up into three categories; general work place practices that should be implemented at the management level, engineering controls (equipment) and lastly how many of the common workplace practices can and should change to help you protect yourself during this uncertain time.

General Workplace Policy

While some people can work remotely from home (best practice), many of us require specialized equipment/facilities, customer interactions or other tools that are simply not available at home. If your work place is welcoming employees back into the office/store, the State of Colorado has set out several guidelines for how work place policy should be setup to protect the employees. First, spread out the hours people work; work from home, work shifts, segregate tasks people are working on to different areas, etc. Second, the employer should be providing ample cleaning supplies, hand sanitizer and soap. In our office we also have an employee tasked with daily cleaning of the common areas and commonly touched surfaces (door knobs, time clock, fridge, conference table, etc). In addition to this I clean my personal desk each morning, it only takes a few minutes, but alleviates any concern about contamination of my immediate workspace. Third, the wearing of masks should be made mandatory for all employees (and customers) when you’re interacting with anybody else (even in passing or in the bathrooms) or moving around the office. The reason this needs to be made a company wide policy is, otherwise it’s too easy for a portion of the population to not adhere, making the effectiveness of cloth/surgical masks far less on a company wide scale, everybody needs to protect everybody else. Additionally, signage reminding everybody about the policies on staying home if you’re sick, hand washing, cleaning of common areas and wearing of masks are helpful. Many of these measures are requirements of the State of Colorado for reopening a business, check with your individual state about their requirements.

Mandatory cleaning supplies near our front entry. All offices should have these available for employee use.
Masks, gloves and all the protective equipment. Despite what Trump recommends, injecting bleach and UV irradiating yourself are not a good idea. But these are good tools for cleaning equipment and surfaces (just not your body).

Engineering Controls

Engineering controls is a term used for physical barriers or equipment that is used to reduce the hazards of a workplace. In regards to COVID-19 in the workplace it’s referring to barriers and office setup that can help reduce interactions with coworkers and thus reduce the risk of someone getting sick. One method of limiting the workplace risk is to spread out employees desks/work spaces. Providing all employees with at least 6ft of space as to reduce the likelihood of infectious transmission. Another way is to setup barriers between employees desks/work spaces. This can be done by putting up plexiglass walls (or other materials) to block the direct line of transmission from one person to the next. So the open workspace system that so many tech companies love, is probably going to need to go away for the immediate future. Cubicles (or closed offices) actually provide a fairly safe way for each employee to have their own protected space, where infection risk is low, and you don’t have to wear a mask all the time. Work with your employer to establish these ‘safe zones’, because not only will it reduce the transmission risk, but it makes the employee far less anxious because they have their own personal space (at least in our office it works that way). For those of you working retail, store fronts or other customer based jobs, many of these rules won’t directly apply. My recommendation would be to establish a safe zone for yourself (back room, office, car, outside). Take breaks to get out of the mask for a few minutes (pretend like you’re a smoker) or just to step into the back room/warehouse for a few minutes to relax and breath. Plan and prepare for the long haul.

The dreaded cube farm, a great way for every employee to have their own protected safe space and to minimize COVID-19 transmission risk.

Common Workplace Practices

While the previous two sections mostly addressed changes that can/should be broadly implemented in the workplace, this section is going to address how the actions of individuals/groups should change. I have a feeling for many people this is going to be the hardest section to incorporate into our daily lives, but these changes are equally as important as those above. The first one is simply an extension of the general social distancing policy that pervades our lives, but applied to the workplace. No group lunches, standing around the coffee/espresso machine, office parties, etc (yes, sad face, I know). It doesn’t mean you can’t chat with coworkers or socialize, but it does mean it has to be done at a safe distance apart and while wearing your masks. If/when you need to use common office equipment (printers, coffee makers, fridge, cash register, etc) either make sure the equipment is well cleaned off or sanitizer/wash your hands afterwards as a precaution. This mitigation measure may be slightly less important for some workplaces, and more important for others (depending on how many people you’re sharing space with). On the far end of the spectrum are people whose jobs require direct contact with others (massage therapist, physical therapist, hair stylist, acupuncturist). For these professions it’s even more important to sanitize all surfaces after each client, wear masks (tough for hair salons), make sure both client and provider clean their hands before interacting, and of course pre-screen your clients to make sure they are not sick or symptomatic.

The last one is probably fairly obvious for many people, but meetings are going to look quite a bit different (if they happen at all). The easiest way to mitigate the risk is to do virtual meetings (Zoom, Skype, Teams, etc) whenever possible. Of course sometimes it’s much faster and more efficient to meet in person, which can definitely be done very safely. The smaller the better to start with, but as meetings grow, ensure there is at least one seat between everybody in the room, and everybody continues to wear their masks when in the same room.

Workplace meetings in the COVID-19 era. Join virtually, space out, masks for all those who attend in person.

Final Thoughts

My office/lab implemented most of these procedures the first week of Colorado’s Stay at Home order and shutdown. We have our own cubicles/workspaces that are our own private areas when we’re not working in the common lab spaces. We wear gloves (because it’s a lab) and masks whenever working in close proximity to others, common surfaces are regularly cleaned, our employees with COVID-19 risk factors spend much of their time working from home, or working off shifts, our meetings are done half virtual half in person (with masks). Using all these measures we’ve had no issues with viral transmission and also minimal issues slowing down our workflow. If you or your employer are hesitant to implement many of these actions, just look at the extreme cases of the meat packing plants all over the country. They stayed open but didn’t implement any infection risk mitigation (employees working in close quarters), and ended up suffering large outbreaks forcing their businesses to shutdown. So it’s really in everybody’s best interest to protect themselves and those around them, to stay healthy and keep the business running without the major setbacks that an outbreak would cause.

While company wide policy is up to the employer, you are your own strongest advocate. So it’s important to assess your work place (and how it operates) and how best to mitigate risks. If an employer isn’t providing you at least the minimum levels of protection outlined above, then speak with your local public health department, as they will come in and further assess what more can and should be done. Going back to work in and of itself isn’t a problem, it’s doing so in a responsible and controlled manner that allows your workplace to implement and test out these new policies. For all businesses there will be a trial period of adjustment to the new way of functioning, just be flexible and understand most of these changes really don’t dramatically affect our lives (and definitely don’t impinge our our civil liberties), we’re all going to get through this.

State of Colorado general Guidelines
State of Colorado Guidelines for Protecting Workers and Customers
Definition of Lab Biosafety Levels
CDC Guidelines for Businesses (far less specific than individual states)

COVID-19; Immunology and the Infection Cycle, 4/22/20

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Sorry for the delay, but this one has taken a lot of time and thought to put together (and reading some 80 odd Covid research papers). My goal in this edition of Covid Science Theater 2020 is to talk about what happens when the virus enters our body, infects our cells and subsequently leads to either mild disease or more severe infections. It’s going to be a fairly dense article, but I’ll do my best to keep the science and terminology to something generally understandable and hopefully educational.

For those who don’t want to delve too much into the specifics of all the virology, immunology and pathology I’ll provide a short 1 paragraph set of clifs notes here. The virus most commonly enters the host through mucus membranes (eyes, nose, mouth) and infects vascular endothelial cells and cells of the lungs, kidneys, GI tract and begins to replicate. The body initially responds to the virus through a host of Innate Immune mechanisms; these generic counter measures are deployed against all invading pathogens as a first line defense and are not specific to the invading pathogen. Unfortunately, these initial immune responses aren’t always adequate to contain the virus (the virus sometimes evades destruction, other times the virus just overpowers the immune response) so our body deploys a second type of response known as the Adaptive Immune response. In this phase, T-cells and B-cells are primed to respond to the specific infectious agent (here, SARS-CoV-2). Often this two-pronged approach works to contain the infection, eliminate the virus and build up lasting memory to subsequent infections. Unfortunately in some people the virus spreads too rapidly and the immune response doesn’t respond appropriately, leading to destruction of their organs (notably the lungs) and potentially death. Sometimes this more severe outcome is caused by the virus itself, but more often it seems to be caused by an overzealous immune system trying to play catch-up. So there’s the quick and dirty; in the following paragraphs I’ll go into more detail about Viral Entry/Binding/Replication, Early Cellular Responses, Clinical Symptoms, Adaptive Immune Response and What Happens and Why the Immune System Sometimes Fails.

The information in the following paragraphs comes from a combination of basic immunology principles (Kuby Immunology textbook), observations and early research released about Covid-19 and conclusions drawn from earlier studies of SARS-CoV-1 (a virus that is very similar to the current SARS-CoV-2, but with some caveats of course). As Covid-19 is still a new disease, we are constantly learning new things about the virus, infection cycle and pathology, so while what I outline here is based on a lot of research, there are definitely aspects of this virus that we don’t fully understand, and need further investigation.

Graphic of the structure of a SARS virus, the S, M and E proteins are the most important in regards to host recognition, Li et al 2020.

Viral Entry and Replication

Coronaviruses get their name from the hallmark shape, a circular capsid (or shell) that is spiked with proteins on the outside and sheltering the virus genetic sequence on the inside. The Spike (S), Membrane (M) and Envelope (E) proteins make up the majority of the viruses outer shell, while the Nucleocapsid (N) protein found inside the virus assists in viral replication. This small assortment of proteins, plus a few others, make up the bulk of the very simple viral structure (Weiss 2005, Li 2020). The novel coronavirus 2019 (COVID-19) shares a lot of homology or similarity with the original SARS virus that was discovered in 2002, genetically 80% similar, while being 76-95% similar for the major proteins listed above (Xu 2020). This allows researchers to draw a lot of conclusions from previous research on SARS-CoV-1, though we must be careful when doing so, as there are some known (and unknown) differences between the two viruses. The infection cycle starts with the virus gaining entry to the host, usually through mucus membranes of the eyes, nose and mouth. Once inside the virus often begins it’s infectious cycle by infecting vascular endothelial cells that line vessels throughout the body. While different viruses have different mechanisms by which they enter host cells, SARS-CoV-2 binds to the ACE2 receptor using its spike protein (same as SARS-CoV-1), allowing it to enter the host cell (Jia 2005, Walls 2020). Like most viruses, SARS-CoV-2 then goes through a multi-stage process by which it hijacks some of machinery inside our own cells to in order to replicate, escape and subsequently infect more cells in a continual cycle (Frieman 2008).

Overview of the SARS viral life cycle inside the host, Frieman et al 2008.

Early Cellular Response

Thankfully our body has a whole host of immune mechanisms it utilizes to deal with infectious agents of all types. Almost as soon as an invading pathogen has infected our cells the immune system starts going to work. The Innate Immune response is our constantly active sentinel, whose cells are constantly circulating all over our body just looking for foreign invaders to attack and kill. These innate cells use Pathogen Associated Molecular Patterns (PAMPs), or markers of foreign invaders, as the initial signals something is wrong and that it’s time to go to work (Li 2020). Some cells go to work directly attacking the virus and infected cells in an attempt to destroy the virus, others release signaling molecules known as cytokines and chemokines that recruit other cells to help in the fight (Frieman 2008), and some cells just go ahead and sacrifice themselves in an effort to prevent the virus from hijacking them, a process known as apoptosis (Lim 2016).

