As the year 2020 got off to it’s expectedly auspicious start, we may not have expected that the reports of a novel (simply meaning ‘new’) virus trickling out of China in early January, would play such an important role in why the year 2020 would become a significant year in world history.
At first they were considered rumors, and public discussion of this virus was largely condemned within China.
However, reports from citizens on the ground in the Wuhan region became increasingly frequent, and concerned that this virus was unlike other viruses seen in recent times.
By February, cases of the virus began to accumulate outside of China, and the rest of the world began to come to terms with it’s reality.
Experts around the world soon identified this virus to be a member of the Coronavirus family (Corona meaning ‘Crown’ in Latin, describes their characteristic shape, which is typically spherical with numerous spikes protruding from an outer envelope).
These spikes facilitate attachment to specific molecules on the tissues of their target host.
It is actually estimated that the common varieties of Coronaviruses are responsible for over 10% of all ‘Colds and Flus’ encountered by almost every population in the world, each and every year.
Viral Cause of The ‘Common Cold’
|Virus||Estimated Proportion of Annual Cases|
|Respiratory syncytial virus||5%|
So what has caused this novel Coronavirus to be so different to other similar viruses that have gone before it?
What Has Gone Before?
In May 1997, a young boy in Hong Kong developed what seemed to be just another cold. However after his symptoms rapidly progressed to such severity that he died, his sputum was sent to laboratories for analysis of the virus that was responsible.
This virus was eventually revealed to be a variant of the Influenza virus that was at the time only known to infect birds (Avian Flu), and became known as H5N1 (owing to its specific combination of Influenza viral components), and was one of the most recent modern examples of how a virus can jump the species gap (i.e. evolve to infect humans).
This demonstrated one of the risks associated with large populations living in close proximity to animals, in less than ideal conditions.
The Chinese government responded by killing 1.5 million chickens, as further human cases were closely monitored and promptly isolated. By the end of that year there were only 18 known cases in humans, however six people had died.
This alarming level of lethality was actually considered helpful in preventing the wider spread of this virus (since those who are infected become very quickly and obviously affected).
Unfortunately, this relative ‘success’ in the containment of H5N1 still resulted in a further 450 people dying from the virus before it was apparently brought under control over the proceeding years.
The Case Fatality Rate (CFR) for H5N1 ended up being around 60% (which means that, on average, around 60% of those who caught the virus, died from disease associated with it’s infection).
This obviously explains the level of alarm that circulates whenever a strong virus emerges, and why it was considered a warning as to what was possible whenever virulent viruses are ever able to emerge and spread.
The World did not need to wait long before another concerning virus was to reveal itself.
In November 2002, the first case of an ‘atypical pneumonia’ was reported in the Guangdong province of southern China.
By March 2003 the US CDC reported that a particular strain of Coronavirus (rather than an Influenza virus, like was seen with H5N1) had been spreading throughout China, Vietnam and Hong Kong and was responsible for the condition, using the term ‘Severe Acute Respiratory Syndrome‘ (SARS) to describe the associated illness (and therefore SARS-CoV became the name of this virus i.e. SARS Coronavirus).
The CDC acted swiftly to contain the virus, via early quarantines, travel bans, vessel inspections, isolation measures, etc.
The US was subsequently able to lift their travel limitations and quarantines by July that year, resulting in only 119 suspected cases (and 0 deaths) within the USA after resolution of the outbreak, which was achieved worldwide by December (not before a brief resurgence occurred after the resumption of Chinese wildlife markets, leading to Bats being identified as a reservoir of the virus).
Ultimately, the worldwide toll of the first outbreaks of SARS-CoV resulted in over 8098 infections, 916 deaths, across 29 countries, making SARS one of the deadliest new infectious diseases of the 21st century.
In January 2004 the US CDC reported that Civets (Weasel-like creatures) in China had also been shown to carry the virus, implicating them as an additional suspected link in the chain from animals to humans (and subsequently implemented a ban on the import of all Civets and associated by-products, which remains to this day).
Beyond the ongoing use of Civets for meat and other food products within China, there is a Civet product that is still consumed around the world known as ‘Kopi Luwak’ (aka ‘The World’s Most Expensive Coffee’), which sells for $30-$100 per cup. ‘Civit Coffee’ as it is also known, consists of partially digested coffee cherries, which have been eaten and defecated by the Asian palm civet.
The resulting coffee is harvested from the droppings of the Civet, and regarded by coffee drinkers around the world to have superior and unique flavor properties (due to the meticulous selection of the civet). There are notable animal welfare (as well as possible health) concerns surrounding the production of this coffee.
How Was SARS 1 Brought Under Control?
Obviously not quick enough for those affected by it, however a combination of rapid, coordinated and effective containment measures, along with the specific nature of the disease made it potentially less infectious, ultimately limiting its spread.
However, once it again, it demonstrated a warning as to what was possible.
It was noted at the time that ongoing vigilance would now be required, since Coronaviruses are known to be capable of genetic recombination (resulting in mutation/evolution), and a strong culture of exotic animal consumption persists within China, that may present an ongoing increased risk of development and opportunity for transmission.
Infectious disease experts have therefore been attempting to plan for such further viruses since. In particular urging the importance of consistent monitoring, early detection and reporting, along with early and aggressive isolation and containment measures through efficient communication and well considered action plans.
SARS-CoV-2 (SARS 2.0)
The novel coronavirus that we have come to know most recently (which will eventually lose its ‘novel’ designation after no longer being considered so new), is therefore most similar to the original SARS virus, and as a result has understandably been named SARS-CoV-2 (meaning SARS Coronavirus 2).
For the sake of nomenclature, it may be important to note the difference between the virus itself and the disease that it causes.
For example, Human Immunodeficiency Virus (HIV) is known to cause Acquired Immune Deficiency Syndrome (AIDS), although it is theoretically possible to have an acquired immune deficiency syndrome that is not attributable to an HIV infection, making clear distinctions in terms potentially advantageous to support optimum understanding, and the most appropriate courses of action.
Similarly, the associated symptoms and condition caused by SARS-CoV-2 was officially labelled ‘COVID-19’ by the World Health Organisation (WHO), simply meaning:
CO = Corona
VI = Virus
D = Disease
19 = Originating in 2019
The Virus: SARS-CoV-2
The Disease: COVID-19
Where Did SARS-CoV-2 Come From?
Sometimes viruses need to go through a complex journey over multiple generations through multiple species in order to develop the capacity to jump from the more exotic animals to humans (more exotic than the chickens and pigs that have more established history and contact with humans).
This may have occurred at one of China’s so called ‘wet-markets’ where a wide variety of often obscure and exotic animals are all housed in close proximity, limited hygiene, and minimal transmission prevention measures.
Although some may be puzzled by the apparent implausibility of events required to result in this type of virus emerging through natural processes, early indications pointed to the fact that a virus 96% genetically identical to SARS-CoV-2 had been found in Rhinolophus affinis bats collected from China’s Yunan Province. (Zhou et. al. 2020)
Although other research (conducted by the South China Agricultural University 2020) claimed to find a virus in Pangolins which shows a 99% genetic similarity to SARS-CoV-2.
However, other research on Malaysian Pangolins found their virus to be closer to 90% genetically similar.
It remains unclear exactly which species facilitated the development of SARS-CoV-2 and how precisely it made the leap to humans.
In any event, the real danger of any virus that transfers from an animal to a human is when that virus then shows the ability to transfer quickly and effectively from that human to any other human.
With the modern scale, speed and frequency of human mobility and travel (between countries and communities), this risk of rapid spread is particularly problematic.
These risks have been highlighted by various researchers over the past decade, suggesting that more attention may be needed to develop better national policies and practices in order to prevent the next outbreak. (Cheng 2007)
Weighing Up The Risks
The truth is that there is no way of knowing in the early stages of an outbreak, what the full extent of transmissibility can and will be, and which people in the population have the greatest susceptibility to infection, and ultimately what the full extent of complications, injury and mortality may be.