Symptoms: What and How They Manifest

While this system works well for many invading pathogens (why we are not sick all the time), allowing our body to control the infection, many viruses (and bacteria) have evolved mechanisms by which to evade, subvert and co-opt the immune response to their advantage. For SARS-CoV-2 it seems to be able to prevent the host immune system from activating one of it’s key anti-viral signaling pathways, the Type 1 Interferon pathway (Lim 2016, Li 2020, Frieman 2008). While it is not known exactly how the virus subverts this system a few hypotheses involve the Nucleocapsid protein (Lim 2016), other non-structural proteins (Lim 2016), and some of the SARS enzymes (Chen 2014). So by reducing the host immune response the virus is able to more effectively replicate and spread, leading to a more systemic infection. This is when we start to experience more of the hallmark symptoms of the infection; fever, sore throat, coughing, fatigue, pulmonary inflammation leading to shortness of breath and possible pneumonia and lymphopenia (a decrease in lymphocytes, more on that later) (Huang 2020, Zhu 2020). Most of these symptoms are a physical outcome of the body’s ongoing fight with the virus, trying to delicately balance destroying the invader, while preserving the host organs and system. The fever is the immune system’s attempt to raise the core temperature enough to burn out the infection. The sore throat/cough is an outcome of our immune system attacking infected cells of the airways and trying to expel the invader (mmm mucus), same for the pulmonary issues (initially, more on this later too). While many of these symptoms may be scary and uncomfortable they are often a normal part of our body’s healing process when dealing with a foreign invader. So under normal circumstances, it’s best to rest and let your body do it’s thing, unfortunately this doesn’t always go as planned, as we’ll find out in the following sections….

Adaptive Immune Response; Stage 2

In the previous two sections you’ve seen how our well intentioned Innate Immune system can sometimes fail leading to illness, thankfully the body has a backup, the Adaptive Immune response. This secondary wave of the immune response goes into action very soon after the initial infection (several hours to few days, infection dependent) and is mostly comprised of two cell types; T-cells and B-cells. When the levels of virus in the body start to rise, several of the innate immune cells can act as activators of the adaptive immune response, taking pieces of the virus to specialized activation centers know as lymphoid organs. These centers of immune activation are spread all over our body and are the primary site of pathogen specific antigen (virus pieces) presentation. The antigen presenting cells (Dendritic cells are most prominent) present the virus to the T-cells and B-cells as if locks in a door, allowing the T-cells and B-cells to go to work making specific keys (receptors and antibodies) that can attack and destroy the pathogen in a very focused manner. The outer proteins that make up the viral capid (proteins S, M, E) tend to be the most effective as this is what is visible to our body when intact virion are released (Liu 2017). So the body makes a whole army of these specific cells that traffic to the sites of infection; T-cells directly attack the virus and infected cells, while B-cells make antibodies that bind to parts of the virus, preventing them from entering new cells and marking them for destruction (Liu 2017).

These two arms of the Adaptive Immune response are also what comprise our immunological memory. Virus specific T-cells and antibody producing B-cells remain dormant in specialized lymphoid organs (sometimes they also remain in circulation), just waiting for the virus to turn up a second time. This time since they are already primed and ready to go, memory T-cells and B-cells start attacking the virus almost immediately, usually preventing the virus from spreading and preventing us from getting sick. Studies of SARS-CoV-1 have found both memory T-cells and memory B-cells (producing neutralizing antibodies) that are capable of rapidly responding to viral reinfection (Li 2020, Liu 2017, Channappanavar 2014). In human patients who recovered from SARS-CoV-1 infection anti-SARS antibodies and memory T-cells were found in most patients up to 24 months after infection (Liu 2006, Ka fai 2008, Liu 2017). While antibody responses did decline over time in SARS-CoV-1 patients (many undetectable at 6 years), memory T-cell responses were conserved for up to 11 years after infection (Tang 2011, Ng 2016, Liu 2017). Similar high quality neutralizing antibodies have been found in COVID-19 patients, but since the disease is so new the longevity of memory responses to this new virus aren’t exactly known. Encouragingly, since SARS-CoV-2 is so similar to the original SARS virus, and lab testing has even shown that their be might cross-reactive protection between the two diseases (Walls 2020), there is much hope that the long lasting memory responses seen for SARS-CoV-1 would also apply to those who have recovered from COVID-19. All of this evidence, both old and new, does inspire a lot of hope that a functional vaccine would both be likely and very effective in providing some duration of immunity from COVID-19, but how long remains to be seen.

Graphical overview of the many cells and pathways involved in the host immune response to SARS. It’s a complex set of feedback loops and interactions with a lot of variables. Li et al 2020.

When the Immune System Fails, Severe Disease

The reason COVID-19 is such a scary disease, isn’t because our immune system has no problem fighting it off, but because in some percentage of the cases (uncertain, but estimates are as high as 10-20%) patients need to be hospitalized due to severe complications. If our immune system is so complex and so strong, why do patients with COVID-19 get so sick that they need hospital care? It comes down to numerous very subtle things this virus does that are different than coronaviruses that cause the common cold. One is the effect SARS-CoV-2 has on Type 1 Interferons mentioned earlier, reducing the body’s initial response to infection. Another early symptom seen in many severe cases is lymphopenia, or a loss of lymphocytes (notably T-cells) early on in disease (Huang 2020, Schmidt 2005, Weiss 2005). While the exact cause of this loss of T-cells is not known, it is hypothesized that the viral proteins may lead directly to T-cell death as a mechanism of immune evasion (Lim 2016, Li 2020). These mechanisms of avoiding immune detection along with the efficiency of viral replication can lead to an out of control infection very quickly.

But in the end, it’s only partially about the virus, and largely about an overexuberate immune response. In an attempt to catch-up to the wide-spread infection the immune response goes into overdrive, ramping up a lot of the inflammatory cells and signaling molecules that tell the body to attack the infection (Li 2020). This response does in fact kill the infected cells, but it also destroys lung tissue (primary target), vascular tissue, liver tissue and other infected tissues (Tian 2020, Schmidt 2005). This is often when the more obvious signs of pneumonia set in; the lungs fill with fluid, the efficiency of aveoli decreases (oxygen absorption) and breathing becomes very labored and difficult. This is the tricky thing about COVID-19, making our immune response more efficient would help prevent early infection, but later on would lead to increased tissue damage. But if we reduce the immune function of the body to prevent self-inflicted tissue destruction, we run the risk of allowing the virus to run rampant throughout our body. COVID-19 is a tricky disease to treat for these reasons, and because the disease severity has a wide range of outcomes for different people. In some, infection is very mild and asymptomatic, in others, their entire body shuts down as the virus (and immune system) destroys the host from the inside. The reason many comorbidities are important as risk factors for severe disease is that most of them either affect the immune system or lung function. Obesity, diabetes, auto-immune diseases all alter the immune system’s ability to function, making it harder to fight off the virus. COPD and asthma (though less prominent then thought) make the host pulmonary system more sensitive to damage caused by the virus and immune system.

But not all hope is lost! Because of the large body of evidence suggesting that SARS viruses create robust lasting immunity, this means a vaccine might be very effective at protecting most of the population. Also, now that there are many patients who have recovered from COVID-19, tests are underway to examine if using their plasma (containing antibodies) can help patients who are suffering from more severe cases of the disease (works for other viruses like Ebola). We also have several promising anti-viral agents that are already in clinical trials being tested against COVID-19, with hopes that one or more of them will help improve patient outcomes and be ready for use later this year. Unfortunately all of this does take time, meaning we won’t have a cure next month, but by slowing the spread of the virus, not only do we allow hospitals to manage the patient load, but we allow all the scientist out there to catch-up and produce much needed data, therapies and vaccines.

Thanks for reading. If you see any mistakes please bring them to my attention and I will correct them ASAP. If you have additional questions or want to discuss the immune response in more detail (this is a very high level overview) I’d be happy to do so via text or email. Stay safe and stay healthy.

Literature Citations:
Chan et al, Serological Responses in Patients with Severe Acute Respiratory Syndrome Coronavirus Infection and Cross Reactivity with Human Coronaviruses 229E, OC43, NL63. Nov 2005, Clinical and Diagnostic Laboratory Immunology.
Channappanavar et al, T cell-mediated immune response to respiratory coronaviruses. May 2014, Immunology Res.
Chen et al, SARS coronavirus papain-like protease inhibits the type 1 interferon signalling pathway through interaction with the STING-TRAF-3 TBK1 complex. Jan 2014, Protein Cell.
Frieman et al, SARS Coronavirus and innate immunity. 2008, Virus Research.
Huang et al, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Jan 2020, Lancet.
Jia et al, ACE2 Receptor Expression and Severe Acute Respiratory Syndrome Coronavirus Infection Depend on Different Human Airway Epithelia. Dec 2005, Journal of Virology.
Ka-fai Li et al. T cell responses to Whole SARS Coronavirus in Humans. Oct 2008, Journal Immunology.
Li et al. Coronavirus infections and immune responses. Jan 2020, Journal of Medical Virology.
Lim et al. Human Coronaviruses: A Review of Virus-Host Interactions. 2016, Diseases.
Lu et al. Immune responses against severe acute respiratory syndrome coronavirus induced by virus-like particles in mice. June 2007, Immunology.
Ng et al, Memory T cell responses targeting the SARS Coronavirus persist up to 11 years post-infection. March 2016, Vaccine.
Schmidt et al. Coronaviruses with a special emphasis on First Insights Concerning SARS. 2005, Birkhauser Advances in Infectious Diseases.
Tang et al, Lack of Peripheral Memory B cell responses in Recovered Patients with Severe Acute Respiratory Syndrome: A Six-year Follow-up Study. May 2011, Journal of Immunology.
Tian et al, Pulmonary Pathology of Early-Phase 2019 Novel Coronavirus (COVID-19) Pneumonia in Two Patients with Lung Cancer. Feb 2020, Journal of Thoracic Oncology.
Walls et al, Structure, Function and Antigenicity of SARS-CoV-2 Spike Glycoprotein. Apr 2020, Cell.
Weiss et al, Coronavirus Pathogensis and the Emerging Pathogen Severe Acute Respiratory Syndrome Coronavirus. Dec 2005, Microbiology and Molecular Biology Reviews.
Xu et al, Systematic Comparison of Two Animal-to-Human Transmitted Human Coronaviruses: SARS-CoV-2 and SARS-CoV. Feb 2020, Viruses.
Zhou et al, Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. March 2020, Lancet.

COVID-19 and Masks, 4/5/20

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There’s been a lot of debate and misinformation floating around about the use of masks for the general public as a measure to prevent the spread of infectious diseases, specifically Covid-19 in the United States. Do they help, do they not? Is an N95 really better than a surgical mask, is this better than a cloth mask? How and when should they be used? On 4/3/20 the CDC in the United States finally came out with a blanket recommendation that ALL citizens of the United States wear some sort of face covering whenever in public. This was a dramatic change of direction from the previous recommendation that masks were completely unnecessary, except for front line hospital workers and for the infected. In this rendition of Eric’s Science Corner I’ll do my best to present some of the data and studies that have looked at the questions above, in an attempt to clarify the misunderstandings and the mixed messages. The topics I’ll try and cover are; what are the different types of masks and what are they designed to do? How useful are the different types of masks for the general public? And finally, a few best practices on how to wear and use a mask or face covering. Rule #1, just ignore anything Donald Trump says, now on with the info.