For these reasons, taking an overly cautious approach to any novel outbreak that demonstrates the scale and magnitude of SARS-CoV-2, can be considered appropriate.
It may be easier to relax any proactive measures taken in the early stages, once things show themselves to be manageable and under control.
However, to wait for the situation to prove itself unmanageable and out of control, before stringent and proactive actions are implemented, may lead to far greater overall impacts to the health of the global population.
|No. Of Infections||Recorded Deaths|
|Typical Influenza||‘Flu’||0.01%||Millions p/year||Thousands p/year|
|H1N1||‘Swine Flu’||0.01 – 0.1%||43 – 89 million||3205|
|SARS-CoV-2||‘COVID-19’||1 – 4%||Millions Projected||100,000s|
(if projections not avoided)
(Wong 2014, Talha 2019, WHO 2020, CID 2009)
The level of concern surrounding a virus is therefore influenced by not simply its Case Fatality Rate but also its potential transmissibility, and ultimately access to human populations who do not possess existing immunity.
How is SARS-CoV-2 Spread?
Coronaviruses have been shown to be present in not only the respiratory secretions of infected individuals, but also their feces and urine, as well as their sweat and tears.
This means that MOST of the common fluids and substances that an infected individual may shed into their environment is a potential source of infection and transmission.
Interestingly, blood is not considered to present a high risk for SARS-CoV-2 transmission due to lower viral presence in blood (although blood obviously does still present a risk for many other diseases, and should therefore always be handled with all typical biological hazard precautions), and it is therefore not expected that mosquitoes or other natural sources of blood transmission will present a substantial risk of SARS-CoV-2 transmission.
Air Droplet vs Aerosol
Droplet and Aerosol transmission may sound similar, but they are in fact regarded as distinctly different methods of transmission.
Droplet transmission involves virus particles being shed in small droplets of body fluids which are ejected into the air through coughs and sneezes, which then drift downward via gravity to land on various surfaces.
(Note: strong air currents like air conditioning ducts, may be capable of carrying droplets a certain distance before the droplets arrive at a resting place – potentially infecting surfaces some distance from the infected person)
Aerosol transmission on the other hand refers very specifically to the capacity for a virus to remain suspended within ambient air (e.g. within minute vapor particles). This makes the entire air supply a potential source of transmission for an extended period of time.
Obviously, it is of great priority to determine whether a virus is capable of the latter, as it makes cleaning and containment of environments considerably more difficult.
Current scientific research has suggested that airborne transmission of SARS-CoV-2 is far more likely via droplet transmission than latent aerosol transmission, however the potential for Aerosol transmission in certain situations should not be ruled out (see environment durability below).
How Micro Droplets Suspend In Air
In experimental studies, using a bacteriophage as a marker of infectivity (not merely viral presence), it has been shown that contaminated hands may pass a virus to 5 or more touched surfaces, and are then capable of passing to 14 additional people, when not disinfected to prevent such spread. (Kramer et. al. 2006)
Gut vs Lung
It appears the SARS-CoV-2 virus has a particular affinity for ACE-2 (Angiotensin-Converting Enzyme 2) receptors in the body (using them as a key method of attachment and invasions into cells).
This becomes relevant when we consider that the tissues in the body with the highest ACE-2 receptor concentrations are Lung alveolar cells, GIT cells (including mouth, esophagus, gallbladder, intestines and colon), as well as cells of the Urinary System (Kidney and Bladder) and Cardiovascular System (Heart and Vessels).
This means that in addition to the potential for transmission to lung tissue via breathing infected droplets/aerosol, there is also a strong potential for transmission via surface to mouth touching, food contamination, and the common feces-to-mouth routes of many diseases (which may explain why some cases of COVID-19 manifest predominantly as gastrointestinal symptoms rather than lung symptoms).
Note: This also means that certain individuals, such as those with existing gastrointestinal complaints, may be more or less prone to infection via this route, as well as those with particular conditions (such as cardiovascular and metabolic) who may be at greater risk of further complications associated with a severe infection.
This also brings up the significance of healthy microbiome balance, as both the lung and gut both share certain bacteria that can assist in the defence of their membranes, and the regulation of inflammation at those locations.
(Wang et. al. 2017)
How Long Do Viruses Last On Surfaces & Objects?
|Virus||Typical Lifespan Out of The Body|
|Herpes Virus||Minutes (rapid drop after 30min)|
|Flu Viruses||Hours to Days|
(Varies from virus to virus)
|Norovirus (‘Stomach Flu’)||Up to 2 Weeks|
1. The long survivability of Norovrius is one of the reasons it presents such a challenge on Cruise Ships and in other high density enclosed environments.
2. While these time-frames are indicated in typical conditions, various other conditions may be more or less favourable (which may substantially reduce or increase times) for certain viruses.
How Long do Coronaviruses Persist in the Environment?
Some previous studies on various strains of SARS-CoV have shown the potential capacity for relatively long persistence times on various inanimate surfaces (with the table below showing an average of around 4 days for SARS-CoV strains, with one specific strain being capable of up to 9 days on plastic in certain conditions (demonstrating plastic as the most problematic material).
Maximum Persistence of SARS Coronaviruses on Various Surfaces
|Type of surface||Virus||Strain||Temperature||Persistence|
|Metal||SARS-CoV||Strain P9||RT||5 days|
|Wood||SARS-CoV||Strain P9||RT||4 days|
|Paper||SARS-CoV||Strain P9||RT||4–5 days|
|SARS-CoV||Strain GVU6109||RT||24 hours|
|Glass||SARS-CoV||Strain P9||RT||4 days|
|Plastic||SARS-CoV||Strain HKU39849||RT||5 days|
|SARS-CoV||Strain P9||RT||4 days|
|SARS-CoV||Strain FFM1||RT||6–9 days|
|Disposable Gown||SARS-CoV||Strain GVU6109||RT||2 days|
RT = room temperature (20 – 25°C)
(Adapted from Kampf et. al. 2020)
This suggests that if quarantining is the only method used to sanitise a surface or item, it may need to extend for a number of days at typical room temperatures in order to be considered sufficient (to account for the potential for strains of SARS-CoV-2 that may emerge with similar capabilities).
Note: This research also highlighted that well below room temperature (at around 4°C) the virus could persist on surfaces for up to 28 days or more!
Which means that particular care may need to be taken to actively sanitise any items being placed within refrigerators and freezers for later consumption (including food packaging, wrappers and containers, that may transfer intact virions to hands during food preparation at a later date).
Although a distinction between the mere presence of viral genome remnants, and intact virions that are viable and capable of infection needs to be made clearer in some of the previous research.
How Long does SARS-CoV-2 Remain Infective in the Environment?
More recent research has been conducted specifically on SARS-Cov-2 (in comparison to its original cousin SARS-CoV-1).
Not only is this research more relevant for SARS-CoV-2 specifically, but it clearly verified the viability, not merely the presence, of the virions, and therefore gives more reliable indications of how long surfaces may remain infective (under studied conditions).
Viability of SARS-CoV-2
(at room temperature (21-23°C)
and relative Humidity of 40% for surfaces, and 65% for air)
(Van Doremalen et. al. 2020)
These results suggest that the virus appears to survive relatively briefly in air (a few hours), however those hours may be long enough to potentially contaminate enclosed air spaces for those immediately entering an area that was recently occupied by a contagious individual (making it desirable to reduce the numbers of individuals frequenting a common space in too quick succession (e.g. such as building elevators), just as much as those who gather in one space all at one time (e.g. such as conference and meeting rooms).
Surfaces on the other hand, did show a higher than desirable capacity to harbour contamination (albeit thankfully not as durable as Norovirus).
It should be noted that the amount of viable virion falls consistently over time after being deposited on surfaces. Therefore the greater the amount of time after the infected person has transferred the virus to the surface, the greater reduction in risk of transmission, or greater reduction in ‘dose’ if transmission does occur (potentially reducing the degree of burden to the body and therefore possibly the speed and likelihood of the immune system being able to prevent/overcome the infection sooner).
The average half-life of various environments was therefore summarised below.
(Van Doremalen et. al. 2020)
Note that whilst some virion particles can linger in the air for a number of hours, the vast majority are nonviable within an hour or two.
It should also be noted that this data is applicable to enclosed indoor air only. Outdoor air with much higher air volume, air replacement currents, and UV sunlight during the day, likely reduce this viability to far more negligible levels (making open air environments less prone to transmission, assuming there is sufficient space to minimise close proximity between individuals)
It should be further noted that since SARS-CoV-2 virion particles can remain viable for days, the reason that air supply does not harbor them for longer than a few hours is not necessarily because they are killed, but because they settle out of the air and onto surfaces.
Therefore all surfaces (such as those tested below) in a known contaminated indoor air space (an area where an infected person has coughed, sneezed, or spent an extended period of time), should also be considered contaminated (whether they were physically touched by an infected person or not) until cleaned or the amounts of time suggested in this study have passed.
Note that SARS-CoV-2 appears to be more sensitive to oxidative metals like Copper than its predecessor SARS-CoV-1, demonstrating Copper-based metal surfaces as the least hospitable environment tested.
Assuming the oxidative mechanism is the reason for this, this may mean that SARS-CoV-2 is particularly sensitive to oxidative sanitisation methods (see below).
Interestingly, in contrast to the lower survivability on copper surfaces, SARS-CoV-2 appears to be able to last substantially longer than the original SARS-Cov-1 on porous surfaces like Cardboard.
This may have relevance to paper also, and shows that all cardboard boxes and possibly paper items (like receipts, invoices, flyers, books, work documents, etc.) should be considered contaminated for at least a few hours (if not the full 24 hours) since a known potential infected person or carrier has handled or come in contact with them.
Note that one of the most sanitisation-friendly surfaces known, still retains a viable transmission risk for up to 24 hours. Therefore, it should be made clear that the reason stainless-steel is so friendly to sanitisation is not that it inherently inhibits viability (like Copper does) but simply that it is so readily and durably cleaned.
Therefore, frequent and effective daily cleaning of any stainless-steel surfaces (that may be at risk of being contaminated), will still be required.
Perhaps most notably of all (considering the ubiquitous use of plastic in our modern environment, including it’s use on permanent surfaces such as toys, appliances, furniture, phones, computer keyboards/mice, etc. as well as temporary surfaces such a product packaging and disposable items) plastic demonstrated the highest capacity to harbour viable virion particles of all materials tested.
It may therefore be advisable to focus on the cleaning of all (durable) plastic surfaces in potentially contaminated environments, and consider quarantining any (less-durable) plastic items for 3 days or more if they have come from a potentially contaminated environment (and cannot be cleaned).
Further Environmental Factors
Various factors influence the survival of viruses in any environment outside a living organism.
Low temperature appears to favour virus persistence.
Warmer conditions tend to accelerate the degeneration of virion particle structure.
Humidity may have variable effects.
Many viruses demonstrate substantially reduced transmissibility in humid conditions (as the moisture level appears to accelerate the settling onto surfaces – and potentially the degeneration of their structure, although certain viruses may be somewhat more resistant to this effect).
Whilst various active drying methods (such as baking and desiccation) may also be sufficient to disrupt a virion particle’s structure and cause destruction of the virus, generally climatically dry conditions usually favour the survivability of viruses for longer in the environment, and in particular the air.
This may have relevance for air conditioning use in summer (that cools and dries air, not to mention provides air currents that may distribute and collect the virus in certain situations).
Although the interaction between temperature and humidity on viability of Cornaviruses has been shown to be more complex than is typically estimated.
Ijaz et al (1985) showed that a moderate humidity (not too low nor too high) was favourable to viral survival at room temperatures.
However they also showed that low temperatures significantly enhance the survival of cornoviruses, and this effect is further increased by higher humidity when the temperature is kept low.
|Half life 26 hrs|
Half life 67 hrs – (High!)
Half life 3 hrs – (Lowest!)
|Enhanced over 20°C level|
Enhanced over 20°C level
Half life 86 hrs – (Highest!)
(Ijaz et. al. 1985)
This once again poses questions not only for cold damp climates, but also for refrigerators in the home.
Some evidence of this in reality has been demonstrated by AccuWeather who has reported a study that shows the parts of China with higher temperatures and higher humidity have seen significantly lower transmission rates between individuals.
Effective Virus Reproduction No. vs Temperature & Relative Humidity (for 100 Chinese Cities)
However other researchers have raised concern that this phenomena is not likely to be sufficient to slow the spread, if basic containment measures are not adhered to.
Effective Sanitisation Methods
|Virus Type||Enveloped?||Resistant To||Sensitive To|
|Enterovirus & Norovirus||No||Strong Acids,|
Heat (up to 60°C),
Heat (up to 60°C),
(Kampf et. al. 2020)
From this summary it seems that thankfully Coronaviruses, being enveloped, are quite sensitive to most sanitisation methods.
Specific Biocidal Agents Against Coronaviruses
Various common and available biocidal agents have been tested for their efficacy against coronoaviruses, with some showing rapid efficacy at reducing infectivity of virions present.
Some commonly used in ‘antibacterial’ products did not show consistent or reliable efficacy, highlighting the need to make a distinction between anti-microbials that have antibacterial vs antiviral activity.
|Agent||Minimum Concentration Required||Duration Required to be Effective|
|Ethanol||70%||within 30 sec to 1 min|
|Povidone Iodine||0.23 – 7.5% (in water)||within 15 sec to 1 min|
|Hydrogen Peroxide||0.5% (in water)||within 1 min|
|Sodium hypochlorite||0.2%||within 1 min|
|? – 10 min|
(Adapted from Kampf et. al. 2020)
– These studies were performed on multiple various types of Coronaviruses (not necessarily SARS-CoV-2).
– These tests were performed either in fluids or on stainless steel surfaces – dirt and residues on surfaces may reduce efficacy (by providing surface area and protective niches for virions to persist within).
– Anti-bacterial cleaners are not necessarily the most effective as anti-viral cleaners.
i.e. common antimicrobial products that use Triclosan, Chlorhexidine and Bezalkonium Chloride may not be as affective at killing Caronaviruses, as simple soap and detergent may be at disrupting and removing them.
– The effectiveness of Chlorine based cleaners can be inhibited by excessive amounts of organic matter (as the Chlorine will bond to organic molecules, leaving less availbe to bond to pathogens)
– One of the most effective, affordable, and non-toxic killing agents for viruses is Alcohol (e.g. Isopropyl Rubbing Alcohol at a concentration of 70% or more – because the mechanism involves physical denaturation).
– Hands and surfaces sanitised via alcohol need to be fully wetted for up to a minute to be fully effective.
– Forms of alcohol intended for drinking do not have sufficient alcohol concentration (spirits being around 40%, wine being around 12%, and beer less than 4%) and are therefore NOT reliable for this purpose, and may even reduce immune function if consumed in excess, and should therefore not be considered helpful during an outbreak.
Are Essential Oils Antiviral?
Beyond the many studies that have analysed the highly antibacterial nature of various essential oils, relatively fewer studies have investigated the specific anti-viral activity of various essential oils.
A comprehensive study investigating the effect of over 60 essential oils on the H1N1 Influenza Virus was completed in 2018. This study demonstrated that a total of 11 essences had notable anti-influenza activity (i.e. over 30% activity).
Three of these essences demonstrated a level of antiviral activity that was over 50% (with one essential oil demonstrating over 70% activity!).
These three essential oils with the highest anti-viral potency, reached an equal or greater activity than the pharmaceutical antiviral medication Oseltamivir (which showed around 50% efficacy), without demonstrating the cytotoxicity associated with this medication (at the same concentrations i.e. a 10% solution).