Defining Mask Types

To start there are three main categories of face masks that I’ll be discussing; fitted N95 respirators, professional grade surgical masks and cloth masks (variety of materials). There are numerous sub-categories for each and also other types of protective face wear I won’t discuss because they aren’t really relevant to the general population, only to those in the hospitals and those of us who work in laboratories. The first type is the fitted N95 respirator, these are face fitted respirator masks that have been certified to filter out approximately 95% of aerosols and particulate matter (when worn properly). You breath through either a small filtration unit in the front of the mask or directly through the filtering material of the mask, NOT around the sides (as it should be sealed). The professional grade surgical masks that many of us have seen in the hospitals are loose fitting non-sealed masks that are designed to block the wearer from inhaling large droplets/splashes and to block their respiratory emissions (protecting others around them). They are not designed to prevent the wearer from inhaling aerosolized particles as they are not sealed around the edges (cdc.gov, crosstex.com). The final group are the cloth masks which can be made from various materials. Their main purpose is to allow more comfortable widespread facial covering for the general public; to reduce the inhalation of larger droplets and to reduce one’s own exhalation and aerosol creation. These types of masks are not specifically certified in any way, though I will discuss the research that has been done looking at filtration, efficacy and utility of the different materials.

On the left is a standard N95 Respirator mask, on the right is a surgical mask.

So now on to how well do these different types filter out microparticles, specifically in regards to viral transmission (because that’s what’s on everyone’s mind). Numerous studies that compare N95s and surgical masks and how they prevent infection in hospital settings have shown both to be similarly effective when dealing with droplet based respiratory viruses like influenza (Randanovich 2016, Smith 2016). Laboratory testing of these two types of masks does confirm that the smaller the particle size, the better an N95 performs compared to a surgical mask (van der Sande 2008, Shakya 2016), thus they are more effective for those dealing with high level risk of aerosolized viral exposure. These two types of masks are certified, so it’s no surprise they perform fairly well, but what about the cloth and homemade masks? The first thing to consider is the type and thickness of material being use for the mask. Things that allow easy breathing or light to penetrate aren’t going to filter the air as efficiently, but if it’s too thick that you can’t breathe through it then it becomes extremely hot, uncomfortable and unwearable (and you breath around the sides, rather than through the material). One study comparing the filtration efficiency (of masks in a lab test, not on a person) of different materials found that items such as tea towels and cotton mixed fabrics did the best job of filtering particulate matter (up to 70% mean filtration) out of the air, while silk, scarves (like buffs), pillow cases and normal cotton T-shirts did not perform as well (45-60% mean filtration efficiency), with surgical masks being their standard (90-96% mean filtration)  (Davies 2013). When commercially available cloth masks were compared to surgical masks on humans (again in a lab) filtration efficiency was more variable; with cloth filtering out 30-50% of microparticles while surgical masks filtering out 60-90% of microparticles and N95s consistently filtering out 80-95% (Shakya 2016). The efficiency of filtration directly correlated to the size of the particle, with cloth masks performing the poorest on particles small than 1µm in size. So that’s a little background about how the masks are INTENDED to be used and how they function in a laboratory, how about in real life?

Use in the General Public

By now you’ve probably heard many times that the public should not hoard or use N95s because we need them for our frontline workers (very true) and they don’t work for the public (partially true). The first piece is that because of the size of this pandemic we don’t have sufficient supplies of N95s for highly trained hospital workers who are coming into direct contact with the virus on a daily basis, thus need this heightened level of protection, first (and most important) reason not to stock up or hoard them. The second is that for an N95 to be at it’s most useful and functional you have to have it fit tested, you need to be trained in proper techniques to don/doff a mask and you have to actually use it correctly (you can’t be taking it off to talk, to eat, to drink, basically you can’t break the seal unless in a clean contained environment). They are also designed to be disposable, meaning you can’t wash them, though sadly our healthcare workers are being forced into extreme measures to try and sterilize/reuse them for lack of options. For the general public a surgical mask would be a descent option because they are designed to reduce droplet transmissions and to block one’s exhalations (protecting those around you), but sadly our hospitals are also short on these too, so for now they need to be saved for the frontline works (and patients) where they’ll do the most good. Also remember that both of these are designed to be disposable, so can’t be washed and aren’t designed to be reused for weeks on end (like the public would need).

So this brings us to cloth masks and their use in the general public. Mistakenly the US government (CDC) originally came out saying that cloth masks don’t work and that they aren’t necessary. By now most people have realized this isn’t exactly true, because why else would they change their minds and recommend people wear them? Yes, cloth masks are NOT designed to stop all tiny viral particles (and aerosols) from passing through, and yes they are not highly efficacious, but that doesn’t mean they don’t help. While a cloth mask won’t fully stop one from inhaling aerosols and microparticles, they do filter out some of the smaller aerosols (30nm-1µm) but more importantly block larger droplet transmission both inward and outward (Davies 2013, Shakya 2016). So while they do filter some of the air you’re inhaling, the major benefit of a mask is to protect those around you by minimizing the amount of aerosols you create. This is especially true with the knowledge that those infected with COVID-19 can be asymptomatic but still capable of spreading the infection. For masks to be most beneficial we all should wear them in any public setting where we’ll be interacting with others (even if we’re socially distancing).

Best Practices for Masks

Now on to a few personal suggestions for best practices when using a face mask. Note that much of this stems from my own personal training having worked in Biosafety Level 3 laboratories (blood and aerosol transmitted infectious diseases) and in hospitals, but some additional guidance can be found on the CDC website (CDC.gov). First off, once you’ve made/acquired your mask, put it on at home and work on the fit, comfort, breathability. A mask that doesn’t stay on or that you can’t semi-comfortably wear (to the point you’ll touch it a lot or take it off) isn’t very useful. Look to make sure it fully covers your nose and mouth, has a pretty good fit around the bridge of your nose and the sides, and that it won’t slip down when you turn/move your head.

Once you’ve established it works, wear it around for 20-30min inside your house to get used to the idea of breathing through a mask. It’s probably going to be a bit awkward at first, as for most people they’ve never had to do it before. This exercise will make it easier to wear in public without thinking about it too much. Now on to that more critical step, wearing it out. The main times the mask should be worn is whenever you’re going into a public area where you might have close contact with others. If you’re just sitting in your car and driving around, no need to wear a mask, but if you go to the grocery store, pharmacy, liquor store, gas station, work, or even walk around your neighborhood it’s best to wear the mask to protect those around you, even if you don’t think you’re sick.

To put on the mask, do so BEFORE entering that public space, meaning your home entry if you’re walking around the neighborhood or inside your car before you walk into a shop. Then clean your hands off so that you are less likely to contaminate other surfaces (hand sanitizer or washing). When you’re wearing you mask you SHOULD NOT be taking it off or moving it off your nose/mouth until you’re back in your non-public safe area. Wearing it half the time, pulling it down half the time, taking a break to eat or drink in public negates some of the benefits and protection and also adds to the chance that anything you pickup on your hands will be transferred to your face. When you’ve exited the public space, wash/clean your hands then grab the strings/band of the mask and remove it (do not grab the front of the mask itself). If you have a washable reusable mask proceed to wash it with soap and water. Disposable masks are supposed to be discarded into the trash (hence why not ideal for daily use in public). While your mask is your barrier of protection, remember it’s not foolproof, and is merely a way to further reduce your risk of becoming infected and infecting others. IT DOES NOT change the fact we should be social distancing and providing each other space or that we should be staying at/near home and avoiding any unnecessary travel/errands. Wearing a mask is just another tool in our arsenal to help slow the spread of the virus and reduce transmission rates.

One last note about gloves. Wearing gloves for most people in a public setting is useless (yes I said useless). Gloves are a very effective piece of PPE for trained healthcare and lab workers, but in our daily lives most people treat gloves just like their normal hands. They touch common surfaces, pick up food items, open doors, text on their cell phone, touch their mask, etc. All of these practices together make the use of gloves just as bad as dirty naked hands. You’re better off just considering your hands as dirty whenever you’re in public and not touching any of your personal belongings (including that cell phone) until you’ve cleaned them. If you have to touch your phone or food items while in public, there are many ways to also clean these surfaces as well. Don’t waste gloves and don’t touch your face.

Citations
Balazy et al. Do N95s respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks. American Journal of Infectious Control, 2006.
cdc.gov/hai/pdfs/ppe/ppeslides6-29-04.pdf . CDC Guidelines for Selection of PPE in Healthcare.
cdc.gov/niosh/npptl/pdfs/UnderstandDifferenceInfographic-508.pdf . Understanding the Differences, Surgical Masks, N95 Repsirators.
crosstex.com/sites/default/files/public/educational-resources/products-literature/guide20to20face20mask20selection20and20use20-202017.pdf . Guide to Face Mask Selection.
Davies et al. Testing the Efficacy of Homemade Masks: Would They Protect in an Influenza Pandemic. Disaster Medicine and Public Health Awareness, 2013.
osha.gov/Publications/osha3079.pdf . OSHA Respiratory Protection Guidelines.
Randanonvich et al. N95 Respirators vs Surgical Masks for Preventing Influenza amount Healthcare Personnel. JAMA, 2019.
Sande et al. Professional and Home-Made Face Masks Reduce Exposure to Respiratory Infections among the General Population. PLOS One, 2008.
Shakya et al. Evaluating the Efficacy of Facemasks in Reducing Particulate Matter Exposure. Journal of Exposure Science and Environmental Epidemiology, 2016.
Smith et al. Effectiveness of N95 Respirators vs Surgical Masks in protecting healthcare workers from acute respiratory infection: a systematic review and meta analysis. CMAJ, 2016.

Covid-19; Testing, Drugs, Vaccines and Seasonality 3/25/20

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It’s been a week since my first Covid-19 blog on 3/18/20, and I will have to admit how amazed I am at the feedback and attention it got. A LOT has happened since that day, and not all of it has not been so positive. Here in Colorado Governor Jared Polis officially announced today (3/25/20) that ALL residents of Colorado are under a ‘Stay at Home’ order. Meaning we’re supposed to stay in our place of residence with the exception of essential trips (medical, food, work for us exempt jobs) and exercise, all the while maintaining social distancing from anyone not in our immediate household (which is just me and my cat). For many of us this isn’t too much of a change, but for those who didn’t think this was serious it’s probably a bit of a rude awakening. Since my post LAST WEEK (now 3/26/20) the number of worldwide confirmed cases has more than doubled to 530,000 (from 219,243), the number of deaths has increased to over 24,000 (from 8,968) and on 3/26/20 the United States confirmed over 17,000 NEW cases, making us the country with the most confirmed cases in the world (go us?) (worldometers.com, washingtonpost.com).

I’m hoping by now that most people realize how serious this is, and that there is definite need to slow the spread; both to allow our medical care teams to keep up and to allow scientist to keep working (please no arguments on the political actions or economic impact, yes it’s going to be bad). My goal in this blog write up is to outline the things that help us bring this pandemic to an end (or at least slow it down). I’ll be focusing on the status of testing in the US (what those tests are), the current drug pipeline and what is being tested, the process and timeline for a vaccine and whether there’s anything to the claim of seasonality with the infection. So here we go, Round 2, diving back into the Science!

Testing

So in my last post I wrote about how much of a mess the Covid-19 testing and surveillance were in the United States, well sadly that has not improved a whole lot. While we’ve definitely tested a lot more people, I’ve been hearing from providers and hospitals all over the country that they’re only testing people who are in high risk populations or have advanced/severe cases of disease. Very recently a rash of new tests have become available to providers and hospitals, meaning the surveillance is starting to grow and hopefully this will continue. There is definitely hope as we are soon to have two different types of tests available, the PCR based tests that we’re currently using for diagnosing active disease and an Antibody based test.