This means that these essential oils may provide potentially useful antiviral activity, without significant toxicity to cells.
Note: This low cellular toxicity does not indicate that there is no metabolic toxicity from the internal ingestion of these essential oils, and therefore internal ingestion is not recommended.
This research is highly relevant to COVID-19 since the H1N1 Flu virus has a similar structural nature to Coronaviruses (also being enveloped single-stranded RNA viruses), and therefore justifies consideration of these essential oils when seeking to clean surfaces, personal items, air spaces, etc.
Top 10 Essential Oils for Viruses
In order of potency:
1. Pimpinella anisum (Anise) Fruit
2. Thymus mastichina (Marjoram) Leaf
3. Salvia sclarea (Clary sage) Flower
4. Foeniculum vulgare (Fennel) Seed
5. Pogostemon cablin (Patchouli) Leaf
6. Citrus aurantifolia (Lime) Peel
7. Cananga odorata (Ylang ylang) Flower
8. Rosa damascene (Rose) Flower
9. Artemisia dracunculus (Tarragon) Leaf
10. Zingiber officinale (Ginger) Rhizome
– The specific species variety, and plant part, may be relevant when sourcing essential oils.
– Numerous other essential oils known to have antimicrobial activity (such as Eucalyptus, Tea Tree, Oregano, Clove, etc.) were all also tested as part of this study, however did not demonstrate the highest antiviral activity in this context.
– It is possible that varying grades of oil, and methods of extraction, could yield differing active constituents and results, therefore quality, purity and freshness should remain a priority when sourcing.
Essential Oil Diffusers & Atomisers may be a particularly appropriate way of using these essential oils, as they do not apply heat (which may otherwise disrupt the chemical structure of the oil), and they also effectively humidify the air (which may be helpful in limiting the amount of time viruses can persist in the air).
The characteristic symptoms of COVID-19 appear to be variable depending on the individual, however seem to include one of the following (although not necessarily all, or even any):
(Dry and Persistent)
(An Internal Body Temperature >37.8°C)
Note: Ear, Mouth or Rectal measurements are often more accurate than Armpit or Forehead measurements (depending on the quality and intended-use of the available thermometer device)
Cough More Than Fever?
Some sources (such as WHO Feb Final Report 2020) have indicated that fever is more common the cough.
However other sources have indicated that only 48.3% of infected patients had fever when admitted to hospital (and that the number only rose to 88.7% of cases during their treatment, multiple days AFTER being unwell), whereas 67.8% presented with cough (with 56.4% of patients shown to have clouding/opacities on chest CT scan).
This suggests that cough is potentially a more universal indicator in the early stages of an infection (and therefore sign to look for when identifying infected individuals in a population), and that fever only becomes more universal after the infection has progressed further.
This may also be interpreted to suggest that the majority of individuals were exposed via lung infection initially, but still brings into question the reliability of temperature scanning initiatives that have been used in major transport hubs, and other places of gathering.
It is likely these initiatives, whilst better than nothing, do not provide much ability to prevent wider spread, if used alone.
According to one study (Guan et. al. 2020) a low lymphocyte white blood cell count was seen in 83.2% of hospitalised patients (suggesting that the initial elevations that mobilise to defend from infection, may be overburden or compromised by the infection, precipitating the more serious cases of the disease)
i.e. it is possible that if a patient can fend off and recover from the infection before white blood cells become compromised and depleted, and subsequent inflammatory cytokine damage, the risk of more serious complications may be minimised.
Loss of Taste & Smell?
According to some reports from doctors in some of the most affected areas in Italy, a distinct and abrupt loss of taste and smell is also one of the early symptoms of infection for some individuals. (NY Times 2020)
This may progress to more significant symptoms, however for many that may be the only symptoms they experience.
According to recent multicenter study published in The American Journal of Gastroenterology, over half of all COVID-19 patients had digestive symptoms (including pain, diarrhea, etc.). (Pan. et al. 2020)
This correlates with the high ACE-2 expression in intestinal tissues, and may be an underestimated source of infection as well as an overlooked source of symptoms (while focus often remains solely on fever and cough) in those who are claimed to be ‘asymptomatic’.
Although it has been suggested that the cause of some experiencing pain in the abdomen is due to referred pain and inflammation from the lower lobes of the lungs.
Additional symptoms that may accompany cough, fever, or manifest alone:
– Extreme Fatigue (with possible muscle aches)
– Sore Throat
– Running Nose & Mucus Production (typically only seen in later stages of recovery)
It should be noted that just prior to, and during, any symptoms (no matter how mild), an individual may be shedding virus, and therefore contagious.
Levels of Symptom Severity
|Asymptomatic||No noticeable (or reported) symptoms, however virus exposure has occurred, and has either been overcome without outward signs.|
Note: This category may include individuals who HAVE had symptoms, however they did not report them, or did not attribute them to COVID-19.
|Mild Symptoms||This category includes a wide range of severities.|
This categorisation may include everything from barely perceptible signs, to being bedridden.
The term ‘mild’ relates to the level of demand for acute healthcare support services (rather than a description the level of discomfort).
|Severe Symptoms||This category encompasses those symptoms that may warrant acute and intensive care, and have the potential to progress to life-threatening complications.|
Course of Disease
According to Song et. al. 2019, severe SARS coronavirus infection is characterized by atypical pneumonia with rapid respiratory deterioration, and potentially failure, due to increased levels of activated proinflammatory chemokines and cytokines (so called ‘Cytokine Storm’), which can cause inflammatory tissue damage, and the impairment of oxygen transfer in the lungs due to fluid accumulation.
In the case of COVID-19, the prevalence of virus wherever there are ACE-2 receptors in the body means that tissues other than the lungs may also be affected and ultimately damaged, causing potentially life threatening complications.
According to ICNARC, the organs most impacted in cases requiring hospitalisation are as follows:
Percentage Of Patients Receiving Specific Organ Support
Clemens Wendtner, the director of infectious disease and tropical medicine at Munich Clinic Schwabing teaching hospital, was asked to comment on what hey have found regarding the contagiousness of SARS-CoV-2.
He stated that in one case an infected individual sneezed during a meeting with one person, and that was enough for infection. In other cases of infection there were simple business meetings where individuals were sitting at a table for 60 minutes, “with no physical contact — just one handshake, that’s all. The infectivity is quite high.”
Duration of Virus Shedding (AFTER Symptoms Start)
SARS-CoV-2 has shown an average of 20 days virus shedding (from onset of symptoms) in hospitalized individuals. But some individuals shed for as long as 37 days.
It is unclear what the average is among those with less symptomatic disease.
Wendtner said that the results of their investigations suggest that isolation periods could be shorter for people who have RNA fragments but no intact virus.
(Researchers have thought that because tests could still detect RNA fragments for up to weeks after symptoms had cleared, patients were infectious for that long).
Wendtner didn’t suggest letting people out of quarantine before their two weeks, but he did say that due to the rapid drop in infectious virus often seen after the early stages of infection, “maybe it’s safe 10 days after symptoms start, but you have to prove they have those neutralizing antibodies.”
Currently, most patients are not released from the hospital until two separate tests, within 24 hours, come back negative for the virus.
Antibody testing remains yet to become standard.
Body Fluids With Highest Viral Load Post Symptom Onset
This study illustrates how 6 different patients all had highly variable levels of virus shedding, from very different body fluids, over different periods of time after falling ill.
It also demonstrates (with the pink bar) how few patients experienced fever, and how briefly for those that did.
What is perhaps even more concerning, is the fact that a study of nine people who contracted SARS-CoV-2 in Germany suggested that people are mainly contagious before they have symptoms and in the first week.
Duration Of Virus Shedding (BEFORE Symptoms Start)
|Virus||Incubation Period||Potential Shedding BEFORE Symptom Onset|
|Potential Shedding AFTER Symptom Resolution|
|Measles||7 – 19 Days||1 Day Before||4 Days After|
|Chicken Pox||10 – 21 Days||2 Days Before||7 Days After|
|Enterovirus||5 – 7 Days||NA||8 Weeks After|
|Herpes Simplex||6 Days||NA||8 Weeks After|
|Influenza||2 – 3 Days||1 Day Before||7 Days After|
|SARS-CoV-2||2 – 10 Days||Multiple Days Before||2 Weeks After|
(may or may not be infectious)
(Kampf et. al. 2020, Woelfel 2020)
It may be difficult to determine SARS-CoV-2 infection from symptoms alone (especially since ‘Cold & Flu’ symptoms are so common, and have such a variety of causes).
Given the amount of evidence that many infections of SARS-CoV-2 do not progress to noticeable COVID-19 symptoms at all, it is possible that the true rate of infection is far greater than has been (or will be) realised.
In Italy, one of the worst affected nations in the early stages of this outbreak, the entire population of the town of Vo ‘Euganeo (around 3,000 inhabitants) were tested for SARS-CoV-2. The results showed that the majority of infected individuals had become carriers, without any outward signs or symptoms.
The Professor of Clinical Immunology of the University of Florence, Sergio Romagnani, said that:
“The vast majority of people infected with Covid-19, between 50 and 75%, are completely asymptomatic but represent a formidable source of contagion”.
Some questions were raised as to whether individuals in the study should be tracked for a longer period of time, (since there could be a very long incubation stage for this virus in some individuals).
However Romagnani pointed out that “with the isolation of the infected subjects, the total number of patients fell from 88 to 7 (at least 10 times less) within 7-10 days. The isolation of the infected (symptomatic or non-symptomatic) was not only able to protect other people from contagion, but also appeared to protect against the serious evolution of the disease in infected subjects because the cure rate in infected patients, if isolated, was in 60% of cases equal to only 8 days”.
Other studies, such as modelling of the Diamond Princess Cruise Ship outbreak, as well as research on Japanese citizens evacuated from the Wuhan region, found the rate of asymptomatic patients occurred at close to 20% and 30% respectively.
This is promising because it shows that the true severity of the statistics are likely lower than initially estimated, however it also suggests that the contagiousness is even higher than first realized.
It also demonstrates the importance of widespread testing (even in the mildly ill or asymptomatic), as well as isolation measures.
It is imperative that accurate, rapid, affordable and accessible testing methods exist for tracking the case diagnosis, and spread of this virus.
However these measures have not taken place in the most crucial early stages of this outbreak.
According to Li et al (2020), they estimated that:
“86% of all infections were undocumented (82%-90% prior to the 23 January 2020 travel restrictions)” and that “due to their greater numbers, undocumented infections were the infection source for 79% of documented cases. These findings explain the rapid geographic spread of SARS-CoV2 and indicate containment of this virus will be particularly challenging.”
Key: Waiting for symptoms is not a suitable threshold for detection.
The Woelfel paper did suggest that people with very mild or asymptomatic infections don’t shed as much virus and aren’t as likely to infect other people as those with more severe cases.
The reasons for milder or even asymptomatic cases may have something to do with various circumstantial factors (such as mutated (weaker) strains of the virus, lower exposure doses, digestive routes of contraction rather than lung), as much as personal susceptibility factors (such as genetics, blood type, etc.)
The fact that proliferation of the virus is highest in the early stages of infection, also means that the greatest opportunity to reduce the severity of the infection is in the earliest stages, and waiting for the severity to worsen before testing justifies treatment, may lead to worsening prognosis for many who may have had milder disease if supported sooner.
The early handling of the outbreak by South Korea (who had first patients at a similar time to the USA), showed the success that can achieved by early, rapid and widespread testing.
Note: Testing methods may matter.
– Testing for the actual SARS-CoV-2 virion using PCR (mere detection of the virion RNA fragments) does not necessarily confirm that they are viable or infectious.
– Testing for antibodies to the virus in patients (indicating previous exposure and estimating long term immunity) may provide greater insights into contagiousness.
Coronavirus virions contain four main structural proteins.
These are the spike (S), the membrane (M), the envelope (E), and the nucleocapsid (N) proteins.
Each are a potential target for testing.
Test Type & Accuracy
In mid-January 2020 China released the genome sequence of the newly discovered SARS Coronavirus 2 to the world.
Since then numerous labs around the world have attempted to develop their own methods of testing for the virus according to that sequence.
Almost all labs use some kind of PCR based gene testing method, however each has tended to look at a different portion or section of the virus’ genome sequence.
This means that each test may have its own peculiarities (e.g. degrees of sensitivity and specificity).
Some tests may be mire able to detect smaller amounts of virus, some may only test for one strain of the currently identified virus (to prevent false positives from a similar virus), and others may include multiple strains (to attempt to catch multiple subtypes of the current virus group responsible for COVID-19, as they mutate – however may also include similar but non-COVID-19 strains).
Sampling procedures, equipment and methodology also vary (e.g. sampling of the throat is preferred by some researchers, and others recommend sampling the nasal passage, as each have differing viral levels at different stages of infection.
Therefore even if everyone in the world got tested, there would still be a high degree of variability in the accuracy of the results (and their appropriate interpretation).
Tests Recognised by The WHO
|Country||Institute||Target Gene Sequence|
|China||China CDC||ORF1ab and N|
|Germany||Charité||RdRP, E, N|
|Hong Kong SAR||HKU||ORF1b-nsp14, N|
|Japan||National Institute of Infectious Diseases, Dept of Virology III||Pancorona and multiple targets,|
|Thailand||National Institute of Health||N|
|US||US CDC||Three targets in N gene|
|France||Institut Pasteur, Paris||Two targets in RdRP|
(as of Mar 2020)
Not All Tests Are Created Equal
According to the National Review, the Czech Republic recently claimed that they spent over half a million dollars ordering 150,000 SARS-Cov-2 test kits from China, however upon arrival it was found that the test kits had an error rate of 80% (80% of the kits gave apparently faulty results), which was only discovered when they chose to verify the accuracy of the Chinese tests (via comparison with their own internal laboratory testing).
Spain has also received these kits from China. This demonstrates how variable the accuracy of results from the world might be.
Why Do Some Countries Minimise Testing?
In an ideal world, the resources would be kept available for rapid and widespread accurate testing right from the earliest (and most important stages) of a pandemic.
The Director-General of the World Health Organization said in early March 2020:
“We have a simple message for all countries: Test, test, test. Test every suspected case. If they test positive, isolate them and find out who they have been in contact with two days before they developed symptoms and test those people, too.”
However realities beyond simply the time required to develop an accurate test, include limitations to materials required to make the kits, logistics in the distribution of kits, returned samples and test results, as well as the availability of Personal Protection Equipment (PPE) required for the personnel who need to take and process the samples.
Limitations in any one of these areas (or all) can drastically reduce the volume of actual testing that can be done.
In an attempt to address this shortfall, the list of approved tests will likely increase rapidly as more private research and commercial laboratories also develop testing procedures and seek approval for their widespread use under emergency EUA (Emergency Use Authorisation) provisions.
This may assist in achieving greater and sooner access to testing, however may also further complicate the data from differing methodologies being used to contribute to the same statistics (making the level of accuracy around those statistics further complicated).
As of March 2020, a number of new testing systems are emerging to fill not only the shortfall in available tests, but also improve the accuracy and speed of testing.
Abbott Laboratories has gained FDA approval under EUA to adapt it’s existing ‘ID NOW’ platform (a small portable device previously used for Influenza strain identification), to successfully identify the SARS-CoV-2 gene sequence in less than 5 minutes (and confirm a negative result within 13 minutes).
This, and other systems like it, could provide far more immediate control over various environments, where test results are not only required, but are required immediately (as opposed to 24-72 hours later, which may miss the opportunity to a control a local situation).
It also means some of the burden of testing could be taken off hospitals, and put back in the hands of GPs and other point-of-care healthcare environments.