The PCR based test is the one I spoke about previously where labs are able to look for pieces of the viral genome in human samples (usually a nasopharyngeal swab). This test can be quite sensitive and is used to identify infected patients even during the early stage of disease. Though, being such a sensitive test it is more prone to errors and false positives (though they are still very well validated), hence why the original CDC test failed. The other issue right now is that because there’s not a lot of top down coordination in the United States we have dozens of different labs who have created PCR based tests that are being used in different parts of the country. Here are a few of the companies/hospitals who have created PCR based tests; ThermoFisher, Roche, Cepheid, Mayo Clinic, Stanford University, University of Pittsburgh, Atrium Health and the list goes on and on. The CDC even setup a website to allow researchers to develop their own tests and to provide some general guidelines. While on the surface this seems smart, it also means we don’t have any national coordination in our Covid-19 testing on the ground.

The second type of test that is just now being release is a test to look for IgM and IgG antibodies in the blood of patients. You might remember in the previous post where I talked about us building immunity to the virus? Well, antibodies are one of the hallmarks of immunity, and we can test for them, even after we’re no longer infected. A simple prick of the finger (a little blood) on a indicator strip and we have a positive or negative for SARS-CoV-2 antibodies in minutes rather than hours or days, think of it like a pregnancy test for Coronavirus (United Biomedical, Aytu Bioscience). The problem with these tests is that SARS antibodies may not be detectable until 7-14 days after onset of symptoms (Chan et al 2005), so there’s a good chance they won’t identify people who are in the early stages of disease. They WILL help us dramatically as we attend to understand the true prevalence of the disease and how many people are now immune. Once a person is immune and recovered you’re very unlikely to pickup or spread the disease.

Drugs and Clinical Trials

Much to the chagrin of many of us in the biomedical research sciences and healthcare, Donald Trump touted hydroxychloronquine as a ‘game changer’….wow wow, let’s pump the breaks for a second, back it up, and talk about the process by which drugs are created, rigorously tested and finally produced for mass distribution (if they even make it there). The first step is identifying potential drugs and targets then testing them in a laboratory to see if they actually work like you hoped and they’re not excessively toxic. This usually involves some mix of cell culture and animals models. If a candidate is lucky enough to make it through the lab testing phase (known as pre-clinical trials, only 1 in 1000 do) then the company can apply to the FDA to move it’s drug on to a multi-stage Clinical trial in human subjects. Phase I of the clinical trials process involves taking healthy individuals and dosing them with the new drug (usually starting low and escalating). They have to look for safety, effects on the body, toxicity, side effects, maximum tolerate dose, tissue distribution, half-life and on and on. IF the drug makes it through this initial phase then it’s on to Phase II where the drug is tested in a medium size group of diseased individuals (in this case Covid-19 positive). All of this under careful supervision of doctors who are specially trained to assess dosing and efficacy. If the drug proves efficacious in this Phase II study it will move on to a larger Phase III randomized double blind study where the drug being tested is compared to a placebo control (sugar pill) to ensure that it’s really the drug having an effect. These large studies can include 1000s of people and take many years depending on the nature of the disease being tested. Finally, once a drug survives Phase III; proving safe, efficacious and with the dosing amount and regimen worked out, the company can file for approval from the FDA (1 in 5000 make it this far)(medicine.net). This whole process can take up to 12 years for chronic diseases, but of course right now things are moving much more rapidly, and a lot of the regulations and paperwork are being modified to speed up the process.

So what about all the drugs that are being tested against Covid-19 right now? There are several drugs that were identified as being potential therapeutics, and thankfully they had already passed Pre-clinical testing and Phase I trials, so this dramatically expedites the process of testing. The most promising seem to be Remdesivir (from Gilead), Favipiravir (anti-viral), and the previously mentioned hydroxychloroquine (cdc.gov, Dong et al, Wang et al). Even though all of these drugs have successfully completed varying levels of clinical trials, using them against a new disease requires a new round of efficacy, dosing and safety testing. Patients with different diseases respond to drugs differently, dosing needs to be adjusted for the new disease and of course the drug needs to be thoroughly tested to ensure that the differences seen in early studies weren’t simply because of patient selection, population bias or other factors that were not controlled for with the small sample set. In short, all these drugs, while promising, are many months away from being approved for safe use in a wide array of Covid-19 patients, if they get there at all. See the comment below from my college friend Aileen, who’s a pharmacist in the San Francisco Bay Area in response to the small test of hydroxychloroquine in patients in France (Gautret et al)….


More PSA from a pharmacist….to detail out certain claims Hydroxychloroquine used in this case is in particular HIGH DOSE (usual dose of the drug is 200-400mg daily, in this case…600mg daily and we only use that dose in Q Fever patients). When the hydroxychloroquine in high dose and azithromycin are taken together, there are risks for GI side effects…and most importantly…POTENTIAL ARRHYTHMIA. First azithromycin is a known QT prolonging agent…but also…hydroxychloroquine can either cause direct mycocardial toxicity or exacerbate underlying mycocardial dysfunction. This is a RISK that must be weighed by physicians and healthcare professionals vs. the unproven benefits.
Is there promise? potentially….but we NEED MORE EVIDENCE TO EVALUATE SAFETY AND EFFICACY.
Please…do not demand for it….leave it to healthcare professionals to make that decision and do our jobs….

The next question is in regards to a vaccine against Covid-19. Unfortunately, the process I outlines above for drugs, also applies to vaccines, but we’re starting from ground zero. Prior to this pandemic there were no coronavirus vaccines available (though plenty of background research), so companies have gone into serious overdrive trying to develop something, and amazingly in just two months Moderna, in collaboration with the NIH, took the first vaccine candidate to Phase I clinical trials this month (March 2020) (nih.gov). A process that usually takes 6-12 months took them 2, let that sink in for a moment. And they’re not the only company working hard on creating a vaccine, as there are numerous others with vaccine designs being tested in Pre-Clinical trials as we speak. But, this bring us back to question of time. Before a vaccine can be deployed to the general public it has many hurdles to pass, and only if it successfully passes those hurdles can it be mass produced and distributed. So, as Dr Fauci has explained many times, we’re looking at best case 12-18months for a vaccine. Guess we’re going to have to hang tight and weather this storm for a bit longer.

Seasonality

Most people have probably heard the claim at one point or another that this thing (Covid-19) is like the flu and it’ll go away when the weather warms up. Even our President claimed “…you know, a lot of people think that (the virus) goes away in April with the heat — as the heat comes in. Typically, that will go away in April.” Is there any logic or scientific evidence to support this claim? The short answer is, no, but it’s definitely more complicated than that.

The idea of seasonality was brought up because the influenza virus does see a very seasonal pattern of spread and retraction. During the cooler winter months in the Northern Hemisphere we see a dramatic rise in influenza infection rates, then a drop as the weather warms in April, as Trump suggested. There are many reasons for this; reduced contact time between people (stuck inside, schools) as weather improves, improvements in immune responses due to people being outside more and increases in Vitamin D, potential increase in duration of infection during winter months, and decreased survival of some pathogens in warmer environments (Fisman et al). While we do have the first three things going for us as they are environmental changes that aren’t pathogen specific, what about the survival time of different viruses? It’s been well documented that influenza viruses survive and transmit best at lower environmental temperatures in the range of 5C and 20C. Though starting at 20C, depending on humidity, influenza virus transmission becomes much more variable, and at 30C a dramatic decrease is seen in viral transmission (Lowen et al). Unfortunately, coronaviruses don’t seem to have the same susceptibility profile. Testing on the original SARS-CoV-1 virus showed that it was fairly stable at environmental temperatures as high as 33C (91F), and only when temperature was increase to 38C (100F) did the virus infectivity begin to dramatically drop (Chan et al 2010). SARS-CoV-2, the causative agent of Covid-19 seems to be more temperature resistant than the influenza viruses that we commonly associate with having seasonal cycles. So with the virus currently spreading in the Southern Hemisphere and in several warm weather countries we shouldn’t expect too much help with the virus from Mother Nature’s change of seasons.

But not all hope is lost! I’ve heard recently that the extreme measures taken by many states have allowed the hospitals in the US a little breathing room. Even if this is short lived it means that staff and supplies can be replenished and that buys more time for widespread testing to come on line. Countries like Germany and South Korea are good case studies for how excellent testing and surveillance can lead to minimizing the number of fatalities (testing large percentages of their populations, and doing so quickly). Even though cases and number of deaths are still increasing, we’re slowly catching up on testing, and keeping our death rate low, but the fact that we have 2,122 serious or critical Covid-19 cases is still a little scary. For now, we’re all going to have to sacrifice a bit, be more compassionate to our fellow humans and just realize that we’re living through unprecedented times, that we will get through, though it’s going to take some time. If you’re interested in reading about some potential scenarios on how the pandemic plays out in the next 3-12months this article from the Atlantic outlines them pretty well in my opinion.

Citations
aytubio.com/covid-19/
cdc.gov/coronavirus/2019-ncov/hcp/therapeutic-options.html
Chan et al. The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus. Advances in Virology, 2011.
Chan et al. Serological response in patients with Severe Acute Respiratory Syndrome Coronavirus infection and Cross-Reactivity with Human Coronavirus 229E, OC43, and NL63. Clinical and Diagnostic Laboratory Immunology, 2005.
Dong et al. Discovering Drugs to treat Coronavirus disease 2019 (Covid-19). Drug Discoveries and Therapeutics, 2020.
Fisman et al. Seasonality of Viral Infections: mechanisms and unknown. European Society of Clinical Microbiology and Infectious Diseases, 2012.
Gautret et al. Hydroxychloroquine and azithromycin as a treatment for Covid-19: results of an open-label non-randomized clinical trial. Journal of Antimicrobial Agents, 2020.
Lowen et al. Roles of Humidity and Temperature in Shaping Influenza Seasonality. Journal of Virology, 2014.
nih.gov/news-events/news-releases/nih-clinical-trial-investigational-vaccine-covid-19-begins
unitedbiomedical.com/COVID-19/
Vincent et al. Chloroquine is a potent inhibitor of SARS coronavirus infection and spread. Virology Journal, 2005.
Wang et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCov) in vitro. Cell Research, 2020.
washingtonpost.com/world/2020/03/24/coronavirus-latest-news/
worldometers.info/coronavirus/

Chaos and COVID-19

22 Replies

Society is in some state of chaos at the moment, and there’s so much misinformation and misunderstanding floating around. So in this blog I’m hoping to provide some of the scientific knowledge based on the research and observations. First, here are my credentials; Masters of Science in Immunology and Infectious Diseases, I’ve spent 14 years in the laboratory doing research (HIV, Tuberculosis, West Nile, Autoimmune diseases, cancer) and worked in a BSL3 laboratory. So with that out of the way, I’m going to try and stay away from giving too many opinions, talking about the politics or debating the models because there’s just too much speculation there. So if you’re interested just in the scientific research about the virus, the immune system and the current case study numbers hang on, this is going to be a long one (all references cited will be at the end).

Background

In early December 2019 a cluster of pneumonia cases appeared in Wuhan, China with clinical characteristics similar to SARS-CoV-1. Of the initial patients studied the mortality rate was extremely high (10-15%, now estimated closer to 2-3.5%), which gave rise to great concern that this virus would be a serious health issue. Sampling from the initial patients and sequencing identified the causative agent as a novel (new) coronavirus that was originally named 2019-nCoV (Huang C et al). Subsequent sequencing and analysis of the virus from those original cases showed that the founding virus has similar characteristics to coronaviruses found in bats, but is also related to those found in pangolins. There are currently two sub-strains of the virus circulating in the population; S-type and L-type. The S-type is thought to be the founding strain, while the L-type is a slightly altered variant that is now the predominant virus circulating in the population (70% of cases), though the consensus sequence for both strains only differ by a few base pairs (Tang et al). As of now (3/18/20) there is no evidence that SARS-CoV-2 can sustain infection and spread through any other animals other than humans. As of 3/18/20 China has experienced 80,894 confirmed cases on COVID-19 (disease caused by the virus SARS-CoV-2 formerly 2019-nCoV) and 3,237 deaths from the virus (worldometers.info). While daily number of new cases in China has significantly waned in recent weeks, it has spread to the rest of the world and is currently spreading rapidly throughout Europe, the Middle East and the United States.

How the Virus Spreads

Viruses can spread by either direct (touching, kissing, sex) and indirect (coughing, sneezing, aerosols) methods. Early on during the epidemic of SARS-CoV-2 it was realized that the virus was capable of spreading by indirect contact and possibly survived in aerosols. Though the primary route of transmission is still thought to be direct or close contact with an infected individual. Studies showed that aerosolized liquids containing SARS-CoV-2 could survive on surfaces (specifically plastic and steel) as long as 72 hours in a controlled laboratory setting (Doremalen et al). Though the half-life of the virus on all surfaces was 16 hours or less. Meaning that while the virus can be detected up to 3 days after deposition most of it dies much earlier, though we don’t know exactly what the survival time in a natural environment is. The main take home from this should be, the virus can be transferred from one host to another fairly easily and surface contamination can be an issue if an infected person sneezes/coughs, so cover your mouth and clean common areas! One thing that has made the virus especially difficult to track and control is the presence of what are known as asymptomatic carriers. These are individuals who become infected with the SARS-CoV-2 virus and are contagious without showing any symptoms (Bai et al). Thus, while they appear fully healthy, they are in fact vectors for the disease without even knowing it. Additionally there can be long incubation times between becoming infected and showing symptoms, thus allowing people to spread the viruses unknowingly.

Preventative Measures (WHO.int)

Standard hygiene rules apply for SARS-CoV-19;
Wash your hands frequently.
Clean common surfaces in shared areas.
Cover coughs and sneezes with an elbow or arm.
Do not touch your nose, eyes and mouth (this is how the virus gains access to the body).
Social distancing (the practice of staying 2m away from potential contacts).
Stay home if you’re sick and self-quarantine. This one is very important and something Americans do not do well.

The question of using masks and gloves has come up numerous times, so I’m going to try and dispel some of the rumors and misinformation. These items are known as PPE (Personal Protective Equipment) to those in healthcare and the medical sciences. They are used to protect one’s self from infectious and hazardous materials when used properly. Both N95 masks (fitted and tested, designed to filter out 95% of microparticles) and surgical masks (loose fitting masks that cover your mouth, no seal) are designed to create a barrier between the user and the surrounding environment. N95 masks when worn properly will filter out most particulate and infectious matter, protecting the wearer, when USED PROPERLY. Proper use does not include wearing it around your chin, pulling it off your nose to breath or touching the mask with unwashed hands, in short most of the public is not trained well enough to properly use these and thus negates a lot of the benefits they can provide. Surgical masks on the other hand are designed to protect those surrounding the user by blocking some of the aerosolization of material, they ARE NOT designed to protect the user from inhaling microparticles (same goes for cloth masks) (Balazy et al). The reason the government does not want the public using and hoarding these disposable masks is that there is a HUGE shortage for our healthcare workers, the people who have to take care of the sick and injured on a daily basis (which may be you). They come into contact with the infectious and at risk at levels exponentially higher than the average person and if they don’t have these protective equipment then it’s almost a certainty they’ll get infected, and then either be forced to take time off (leaving our hospitals understaffed) or infect those around them such as patients who are at risk. If you’ve been hoarding masks or bought a bunch think of donating them to your nearby hospital, every nurse or doctor I’ve spoken with says they are rationing and running very low on these supplies. If you need to wear a mask buy a cloth reusable mask (and wash it regularly) in order to protect those around you from anything you might be carrying. As with the N95s above, disposable latex and nitrile gloves are not very practical or helpful for most people. Every time you touch your body, your cell phone, your hair, your mask on your face, you contaminate the gloves and spread that contamination around. Save yourself the waste and trouble and just regularly wash your hands.

Symptoms and Testing

The main symptoms as outlined by the Center for Disease Control (CDC) are; fever, cough and shortness of breath along with a host of other minor symptoms (CDC.gov). What sets SARS-CoV-2 apart from influenza or the common cold is the lower respiratory involvement. Symptoms usually appear in 2-7days, but there have been cases where symptoms are very delayed (beyond a week). The state of Colorado recommends that if you have these symptoms or are concerned due to exposure to a positive case to call your primary care doctor first, do not go to an ER unless it’s an Emergency.

Once the virus enters the body it binds to ACE2 (Angiotensin-Converting Enzyme 2) receptors on vascular endothelial cells and uses these cells as a host to replicate. ACE2 receptors are also found in the lungs, kidney and GI tract, all locations known to harbor coronaviruses (Jia et al). In addition to the more general symptoms, in moderate to severe cases pulmonary inflammation and damage are seen and these are considered the more critical issues when looking at long term prognosis. CT scans of the lungs were found helpful in diagnosing patients with more advanced disease (Zhu et al). Patients over the age of 65 and those having a host of other chronic disorders (hypertension, diabetes, auto-immune diseases, immunocompromised) are more likely to progress to severe COVID-19 disease than those without (Zhou et al). Though recently it has been seen that even younger patients can have lasting pulmonary damage beyond disease resolution.

Which brings us to the next issue, testing…oh testing….. When the epidemic first began in China researchers isolated and sequenced the viral genome (this is an RNA virus). Allowing them to identify unique sequences in the virus that they could use as a genetic finger print. In January of 2020 a group at the Charité University Hospital in Berlin released information on an assay that would guide the creation of the first large scale PCR testing to be adopted by the WHO (Corman et al). Since then several other countries have released different versions of the test. Since January over 1million tests have been run around the world, with China (320,000), South Korea (286,000) and Italy (148,000) leading the way (ourworldindata.org). Sadly the estimates in the United States are that only 41,000 people have been tested. I say ‘estimates’ because right now we have no National testing strategy or centralized facility monitoring our testing. Tests are being run by government labs, hospitals, private diagnostic labs and even some private biotech companies have created their own tests, but the short of it is there’s no central coordinated effort as of 3/18/20. If you’re interested in reading more about what went wrong with our testing, check this article from the New Yorker.

Which brings us to how can you get tested? Well, the short answer is most people can’t. Because of testing shortages the guidelines on who can get tested vary wildly from state to state and county to county. The standard criteria in Colorado as of 3/18/20 is that you must have an order from your healthcare provider, stating known contact with another infected patient and/or presenting with symptoms. Even if you do meet that criteria there’s no guarantee you can or will get tested right now, I personally know several people who fit the criteria but have been turned away to self-quarantine and monitor. So how do you know if you are infected with the virus? Well, in the United States right now you really don’t, and in lieu of broader testing to identify the spread of the virus social distancing and limitations on group gatherings (including concerts, bars, restaurants) have been put in place.

Treatment Options

Right now there’s no fully validated and approved treatments for COVID-19 (SARS-CoV-2). For those with more mild forms of the disease the CDC recommends; quarantine, rest, monitor your symptoms and continue with the preventative measures listed above. For those with more severe symptoms go to the hospital for care.

As of 3/18/20 there are numerous companies in the early stage of testing vaccines against COVID-19, one has even begun Phase I human trials, which simply looks at whether or not the vaccine is safe in humans, it’s a long way from mass production though. There are also several approved medications that are being tested in Phase II and III clinical trials in patients suffering from COVID-19; Remdesivir, Chloroquine and Favipiravir appear to be the most promising. All three were originally developed for other diseases (Ebola, malaria, influenza) but are being repurposed to fight COVID-19 and have shown promise in early patient testing. It’s quite common for drugs to be tested and used for numerous different indications, because this expedites testing as the safety has already been proven in previous studies. EDIT:
Because Trump and the FDA made specific announcements about Hydroxychloroquine today (3/19/20) I’ll add an extra note here. Hydroxychloroquine has been been used as an anti-malarial (parasite) for almost 70 years, and is also used to treat Lupus and rheumatoid arthritis, so you might ask, how does this drug help us fight a virus??? The drug alters the pH inside special compartments inside our cells (for the scientist; lysosomes, endosomes and the Golgi) having an affect on several pathways. One such pathway is the process of breaking down antigens and presenting them to immune cells (Fox et al). For autoimmune diseases this means the drug helps slow the immune response to your own body, but this is counter productive to fighting a virus that we want to kill, so what gives? Ah, but there’s an alternate pathway that the drug affects, modification of proteins in the Golgi. These modifications are essential for viruses to replicate and produce more functional virion! So the drug does function to slow down some parts of the immune system (not all) BUT it also serves to reduce viral replication (in experiments with HIV showed modest reduction, SARS-CoV-2 specifically has not been tested yet) (Romanelli et al).

Immunity?

With most infections, your body has two stages of response. First is the non-specific innate immune response where our body recognizes that there’s a foreign invader (bacteria, virus, parasite, etc) and attempts to kill it. Sometimes the number of the microbe is too great and they infect and spread in the body causing disease. All infectious organisms have a minimum infectious dose that’s required to get a person sick, though this exact amount varies from person to person, for route of entry and is different for each microbe. Once the initial non-specific response fails our body goes into overdrive to try and kill off the rapidly replicating organism. This includes running a fever to burn the pathogen out and creating a pathogen specific memory response via T-cells and B-cells selection. These specific memory responses are the backbone of what is known as pathogen specific immunity, or our ability to fight off a disease. As of now (3/18/20) it appears as though people who survive and recover from COVID-19 are immune to the virus. Recently there have been news articles about how several recovered COVID-19 patients have retested positive for the virus, these cases most likely fall into one of two categories; first that the patients were released prematurely from the hospital and thus still had low levels of virus remaining in their system, second the recovered patient came into contact with another infectious patient who transferred the virus to them allowing them to retest positive. Being immune does not mean that another person who is infected can not transfer the virus to us, it simply means our body is able to destroy the invading pathogen before it causes disease, this is how a vaccine works. Note that in both cases the affected individuals did not get sick a second time (as far as we know) and for those who become immune it is not believed they can further spread the virus once fully recovered.

Current Statistics (3/18/20)

As of 10pm on 3/18/20 there have been 219,243 people who have tested positive for COVID-19, 124,530 cases are still active (6,814 are in serious/critical condition), 85,745 have recovered (mostly in China) and 8,968 have died (worldometers.info). The current world wide mortality rate stands at 4.09% but as many have and will point out that is a flawed number because of the lack of testing and the lack of understanding what the actual case load is. COVID-19 is different than other viral infections we have because it does seem to be killing patients at a higher rate than other viruses currently in circulation. On Wednesday March 18th alone 976 people worldwide died from COVID-19, that’s a pretty astounding number, especially considering the pandemic is still spreading in many countries. In the United States we had 2,848 NEW cases on March 18th, and that’s with our testing infrastructure greatly lagging and many people not being tested. What makes the potential for this virus so scary is that it has a disproportionately negative effect on those who are elderly, immunocompromised and those who have a number of specific risk factors that depress the body’s normal immune responses. The pandemic is far from over and while none of us know exactly what will happen, it’s not looking good in the short term.