Testing Viral Presence vs Viral Immunity
Beyond simply testing for the presence of the virus in an environment or an individual, it may be particularly important and useful to be able to actually test for the body’s immune response to the virus.
This not only serves as a confirmation that an individual has been exposed to the virus, but it also may indicate the degree of immunity that individual may have to the virus (in case the exposure was in the past, and the virus is no longer present or being actively shed by the person).
GeneSystems Inc. is another company that has been given FDA approval under EUA to begin producing its CoronaCheck ™ COVID-19 Rapid Antibody Test Kit.
This test kit measures antibodies to the virus (rather than merely fragments of the virus itself), and it can do so in less than 15 minutes, with a high sensitivity of ~97% and specificity of ~92%, validated by an extensive cohort of patients.
This level of speed and accuracy, as well as ability to determine previous exposures, and potential resistance to future exposures, makes this test a highly promising development in the fight against COVID-19.
Infectious disease experts have estimated that a population needs around 60% or more of its members to have been exposed to (and recovered from) a virus, for the saturation of immune individuals to be high enough that the virus cannot continue to spread.
However this modeling and theory relies on certain assumptions that immunity is durable (persists for a long time after exposure/recovery).
These attributes of durable immunity, whilst applicable to most viruses, have not yet been confirmed for SARS-CoV-2, and perhaps worryingly, some evidence for the contrary has begun to emerge in some cases.
This issue has attracted controversy, as Australian and UK health authorities criticise Holland for prematurely making herd immunity part of their national health strategy, before reliance on this strategy has been proven safe and effective in this case. (ABC 2020)
Is Re-Infection Possible?
Even the CDC (and other health agencies around the world) delivered their standard viral guidelines in their early response to COVID-19, which includes the claim that “someone who has completed quarantine or has been released from isolation does not pose a risk of infection to other people” (because this is indeed usually the case with most viruses), however in this case that may turn out to be a too absolute statement to make.
Numerous reports have emerged from medical experts around the world suggesting that patients who had apparently recovered from COVID-19, tested negative, and sent home, had returned later requiring acute care from an apparent ‘re-infection’.
Some possible hypotheses to explain this have been:
1. Test Sensitivity
The sensitivity threshold of the test is potentially not sensitive enough to detect the shedding of the virus once it reaches low enough levels, and once the patient is removed from treatment, those low levels may resurge and overwhelm the patient’s immune system once again.
2. Nervous System Dormancy
Many viruses have the ability to invade the central nervous system (where they can hide in the slower turnover cells of the dermatomes, spinal cord, and brain), and evade some of the immune system’s strongest activity, and lay in wait for an opportune time to resurge when the patient is weakened.
This neuro-invasive potential has been demonstrated for the SARS-CoV virus, and has been posited as one the main mechanisms for how the virus may travel to and from the lung and other tissues in the body during the acute stages of respiratory distress.
This also explains some of the neurological symptoms presenting in some cases of COVID-19 (headache, pain, loss of sensation, etc.). (Li, Bai & Hashikawa, 2020)
3. Multiple Strains
It has also been theorized that some viruses may have an increased speed of mutation, that causes multiple sub-strains to appear during the same outbreak (as it migrates through large populations, of different genetic heritage, and geographic location). Therefore immunity to one sub-strain may not fully protect from further infection from similar varieties of the same type of virus.
4. Immune Evasion & Adaptation
Another possibility that has been theorized involves the virus developing the mechanisms to evade proper identification by parts of the immune system, or compromise the immune system cells themselves, so that they are less able to properly resolve the infection, and retain durable immunity.
At this stage it is too early to ascertain the reality of this, and if so to what degree this phenomena could hamper any treatment and containment efforts, not to mention future vaccine and eradication strategies.
Should We Be Concerned?
The fact that a substantial number of individuals will get it, but will never be confirmed to have gotten it, does dilute some of the actual severity to the numbers indicated for Case Fatality Rate (i.e. if all the people without sufficiently notable disease symptoms where included in the statistics, the percentage of cases recorded as severe cases would be regarded to be far less).
However, this does not change the reality for those who DO experience severe symptoms, and in that regard the percentage who do, seem to experience a severity of symptoms far greater than the Flu.
It may be considered trite for those of younger age to dismiss the concern around this virus due to its apparent greater risk to those of more advanced age. Compassion, regardless of age, is a community exercise, and whilst humanity currently accepts the unavoidable reality of the seasonal Flu, the same thinking applied to this virus, may in time be considered inaccurate and insensitive.
It should therefore be a collective community priority as a whole to address this virus in every way possible.
The motivation to do this on a societal level may be increased by the growing reports that whilst statistics invariably put the aged and those with preexisting conditions at greater risk of succumbing to this disease, those who are healthy and of young age, are also succumbing to the disease in certain instances.
This was phenomena was also seen during the Spanish Flu (which resulted in the deaths of millions).
So whilst we do not yet know all the factors that make a given individual at risk, regardless of their age and health status, we should probably be regarding everyone at risk, and taking global and community level approach.
Factors That Influence Susceptibility
Particularly over 65 years
Some initial reports suggested higher incidence in men than women
(although further data has also shown a more even balance)
The largest represented group of patients are over 30 BMI
Especially conditions involving lowered immunity, or kidney dysfunction.
High Blood Pressure
Whether being treated or not, higher blood pressure may increase severity.
According to one study (by Zhao et al 2020), “people with blood group A have a significantly higher risk for acquiring COVID-19 compared with non-A blood groups, whereas blood group O has a significantly lower risk for the infection compared with non-O blood groups”.
Allergies & Autoimmunity
It has been theorised that those with a propensity towards a stronger inflammatory response, especially inappropriately strong in other contexts such as allergy and autoimmunity, may be at higher risk of severe complications that involve cytokine overproduction.
However there have been conflicting case reports on this factor, which suggests that there may be some further research detail required to find specific pathologies within this broad group that do or do not increase severity of COVID-19.
It may turn out that those with higher inflammatory responses are somewhat protected by being more likely to fight off the infection in the initial stages, although are more likely to suffer severe complications if the severity of the infection becomes more established and overwhelming to the immune system, however these theorisations remain conjecture at this stage, and are worth monitoring for further indications.
(CDC 2020, ICNARC 2020)
Flattening The Curve
The important thing to understand is that whatever the average case fatality rate for a respiratory disease is in a typical modern healthcare setting, this rate escalates rapidly in a situation where medical care is no longer available.
A Real World Example
Back in 1918 when the Spanish flu outbreak was spreading around the world, the US cities of Philadelphia and St. Louis had two different approaches to the disease.
In an effort to boost morale the city of Philadelphia threw a parade that drew 200,000 people, despite warnings that the Spanish flu was spreading.
Within days the hospitals in the area were filled with infected patients and within weeks 4,500 in Philadelphia had died from the infection.
In contrast, after detecting the first cases of Spanish Flu within their community, the city of St. Louis closed public buildings (such as schools, churches, halls, libraries, etc.).
Gatherings of more than 20 people were banned, work shifts were staggered, and the use of public transport and taxis was limited.
The social distancing measures resulted in half the rate of deaths per capita than Philadelphia during the outbreak (which ultimately claimed the lives of 20 – 50 million people worldwide over a span of only 2 years).
This example demonstrates the effectiveness and necessity for such social distancing measures among conscientious communities during any pandemic.
(Hatchett et. al. 2007)
During the original SARS outbreak it became apparent that transmission rates could be worsened within healthcare settings through the use of nebulizers, bronchoscopy procedures, and cardiopulmonary resuscitation.
All of these activities result in the generation of a large quantity of droplets containing infectious virus particles. Unfortunately hospitals were unwittingly involved in amplifying the spread of the epidemic. (Tomlinson and Cockram, 2003)
This was seen very clearly in the Prince of Wales Hospital in Hong Kong, where within only three weeks of admission of the first index case, 156 further cases had been diagnosed, all capable of being traced back to this single case.