Cited Literature and Sources
Bai et al, Presumed Asymptomatic Carrier Transmission of COVID-19. JAMA Network, Feb 2020.
Balazy et al, Do N95 respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks? American Journal of Infectious Control, March 2006.
cdc.gov/coronavirus/2019-nCoV/index.html
Chiang et al. Inhibition of HIV-1 replication by hydroxychloroquine: mechanism of action and comparison with zidovudine. Clinical Therapeutics, November 1996.
Corman et al, Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR. Eurosurveillance, Jan 2020.
Doremalen et al, Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1. New England Journal of Medicine, March 2020.
Fox et al, Mechanism of action of hydroxychloroquine as an antirheumatic drug. Seminars in Arthritis and Rheumatism, Oct 1993.
Huang et al, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet, Jan 2020.
Jia et al, ACE2 Receptor expression and severe acute respiratory syndrome coronavirus infection depends on differentiation of human airway epithelia. Journal of Virology, Dec 2005.
Newyorker.com/news/news-desk/what-went-wrong-with-coronavirus-testing-in-the-us
Ourworldindata.org/covid-testing
Romanelli et al. Chloroquine and Hydroxychloroquine as Inhibitors of Human Immunodeficiency Virus (HIV-1) Activity. Clinical Pharmaceutical Design, 2004.
Smith et al, Effectiveness of N95 respirators versus surgical masks in protecting healthcare workers from acute respiratory infection: a systematic review and meta-analysis. Canadian Medical Association Journal, Dec 2015.
Tang et al, On the origin and continuing evolution of SARS-CoV-2. National Science Review, March 2020.
Wang et al, Establishment of a reference sequences of SARS-CoV-2 and variation analysis. Journal of Medical Virology, March 2020.
Who.int/emergencies/diseases/novel-coronavirus-2019
Worldometers.info/coronavirus/
Zhou et al, A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature, Feb 2020.
Zhou et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet, March 2020.
Zhu et al, Initial clinical features of a suspected Coronavirus disease 2019 in two emergency departments outside Hubei, China. Journal of Medical Virology, March 2020.

Rocky Mountain National Park Skyline Traverse

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We threw up our hoods, put our heads down and leaned into the wind as we left the Alpine Visitor Center. The wind ripped across the Continental Divide and we ran, partly to make good time, partly to stay warm. An already challenging route promised to be extra challenging on this day.

11hours in and I’d made it to the Narrows on Longs Peak!

Twelve years after running my first National Park ultramarathon in the Grand Canyon I still hadn’t completed my Rocky Mountain National Park (RMNP) ultra, despite it being my home park. I’d spent a lot of time debating the best route, settling on a ridge traverse through the park’s interior. The difficulty of the route was that almost the entire route was above treeline, holding snow late into the summer and being exposed to thunderstorms for most of the summer. My friend Ben and I picked a nice clear crisp September day (9/22/19), the one factor we didn’t count on was the wind. As we traversed the Ute trail along the Continental Divide a bone chilling wind howled from the NW.

Sunrise from the Alpine Visitor Center with the Continental Divide stretched out in front of us.
Following a section of the Ute trail early in the run. Most of the ridgeline was trailless.

We soon bailed off the trail and onto the ridge proper, where we’d stay for most of the day. As we made our way to Mt Ida, the first summit of the day, we had to duck onto the East side of the ridge to warm our hands and put on all our layers. The wind chill was brutal, and we could barely feel our hands and face. We trudged our way up and over Mt Ida to Chief Cheley (2:11, 7.3mi). Lake Azura and Highest lake were still crusted in ice and the views of the park were phenomenal. This section of the park is one of the most remote and seldom visited, miles from any trailhead and the nearest trail. We put our heads down and continued our trudge into the wind.

Proper Rocky Mountain ridge running near Mt Ida.
Highest Lake near the base of Chief Cheley, with Forest Canyon far below.
Tundra running near Sprague Mountain. Longs Peak still looks really far away (square top)

I tagged Sprague Mountain, Gabletop and Knobtop before finally reconnecting with the Flattop mountain trail (5:35, 15.6mi). Ben opted to bail off Flattop back to the car, as the wind was getting worse and there was uncertainty whether the route would go under the conditions. Solo, I crawled my way up Hallett and Otis, barely able to stand without being blown over. As I huddled in the wind block atop Otis peak, I debated my options….. Push on to the technical part of the route (the Class 5 McHenrys Notch), bail down the long East ridge of Otis Peak or return back the way I’d come to the Flattop mountain trail. Being over halfway across the traverse I opted to push on and try my luck.

Flattop Mountain with Hallet and Oatis in the background.
View from Taylor Peak towards Powell with Longs looming behind.

On the long slog up Taylor Peak (the first 13er of the day) my legs were starting to feel heavy, but the wind was actually lessening. From atop Taylor Peak (7:21, 19.1mi) I peered down on Skypond far below, and for the first time all day it looked as though the traverse would actually go! The traverse over to Powell Peak went slowly, but soon I found myself on the summit staring down the SE couloir, ready for the fun to begin. I descended a little over 200ft and located the grassy ledge system to skier’s left that would allow easy passage to McHenrys Notch. From McHenrys Notch the route is obvious, but far from easy. Directly across the Notch are two vertical Class 5 gulleys that lead to the NW ridge of McHenrys Peak.

Looking into McHenry’s Notch. The two gulleys in the middle are your class 5 options to reach the ridgeline above.

I scrambled my way up the lefthand ledge system to the broad ledge on the South side of the peak, and finished the easy traverse over to the summit of McHenrys Peak (8:39, 21.3mi). It felt great to have surmounted the crux, until I looked across Glacier Gorge at Longs Peak, oy vey, I still had a long way to go. I picked my way down through the talus field to Stoneman Pass (not the low point, but the first notch) and descended into Glacier Gorge. This would be the only time I descended into the valley. Glacier Gorge (especially the upper section) is an absolutely magical gem and one of the most iconic hiking destinations in all of Rocky Mountain National Park. Sheer granite faces surround one on all sides, Arrowhead and Spearhead jut abruptly out of the middle of the valley and numerous alpine lakes have carved out depressions amongst the barren white landscape.

Looking across Glacier Gorge from Stoneman Pass. The Trough is the obvious gulley that ascends just right of the Longs Peak summit block.
Frozen Lake tucked in the shadows of Chief’s Head Peak.

I refilled my water in one of the side streams, crossed over the head of Frozen Lake and made my way to the base of the Trough, a 2500ft gulley that swoops its way from Glacier Gorge up to the West face of Longs Peak. I felt like death as I crawled my way up through the talus and slabs just climbers right of the gulley. Time seemed to be passing in slow motion, 100 vertical feet at a time. At last I pulled myself through the windy notch at the top of the Trough and out onto the Narrows. For as many times as I’ve climbed Longs (30?), this was the first time I’d been on the Keyhole route in non-winter conditions alone. I pulled myself up the Homestretch and onto the summit block (11:16, 24.4mi), collapsing with exhaustion, but also with a smile on my face. It was 6:15pm, I was the only person on the summit, the wind had stopped, and long shadows draped themselves across the park.

Feeling like death as I slog my way up the Trough towards Longs.
The shadows of Longs Peak stretching East into the foothills.

After taking a few long breaths in, I knew I had to get moving, sunset was only an hour away, and I wanted to be below the Loft before it got dark, so back down I went, dropping down Keplinger’s couloir, ascending up past Clark’s Arrow and into the Loft between Longs Peak and Mt Meeker. I summitted Mt Meeker just as the final rays of warm sunlight disappeared over the shoulder of Pagoda Peak (12:04, 25.6mi), bathing the talus in a soft orange glow. I took off at a fairly rapid pace down through the talus, in search of the climbers ledge that would lead below the cliffs. As the light began to fade, I started to panic a little bit as I hadn’t reached the climbers trail yet, but luckily, as the last bit of daylight turned to darkness I spotted the trail just below me. Once on the ledge I knew I would be able to navigate myself back down to trail, and in the end the Longs Peak Trailhead.

The Pallisades guarding easy entry to the Loft, down and around I go.
Sun flare over the shoulder of Pagoda Peak with the Longs Peak summit block on the right. What a day.

Progress was slow as I picked my way down the Class 3 slabs and into the talus below. Once I reached the trail in Chasm meadow I was finally able to jog again….it had been over 13miles since I’d last been on trail, so being able to slowly jog felt wonderful. Tired, beat down and totally satisfied I took my time jogging down the Longs Peak trail back to the trailhead. At 8:45pm, 13:46 after leaving the Alpine Visitor center early that morning I stumbled my way onto the pavement, sat on the bench and hung my head in exhaustion. I had only covered 30.6mi and 12000ft of vertical gain, but it had taken 13h46min and I was worked.

At first glance Rocky Mountain National Park may look just like the rest of the Colorado Rockies, but for those with the time and energy to delve a little deeper into it’s depths, the rewards are some of the most stunning scenery anywhere. From the 2000ft high Diamond of Longs Peak to the glacial carved valleys of Glacier Gorge, Sky Pond and Dream Lake to the deep forests teaming with wildlife of the North Boundary; RMNP has it all. I chose my route because it showcased some of the most remote sections of the park, the high alpine terrain, the crystal blue lakes, the glacial carved valleys and of course Longs Peak in all her majesty. There are countless number of adventures within the park, but for me this route offered a taste of all the best. For those looking for something less committing I highly recommend the hike to Glacier Gorge and Mills Lake, Dream Lake and Emerald Lake and for those with summit fever and some scrambling skills Longs Peak.

This route, being a point to point was not possible without the help of a couple of good friends. So a special thanks to Michael Hodges from McGregor Mtn Lodge for helping with the car shuttle and to my friend Ben for the company on the first half of the loop and for waiting patiently at the end for me to slog my way home. And as always a special thanks to Vfuel for keeping me trudging along through such crazy adventures. My RMNP traverse was National Park Ultra #20, and I completed #21 only 3 weeks later in the Great Smokey Mountains. Even after all the time, suffering and misery I can say I’m super excited to see where this project continues to take me.

Great Smokies Challenge Adventure Run (SCAR)

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Well here goes nothing…. At 5am I set off into the darkness, slowly climbing my way up from Davenport Gap into the silence of the hardwood forest. It was Oct 14th, just over a month after my disappointing race at Ultra Trail Monte Rosa, a very unfulfilling would be end to a big year of training, so I immediately went searching for the next big challenge. Naturally my National Parks project came to the forefront, and at the very top of that list was the “Smokies Challenge Adventure Run” (SCAR). If you’re not from the East Coast I totally get your confusion at the name of the route, I was equally surprised when I first came across it in blogs in early 2019.

Pre-scouting Davenport Gap the day before the big dance. Oh boy, oh boy!

In short, the SCAR is a 72mile traverse of Great Smokies National Park from Davenport Gap to Fontana Dam (or the other way) along the Appalachian Trail, it was a logical, aesthetic and seriously challenging line (72mi, approx. 18000ft, current FKT 14h28min). My goal was to simply survive it, experience it, and take a lot of photos (it would be my first time in the Smokies). So as I power hiked and jogged up the hill from Davenport Gap, my head was swirling with doubts… was I trained enough, did I pack enough food/supplies, would the natural springs be flowing, would the weather hold? The only thing I was certain of was that I was in for one hell of an adventure.

First light hitting hitting the Appalachian Mountains in Great Smoky National Park.
A little splash of fall colors along the AT.

The initial climb went by fairly quickly, and as I crested the ridgeline near Mt Cammerer the first glow of sunrise was showing in the East (5.2mm, 2:45). Now atop the ridgeline I settled into my goal pace for the day, hike up each knob/peak, then jog the descents and flats. The trail was a mix of deep hardwood forest with fleeting views from the various lookouts and knobs along the trail. Finally, I crested Mt Guyot and jogged my way down to the Tricorner Knob shelter (15.7mm, 4:10), my first reliable water source. 2019 was a dry year in the Smokies, as such many of the springs had dried up, and even the ever reliable Tricorner Knob was reduced to a piped trickle, though just enough to treat a bottle before moving on.

Early morning light filtering through the deep forest.
Tricorner Knob shelter, the trickle of water is on the right.

The route stuck pretty close to the ridge for the next section, with several beautiful narrow sections of ridgeline where one could look down both the North and South sides of the ridge. Over Mt Sequoyah, Eagle Rock, Laurel Top, Porter’s Gap and The Sawteeth. The foliage was several weeks behind, but the hillsides were dotted with yellows, oranges and reds, just enough to break up the endless sea of green. As I passed Charlie’s Bunion I began to encounter a steady stream of hikers. By the time I reached Ice Water Spring and Mt Kephart there was an almost endless line of hikers strung out along the trail. Thankfully most people were aware enough to allow me to cruise on by, and I soon popped out of the woods into the madness that was Newfound Gap (30.3mm, 7:15).

Splashes of yellow adorn the Great Smoky Mountains.
A little fun rocky single track along the AT.

I knew Great Smoky NP was the most visited National Park in the US, but I was definitely not ready for crowds. Cars were backed up for a mile on either side of the pass as many more endlessly circled the parking lot. By a stroke of luck I was actually able to find my mom, who had offered to meet me at the trailhead for a food and water resupply. I reloaded my S-lab 12 and jogged out of the parking lot, quickly leaving the masses behind. I hike/jogged along the rolling forested AT up towards Clingmans Dome, the high point of Tennessee and the day. As I neared Clingmans Dome I had my first low point of the day, I bonked hard, slowly slogging my way up the Clingman Dome fire tower (39.6mm, 10:05).

Selfie atop the lookout at Clingmans Dome, back from the dead….for now.
View from Clingmans Dome into Tennessee.
The soft afternoon light makes the forest glow.

The views were 360 degree panoramic and the air was unusually clear, allowing one to see a long way into both Tennessee and North Carolina. After taking in the views I again disappeared back into the dense hardwood forest, losing all the crowds instantly. It was all downhill from here, literally and figuratively. The trail slowly became rockier, and my legs were definitely not getting any spunkier. Down, then up, then down again, then up…. I didn’t seem to be losing any elevation, even though I’d passed the high point? I finally reached the Derrick Knob shelter (49.3mm, 12:45) for a water resupply, the pipe was again trickling, just enough.

Derrick Knob shelter, water refill station and new friends.
A little solo silent single track running soothes the soul.

I paused for a moment to chat with the group staying at Derrick Knob, and the inevitable question came up…”So where are you coming from”….”Davenport”….”How many days did it take you”……”I started this morning”……”WHAT?!?!?”. I don’t know why I bother trying to explain, but they were nice enough to point me in the right direction, so off I went. The light was slowly fading away, and the end didn’t seem to be getting any closer. The short steep climbs up Thunder Mountain and Mt Squires were soul crushing, the last just as the sunset faded away in the West, it was going to be a long dark road (54.4mm, 15:15).

Sunset from Mt Squire on a long day, with many miles to go.

The miles seemed to drag on, over Mollies Ridge and down to Ekaneetlee Pass. I had been dreading the climb to Doe Knob, though knew it was my last significant uphill before what I hoped would be a cruiser downhill to the Fontana Dam. The power in my legs had disappeared on Thunder Mountain and it took all my concentration just to stay upright and on my feet. The dense forest seemed to wrap the darkness tight around me, and it felt as though there was nothing but me and the trail. Finally, I reached the turn where the AT leaves the ridgeline of the Great Smoky Mts and heads due South (64mm, 17:18). I started to jog down the overgrown track, only to find my legs were jello, and I was struggling to not stumble off the trail with every single step. I finally gave up and settled into a soul crushing 16min/mile stumble down the trail, frustrated I couldn’t run, usually my strength.

Just after midnight at the Fontana Dam, happy to be done, and completely worked.
Spending the day after the SCAR quietly recovering along one of the many gentle rivers in Great Smoky National Park.

The miles seemed to pass be excruciatingly slow in the darkness, but at last I popped out of the dense woods at the trailhead, only 0.5mi of road left to the dam! Now back on smooth ground I was able to slow jog down to Fontana Dam and the sign marking the boundary of Great Smoky Mts National Park. 72miles (+/-), 18000ft (+/-) and 19h and 25min after leaving Davenport Gap I’d completed the SCAR. I had received a thorough ass whooping on some beautiful but challenging East Coast trail and my first introduction to the Great Smoky Mts had been one hell of a ride. I definitely underestimated the run, but was grateful to have had the opportunity to experience such a classic AT route. Special thanks to my Mom for helping me out with logistics and making the run possible, and to Vfuel for keeping my energy up throughout most of the run. 21 National Park ultramarathons down….only 35 more to go!

Mt Rainier NP; Great Northern Loop Ultra Run

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Wow…I just….wtf???? The scene in front of us was beyond words and comprehension, the glaciated massif of Mt Rainier glowed in the early morning light, fields of wildflowers surrounded us on all sides, and not a soul was in sight, this is what we had come for.

Running across the Sourdough Ridge Trail at sunrise, what a start to an epic run.

Mt Rainier National Park was created in 1899, America’s 5th National Park, to protect the glaciers, alpine meadows, roaring waterways and lush forests of the mountain known to the natives at Tahoma (or Tacoma). The last time I had visited Mt Rainier National Park had been in 2004, and on that trip I’d barely scratched the surface of what the park has to offer. This trip was to be a bit different, a whirlwind tour of the North side of the peak, somewhere in the range of 50miles on already tired legs, game on. I’d convinced my friend Ely Gerbin to join me for this epic adventure of stupidity, and what a day we were in for.

Mt Rainier as seen from the aptly named Sunrise parking lot.

We left the Sunrise parking lot at the crack of dawn, just as the pink alpenglow lit up the hulking massive in front of us. As we jogged our way across the Sourdough Ridge trail the views were nothing short of spectacular, and we were only a mile in! Our route consisted of combining two loops; the Northern Loop with the Spray Park Loop. We opted to start by traversing the Southern portion of the loop first along the Wonderland trail, finishing with the Northern section along the Northern trail. As we rolled along the Wonderland trail through fields filled with wildflowers, the mountain loomed above in the sunlight. The trails were buttery smooth, the morning air was cool and the views were ever changing and stunning. Past the toe of the Winthrop Glacier, the clear reflection of Mystic Lake and on to the bridge over the Carbon River and the looming Carbon Glacier (mm13.4, 3:05). As we started the long climb up from the Carbon River the sun began to bake and the flowers were again popping. The creeks in Spray Park were our own private oasis, and we filled our bottles, drank our fill and dunked out heads (mm17.3, 4:37). Even during our brief stop the mosquitoes swarmed, so we couldn’t stop to smell the flowers for too long.

Reflection in Mystic Lake along the Wonderland Trail.
Ely running through fields of flowers with Mt Rainier looming behind us.
Ely cruising up the single track above the Carbon River.

The views were spectacular as we rolled through the high alpine meadows, then began the slow descent back into the forest and Mowich Lake. Ely and I rolled past the masses at Mowich Lake (mm22, 5:50) and onward to Ipsut Pass (mm23.2, 6:06), the halfway point of our big loop. From the top of Ipsut Pass we stared straight down 2500ft to the Carbon River far below, time to get those quads working. We cruised down down down, through lush green forest, along cascading creeks and past towering evergreens, finally crossing the raging glacial grey Carbon River (mm28.7, 7:21). We took a few minutes to refill our water and to cool off in a small tributary before the long climb up to Windy Gap.

Trudging our way up into Spray Park, the flowers were poppin.
More fields of alpine flowers, all is good.
The alpine gardens of Mt Rainier NP, totally worth it.
Looking down from Ipsut Pass toward the Carbon River.
Ely taking pausing for a moment of serene splendor.

We plodded on up through the trees on what seemed like endless switchbacks, finally breaking out into alpine terrain near the Yellowstone Cliffs into a massive field of bear grass. It was a spectacular site, cruising through the green meadow dotted with white puff balls as far as the eye could see. We continued our trudge up to Windy Gap (mm33, 9:11) and down the other side on some beautiful single track to Lake James. After a little off trail wandering we hit the long and steep switchback descent back to the West Fork of the White River (mm36.7, 10:17). After another water refill we started our final climb of the day up the Northern Loop Trail. The long miles of the weekend hit me like a sledgehammer, and the death march was on. Ely was very patient with me as I slowly trudged up the trail, deep in the pain cave, but the scenery was too spectacular to be too grumpy (but maybe a little).

Ely crossing the Carbon River on the inbound part of our journey.
Ahhhhh, fields of Bear Grass!!!!
View of Mt Rainier from the final climb up above the West Fork of the White River. My grumpiness faded away pretty quickly.

After what seemed like an eternity, we crested the climb to a spectacular view point of Mt Rainier looming high above the White River (mm39.8, 11:32), glowing in the afternoon light….a perfect moment to remind me of why I was enduring all the fatigue, all the suffering, all the soreness in my legs. I finally gained a little of my strength back as we rolled through the flat open plateau and down to Lodi creek. One last final little climb would take us back to Sunrise, and while it seemed to drag on, ambling along the creek through fields of wildflowers was a pretty spectacular way to end the day. As we neared Frozen Lake I was very ready to be done, and just at that moment Ely and I rounded a corner to a herd of mountain goats lazily grazing with the looming mass of Mt Rainier as the backdrop. The day wasn’t over, and the constant reminders of how spectacular the mountain and it’s surrounding environment was kept slapping us in the face. The final traverse back across the Sourdough Ridge trail was a fitting finish to an unbelievable day. Spectacular views and amazing trails start to finish, we’d been thoroughly brutalized (me more so than Ely) and had come out the other side, beaten but with our souls fully filled with an amazing appreciation for all that Mt Rainier National Park has to offer.

The amazing just didn’t stop, running our way up Lodi Creek to the finish of the loop.
Yeah that happened. A herd of mountain goats casually grazing along the Wonderland Trail in the shadow of Mt Rainier.

In the end our route totaled 46.5mi and 13,500ft, taking us a little over 13:30 (because of my slow death march finish). Without a doubt, my first real adventure in Mt Rainier National Park was a resounding success, and the route had been more than I’d ever have hoped for. For anyone who hasn’t had the pleasure of experiencing Mt Rainier National Park either half of our super loop would be spectacular, or any portion of the Wonderland Trail well worth the effort. I’m incredibly grateful for experiences like this, and for the fact that places like this have been protected for me to enjoy, hopefully for many years to come. Run fast, run healthy, but most importantly run happy.