The major reasons given for the spread of infection in this hospital were failure to apply appropriate isolation precautions to cases not yet identified as SARS-CoV and breaches of such precautions, and the use of a nebulized bronchodilator that released huge amounts of droplet contamination in the original patient’s environment.
Therefore, efficient and effective isolation procedures and lab testing remain key (as well as minimisation of aerosolised of infected material, and the spread of contaminated air flows).
It is important to not only communicate correct protocols, but to ensure they are adhered to.
A case control in 5 further Hong Kong hospitals demonstrated that adhering to such precautions (i.e. the use of a mask, gloves, gowns and hand washing) resulted in no secondary cases in 69 staff who followed these measures.
In contrast, all of the 13 staff who became infected after caring for SARS cases reported not adhering to at least one of these measures. (Seto et al. 2003)
The Importance of Speed
A study has indicated that if Chinese authorities had implemented intervention strategies three weeks earlier than they did, the number of initial COVID-19 cases could have been reduced by 95% and its geographic spread limited. (Lai et al 2020)
The likelihood that an outbreak can be contained is often directly related to how quickly and effectively intervention strategies are put in place.
Likewise if any of the actions that have been taken to date, had not been taken when they did, the degree of impact would have been exponentially greater.
Quarantine vs Isolation?
To clarify terminology, it may be worth clarifying the use of terms during an outbreak.
‘Quarantine’ is the term typically used to refer to a theoretical or potential source of infection being restricted from the broader population, by being withheld and delayed contact (not exhibiting symptoms, but enough time for symptoms to emerge, and then warrant further isolation and treatment if necessary)
‘Isolation’ is the term for a person being separated from contact with others due to a strongly suspected or confirmed infection (exhibiting symptoms).
‘Social Distancing’ is a term used simply to describe infection prevention measures that involve individuals spacing themselves at least a ‘cough’s distance’ away from other individuals (usually 2 meters), and the avoidance of any physical contact (such as hand shaking, kissing, hugging, etc.), especially in public places (and may extend to the avoidance of those places altogether or minmising the number of individuals allowed to gather in one place).
How Social Distancing Slows The Spreading Of Disease
Seeing as it is often difficult to visualise and comprehend the rapid expansion of exponential growth, the following video provides some excellent perspective.
Narrator: Professor Hugh Montgommery
Visualisation: Declan Animation
Shelter-In-Place / Lockdown
The terms ‘Shelter-In-Place’ (self imposed) or ‘Lockdown’ (externally imposed) are used to describe the complete isolation of all individuals (or households) within a specific community, in an attempt to completely halt transmission.
The severity of a pandemic like COVID-19 appears to justify a combination of Lockdown (for all who do not fulfill essential community services), and strong Social Distancing measures (for all individuals interacting with essential services personnel who continue to service the community during this time).
As an example, Washington state, (one of the US states first affected by COVID-19, and therefore first to act), will still only be able to stay within their hospital capacity by mid 2020 if residents adhere to strict home lockdown measures for a number of months. Even lax adherence to home lockdown guidelines may not be sufficient to prevent exceeding the available hospital capacity.
The standard ‘quarantine’ period of 14 days that has been recommended is to allow a period of time for the emergence of symptoms (e.g. after possible exposure), due to a potentially long incubation stage.
If an individual becomes an officially confirmed case of COVID-19, then longer than the typical 14 days may be required (i.e. in some cases it may take multiple weeks for symptoms to subside, and to stop shedding the virus).
Acknowledging Tireless Service Workers
As the world rapidly adapts by taking more and more business online, and with physical product purchases being made by delivery rather than in-store, it may be worth considering the delivery personnel who fulfill this essential service.
Can You Catch Contract COVID-19 from Delivered Packages?
There has not been substantial evidence to date that shipped items are a notable source of transmission.
This is likely due to the inability for the virus to survive the period of time it takes for many items to be delivered. However as the speed and volume of modern deliveries increases, and the likelihood that the delivery person themselves may become a source of contamination right at the point of delivery, it may become prudent to take certain precautions.
– Have a designated area for receiving parcels, packages and deliveries (effectively a quarantine)
– If not time urgent or temperature sensitive, simply leave the delivery in ‘quarantine’ for at least 3 days before opening.
– For time urgent items, wipe down any packaging surfaces that may have been handled in the previous 2 days (internal packaging that wouldn’t have been handled so recently should not require cleaning), and wash hands before touching food or face after handling goods.
– For food items, transfer to designated containers for storage (that are cleaned periodically).
– Fresh produce that will be consumed within a few days, and not be cooked, can be washed with mild detergent, brushing, rinsing.
– For immediate hot food deliveries (e.g. take-away), transfer the food into alternate food serving or storage containers, and reheat before consuming.
Note: These steps may not be required in most situations, however they may provide peace of mind for those concerned about this possibility, and if certain situations evolve to justifiably include this concern.
Interestingly, when each of the four primary infection-control measures was examined by researchers (Zuckerman et. al. 2009), only the wearing of N95 masks was shown to be essential for protection against infection. They concluded that this supports the principal mode of spread of SARS being by respiratory droplets, and that unlike most other respiratory viruses, wearing an N95 mask (which is capable of trapping 95% of airborne particles around 0.3 mcm in size), adds a further level of protection to staff.
According to the WHO (2009), the following recommendations were made regarding the SARS outbreak:
“recommendations are centered around rapid case identification, triage and immediate isolation, with droplet and if necessary airborne precautions. Thus when a suspected case enters a hospital, these conditions must be strictly enforced, the patient must be isolated in a single room and, if procedures which may generate an aerosol are necessary for patient diagnosis and management, this should be a negative-pressure room. If mechanical ventilation becomes necessary, this must take place in such a room. However, if the only patient requires supplemental oxygen, the use of nasal cannulae is believed to reduce the risk of airborne spread compared with a high-flow face mask. If no additional oxygen is required, patients who are proven or who may represent possible cases of SARS-CoV should be given a face mask to wear, preferably one that filters exhaled air, in order to prevent the spread of SARS-CoV in hospitals. Furthermore, after discharge the patient must be told to adhere to strict personal hygiene. The staff involved in the initial contact must wear a mask, for example N95 with 95% filter efficiency and goggles. They must wash hands before and after contact and wear gloves. Standard disinfectant solutions such as household bleach and alcohol gel preparations should be readily available in the immediate vicinity of the patient as the virus is easily inactivated. Further infection-control measures include restricting visitors and supervising them in the use of protective equipment. It has also been suggested that the wearing of footwear that can be easily decontaminated should be considered. The removal of linen should be done by staff wearing full protective equipment (goggles, N95 or N100 masks, gloves, disposable gowns/aprons). The linen must be placed in biohazard bags and destroyed by incineration. As virus has been shown to survive in faeces and respiratory secretions for 4 and >7 days respectively, room cleaning should take place using a broad-spectrum disinfectant, for example household bleach.”
Masks vs Respirators
Surgical Masks and Respirator Masks may both be referred to as ‘masks’, however they are not the same thing.
A Surgical Mask is designed to crudely catch/filter air and fluids coming from an individual (to protect the environment from being sprayed with particulate matter and aerosol that may settle and carry infective risk).
A mask will therefore usually simply loosely cradle the mouth and nose region of the face (as a form of ‘cough barrier’).
A ‘Respirator’ on the other hand is designed to protect an individual from particles in the environment.
A respirator will therefore require a tight seal on all sides, and will include either ‘half face’ (nose and mouth) or ‘full face’ types (including eyes as well).
A ‘Filtering Facepiece Respirator’ (FFR) will usually have a valve to allow unfiltered exhaled air to escape easily into the environment to assist breathing (given the tight seal), and is therefore not the best choice for someone who is already infected, and could be shedding virus out of the vent).
The Australian rating system uses ‘P2’ to refer to masks equivalent to N95.
Do Masks Work?
To answer that question, it may be worth first understanding the size of various viruses.