North Cascades NP; Copper Ridge Loop

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One of the many amazing views along the Copper Ridge Loop.

The North Cascades are a massive wilderness full of jagged peaks, alpine lakes, towering glaciers and some of the last true wilderness in the lower 48 states. The National Park portion of the North Cascades Complex (which also includes Lake Ross and Lake Chelan National Recreation areas) encompasses a 500,000 acre nearly roadless wilderness. One that can not be experienced from roadways and lookouts, but must be explored on foot (or boat). It seemed only natural to ultra run the park, but the question is what set of trails best represented everything that makes the North Cascades amazing?

After doing some of my own homework and asking several locals with more knowledge than I, one recommendation kept hitting the top of the list…the Copper Ridge Loop. Well, if everyone (even locals) think it’s that amazing, it must be the proper North Cascades experience? So planning was set in motion for an epic weekend in the Washington mountains (also see Mt Rainier Northern Loop). The first weekend in August (8/2/2019) I flew into SeaTac (2h delays), met my friend Jason and we started our drive North towards the Mt Baker Highway and the Nooksack River. After crashing in a rest stop for several hours, we awoke the next morning to light rain, but a forecast that promised clearing skies, so off we went for the trailhead. Jason and I spent the entire drive catching up, as he is still to this day one of the people with whom I’ve logged the most trail time (cumulative in the months!). He was very nervous though, as this was to be his longest run (by almost double) since badly breaking his leg several years ago, but he welcomed the challenged.

Officially entering North Cascades National Park.

When we rolled into the Hannegan Pass trailhead we were greeted by a road closed sign, marking a huge washout that had undermined the last 200ft of the road. So we parked and packed up our gear, in no rush as the drizzle continued to fall. We cruised out of the trailhead at 9:30am, slowly jogging our way up through the forest towards Hannegan Pass. The low clouds and light drizzled continued to swirl around us, but every once and a while we’d get a glimpse of the mountains looming overhead. From the pass (4.3mi) we opted to do the loop CCW, dropping down to the Chilliwack River first, before climbing to the ridge on the return. As we descended to the river we passed through sections of overgrown trail and sections of open forest, and soon we were soaked from the rain drenched leaves.

Jason getting in touch with his inner tree hugger. Colorado just doesn’t have big trees like this <3
Buttery smooth forest single track in the North Cascades is so serene.

The weather was starting to clear, and we could see glimpses of blue sky overhead, we’d momentarily dry out, just to be drenched by another set of wet dense brush. The river trail was mostly smooth running (where we could see our feet) and we soon found ourselves at the first Chilliwack river crossing, the cable car (11mi)!! But I was a bit dismayed to discover the cable car was down for repairs, so we’d be fording the river instead, sad face. So Jason and I linked arms, and slowly shuffled our way across the knee deep rapidly flowing stream, thankfully making it across without incident. We continued our hike/jog on the undulating descent to the second ford (16.2mi), thankfully the water here was far more docile, making for an easy crossing. This was our first moment of full sun all day, so we basked in the warm glow along the rocky shore for a few minutes, treating water and savoring the moment.

Crossing one of the side creeks along the Copper Ridge loop, somewhere deep in the Chilliwack valley.
Basking in some of that elusive PNW sunshine after our second crossing of the Chilliwack river.

We knew that what came next would be our physical test of the day, a 4000ft climb straight up to the ridgeline. We settled in for the long haul, switchback after switchback up through the forest, the sun percolating through the slowly thinning trees. As we neared the final switchback below the ridgeline, the trees began to open and the views began to explode behind us. The clouds had finally lifted and the jagged glacier capped peaks of the Cascades loomed across the valley. When we finally reached the top of Copper Ridge the weather was beautiful mostly blue sky, and we were completely awe struck by both the verticality and the depth of the mountains surrounding us on all sides (19.2mi).

Mountain views and wildflowers, welcome to the North Cascades!
So amazing and so runnable we couldn’t help ourselves.

The single track along the ridge was a mix of beautiful flowing dirt and rocky steep climbs/descents. This was the wow factor part of the loop without a doubt. We finally reached Copper Lake, set in a steep walled cirque, it’s blue waters glittering in the sun. Jason’s legs were definitely feeling beat up (this being his longest run in 3 years!), but we put our heads down and trudged our way up to the Copper Ridge lookout tower (24.3mi), the high point of the day. We met up with several groups of backpackers, all of whom were soaking in the expansive vistas, oogling the craggy summits, marveling at the hanging glaciers. In the soft evening light it was truly a spectacular site, the only sounds of civilization being the chatter of our neighbors. Unfortunately we couldn’t linger long as we still had 10miles to go and darkness would soon be descending upon us, so we began the long jog back towards Hannegan Pass.

Some rocky trail running near the Lookout, oh and the views were pretty ok.

As we descended the ridge the clouds began to roll back in, completely enveloping the ridge, then bursting apart to reveal the mountains around (finally including Shuksan, but not Baker). It was truly a surreal experience and some of the most beautiful trail running I’ve ever done (right there with Four Pass loop). After dozens of photos stops we finally made it back to the base of Hannegan Pass, all we had to do was conquer this final 500ft climb and it was a short few miles of downhill back to the car. Thankfully the final uphill was littered with fields of lupine, lilies, columbine and wildflowers of every color, a welcome distraction for the tired minds. After a quick snack atop Hannegan Pass (30.3mi) and one last moment taking in the Chilliwack valley that stretched out below, we scooted our way back down towards the car. I ran ahead a little bit, rounded a bend and stopped dead in my tracks…. A noise off to my right had perked my ears up, and when I paused to assess I was astounded to see two baby black bears clambering up trees not 50ft away. Where babies play, mamma isn’t far away, so I slowly backed off, signaling to Jason to stop and do the same. Mamma came sauntering through the woods, finally coaxing the two babies down and they went crashing off through the brush when she finally caught our scent. Wow, did that really just happen????

Moody weather along the ridgeline, watching the clouds roll back and forth.
Almost back to Hannegan Pass, this place is a trail runner’s paradise!

We rolled back into the parking lot just as the last bit of sunlight was fading out of the sky, tired but our hearts so full from the amazing experiences of the day that instead of worrying about camp or cleaning up, we sat next to the car eating ‘dinner’ and just recapping all the memories of the day. The Copper Ridge loop (or lollipop) had lived up to its reputation; beautiful forest single track, meadows full of wildflowers, crystal blue glacial rivers, and stunning mountain vistas. While the North Cascades have far more to offer, if you only have one day, this loop definitely encompasses what makes the North Cascades so special. I was very fortunate to be able to share this experience with such a good friend, on such an imperfectly perfect day. We may not have gotten the clear blue skies (and thus no views of Mt Baker), but the mist and drizzle giving way to a mix of low clouds and blue sky made for such proper PNW experience. This loop has easily jumped into my top 10 for National Park Ultras (it was my 18th completed NP Ultra) and should be on every ultra runner’s to do list. 34.5miles, 8950ft gain/loss, 10h35min.

Bonus shot of Mt Baker from the Mt Baker Hwy the day after our Copper Ridge run. Sometimes being a tourist is pretty A-Ok.
Mt Shuksan reflected in a small tarn along the Mt Baker Hwy. Just touristing around the day after our Copper Ridge run.

Wind Cave National Park; Wildlife and Boxwork

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Wind Cave National Park was founded in 1903, the seventh National Park within the system. Even though it was one of the first National Parks, it ranks far down the list of visitations (<700,000), and many have never heard of Wind Cave. Tucked away on the edge of the Black Hills in South Dakota, Wind Cave is the 7th longest cave system in the world (over 150 miles) and new cave is still being discovered every year. Though what makes Wind Cave National Park so special is the intricate boxwork that adorns the cave (found almost no where else in the world) and the wildlife that roams the above ground portions of the park.

Bison are quite large and intimidating animals, keep your distance.

Fresh off my 6h sloppy mud run in Badlands National Park, and with bad weather looming the following day, I opted for a nice back to back National Park ultra combo. I had tickets for a 3pm cave tour along side my friends Ben, Amanda and Kedar, so at first light on 5/26/19 I hit the Wind Cave Canyon trail, jogging along the gravel road into the plains of Wind Cave NP. I soon turned north onto the Highland Creek Trail (3.5mi), traversing across the high plains, past endless herds of bison, several groups of elk and even a few pronghorn. Large sections of the trail were little more than a faint path cairned through the grasslands, and quite a few times I found myself glancing around looking for the path, but overall it was pretty smooth running.

Cruising through plains and along the rivers of Wind Cave National Park.
Smooth cruiser open plains single track in Wind Cave National Park.

Things were going smoothly and I soon found myself at County Road 5 (10.7mi), my lone 1.5mi stretch of road running for the day (dirt). I hit the Centennial trailhead , turned South and headed back into the park. The running continued to be smooth, as I rolled across the never ending plains, finally dropping into Beaver Creek canyon (16.5mi). I cruised up the creek through the narrow but shallow canyon alongside the creek, a nice change of pace to the expansive plains. I hadn’t passed a single person (or car) the entire morning, though I finally started to pass a steady trickle of people as I neared the Lookout Pt trailhead. I exited the canyon, passed through the trailhead and onto the Lookout Pt trail, headed back across the plains again.

Cruising along Beaver Creek in Wind Cave National Park.
Some elk scampering across the plains of Wind Cave National Park.

As I connected back onto the Highland Creek Trail I could feel the fatigue building in my legs from the past two days of running. When I got back onto the Wind Cave trail, I made a quick turn south onto the final leg of my run, an out and back of the East Bison Flats trail (23.3mi). As I slowly climbed my way back up to the high plateau the sun began to beat down on me, and I quickly realized I was running out of water. Onward I slogged, steeply back down into the river canyon, only to immediately climb right back up to Gobbler Pass (26.6mi). I was definitely feeling beat up now, but as I turned around with just under 4miles to go I had really no other choice than to finish up the run. The fatigue and dehydration were taking their toll, so the final miles seemed to drag on in a blur. At last I descended back to Wind Cave Canyon and slowly shuffled my way to the car. I still managed to finish the 30.4mi lollipop in under 6h, not too shabby for a back to back weekend, and in time for the 3pm cave tour!

Boxwork in Wind Cave.
Frost work crystals in Wind Cave.

After chugging a cold soda, tasted so good, I dragged myself over to the Wind Cave visitor center to meet my friends and to catch the 3pm cave tour. I felt a little pathetic, slowly hobbling my way at the back of the tour group (legs were getting stiff), but it gave me an extra chance to photograph some of the cave formations and to take in the smaller intricacies of the cave. Wind Cave is most famous for it’s boxwork formations, a lattice of spiderweb like crosshatching that is found almost no where else in the world. We admired some frostwork (tiny white crystals), spar and a few stalagmites and stalactites. While Wind Cave may not be the most ornately decorated cave, it’s combination of unique features and above ground wildlife make it a special place to visit. For the runners out there the trails are beautifully runnable and very unpopulated (other than the herds of wildlife). So next time you’re in the area (Custer, SD), stop on in to Wind Cave NP and it’s sister Jewel Cave NM right next door, for a little tour of the above and below ground wonders.

Dog tooth spar in Wind Cave.