How Big Are Viruses?
Note that as far as viruses go, SARS-Caronavirus-2 is actually relatively ‘medium-large’ in size.
This may have an impact on the efficacy of various attempts to filter it out of air.
The Filtering Capacity of Various Masks
A study measuring the filtration capacity of various masks, assessed what percentage of diesel exhaust particles (at an air concentration of 500,000 particles/cm3 – to emulate high pollution) would be captured by the mask and prevented from reaching the wearer.
Note: According to Kittelson (2000) the majority of diesel exhaust particles occur between 10 – 40nm, and the device used to detect the particles in the study (a model 3022 TSI Condensation Particle Counter) was capable of detecting particles as small as 7nm.
Therefore this study has strong relevance to coronavirus particle filtration, since the average SARS-CoV-2 particle is around 120nm (up to 10 times larger than most particles measured in this study).
Amount of Particles Let Through Various Masks
– Even though an N95 mask is rated to provide over 95% filtration protection, based on this study, a surgical mask could still provide up to 80% protection, and even a cotton handkerchief may filter as much as 30% (demonstrating that anything may be better than nothing in a high risk/burden environment).
– However differences in materials, and the poor seal of surgical masks, may result in much lower filtration performance in some instances, as has been seen in some other studies (such as Lee, Grinshpun & Reponen 2008) where N95 masks have been shown to provide a factor of protection 8-12x greater than surgical masks.
The image above shows the difference in fabric density between various mask materials, (which therefore influences the size of particles they are able to effectively capture).
The yellow line for each image represents 500 microns (micrometers) and clearly shows how much more filtration is possible with the high microscopic density of an N95 rated mask.
Can Surgical Masks Catch Coughs?
Beyond the capacity for various masks to filter the environment for the wearer, the main purpose of a surgical mask is to protect the people and spaces around the wearer.
It may therefore be important to assess the ability for surgical masks to sufficiently contain any expelled oral, respiratory, and nasal Caronavirus particles (and prevent them being deposited on the various surfaces and air around an infected person).
A very small study (by Bae et al 2020, on only four individuals) sought to do this, and found that:
– The number of virion particles in the nasal fluid of three of the individuals ranged from
1,000,000 – 10,000,000+ copies per ml.
– The concentration of virion particles that were deposited on surfaces after 5 coughs was around 150 – 3,200 copies per ml.
– When wearing a surgical mask during the 5 coughs the concentration arriving on surrounding surfaces reduced to around 60 – 1,300 copies per ml.
– When wearing a standard cotton mask, the concentration arriving on surrounding surfaces reduced even further to around 160 copies per ml or less.
This study concluded that these masks were therefore not sufficient to prevent the spread of SARS-CoV-2.
– A distinct reduction was seen, so it cannot be concluded that the masks did not provide any benefit at all.
– The study size was far too small, and results of each patient were highly variable, to draw broad conclusions from.
– There were some anomalies in the data, such as high levels of virus detected on the OUTSIDE of the mask, and NONE detected on the inside.
– This, and the fact that cotton masks performed better than surgical masks, were attributed to the poor seal of surgical masks (potentially allowing air flows out the side of the mask).
– Therefore further research is certainly required in this area, and whilst surgical masks should not be solely relied upon to protect people and spaces from infectious individuals, the wearing of surgical masks (whenever available) within populations experiencing community spread may still be expected to reduce the speed, severity and burden of disease.
Note: An N95 respirator would provide no protection of the surrounding environment if the wearer was already infected (as the valve would allow exhaled air to escape unfiltered).
Therefore N95 masks should perhaps be preserved for those that are not yet infected.
– A Respirator must be fitted correctly in order to provide the rated level of protection.
– Regardless of which mask is used, even with proper fit, filtration is never 100% (as it would become impractical to breathe through), however every bit helps in reducing the likelihood of infection, and ultimately the burden of any particular exposure.
Some advisories have suggested against the use of masks on the assumption that the average person does not know how to wear them correctly, and they are sorely needed for medical staff who have not been given a sufficient stockpile.
Therefore, for all individuals who have access to a mask when needed it is imperative that they know how to wear it correctly in order to make full use of the mask.
Respirator/Mask Wearing Guide
Step 1: Wash hands thoroughly (Important!)
Step 2: Apply Mask (See procedure Below)
Step 3: Perform ‘Fit Test’
– Place pressure on the mask with one hand to ensure an optimum seal and smoothly blow outwards (if air escapes out any of the edges of the mask (rather than the mask filter itself, or the designated outflow valve (if present), refit or chose an alternate model/shape/style that can provide a suitable/sufficient fit.
– Make sure the mask rests with this same degree of fit when no longer touching the mask, in order to maintain a sufficient seal during activity (some masks even include sticky edges to adhere to the skin to assist this).
– Avoid touching the face mask after correctly fitted.
– Wash hands before AND after removing mask.
– Place mask in a contained environment once used (as it should now be considered contaminated)
Can You Reuse a Mask?
In terms of mere filtration capacity, respirator masks can in fact be worn multiple times (every day for multiple weeks) and still maintain their N95 effectiveness rating.
However this physical capacity has been assessed in relation to simply maintaining ability to exclude inanimate pollution particles. (Smart Air 2017)
When trying to assess filtration of infective particles, things get a little more complicated.
Whenever a mask is worn for any extended period of time in a potentially contaminated environment, that mask should then be considered contaminated (as it may have virion particles trapped within its fibres).
The longer it is worn within that environment, the more virion particles it may have accumulated.
Therefore it is quite important not to touch a mask’s filter area directly with unprotected hands once the mask has been worn for some time (as those hands could then become contaminated as well), or at least to wash hands immediately after handling a used mask.
In order to reuse that particular mask, a suitable sterilisation process would need to take place.
It would obviously be ideal to discard all masks after use, however in a situation where there are mask and respirator shortages, ensuring their maximum safe and effective lifetime of use should be considered appropriate and necessary.
Some measures that have been taken by those without access to additional masks include:
1. An extended quarantine period (e.g. 2 weeks), before a mask is reused.
(Caveat: requires at least a few masks to cycle through rotation, and does not provide any guarantees, therefore the longer the better)
2. If no further masks are available, and the need to reuse a mask is more urgent, some direct sterilisation techniques have been shown to be suitable and effective.
Ultraviolet light irradiation has been shown to be one of the most effective medical methods of sanitising a mask, without interfering with its performance (however requires the appropriate medical-grade equipment).
Microwave Steam Bags are a potentially more accessible method for many, and has also been shown to be effective for sanitising a mask, without substantially reducing the masks performance.
(Fisher, Williams & Shaffer 2011)
– Do NOT attempt to wash a mask.
Whether water, alcohol, or any other fluid is used, or if any rubbing or scrubbing is applied, almost all other methods that have been evaluated have caused some degree of disruption to the fibre structure of the mask, which has invariably shown a reduction in the efficacy of the mask (and many of these methods did not sufficiently sterilise the mask either).
– Vaporised Hydrogen Peroxide is one other method that has shown to be effective without disrupting the efficacy of the mask (as it uses vapor rather than fluid), however it usually requires commercial equipment to perform (some commercial services exist for hospitals to have their masks restored via this method).
(Viscusi et. al. 2009)
Why Has Mask Wearing Been Discouraged By Some?
It is likely that a shortage in available masks has resulted in various government and health agencies needing to prioritise access to essential healthcare services and personnel. Discouraging the non-essential use by the average citizen, may reduce burdens on demand, however is not consistent with the evidence for reducing transmission.
Beyond social distancing, if everyone wore a mask when in public spaces, the ability to inhibit spread would be greatly enhanced.
For this to happen, the availability of masks needs to be increased through increased national and global production, and the adjustment of social norms around the wearing of masks.
Medical Treatment Strategies
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The Functional Medicine Approach
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This page will continue to be updated with any key developments as they unfold in the course of the COVID-19 Pandemic.
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