There is an overwhelming amount of information available on the disease that has created the pandemic,
but much of it is social media malarkey. To help separate the fact from fiction, KTW editor Christopher Foulds contacted three Kamloops doctors, who agreed to take part in a multi-part Q&A series that began in the
Jan. 6 edition of Kamloops This Week. This is part 2 and the Q&A series will continue in subsequent editions until the queries are exhausted. Dr. Elizabeth Parfitt is a physician specializing in treating and diagnosing patients with infections at Royal Inland Hospital. Dr. Annemie Raath is a hospitalist at RIH, a family physician skilled in caring for hospitalized patients and who has been working on the COVID unit throughout the pandemic. Dr. Carol Fenton is a Kamloops-based medical health officer for Interior Health, a position that is a public health and preventive medicine specialist. Neither of the doctors are vaccinologists, virologists or immunologists. The information in the Q&A reflects current understanding as of Dec. 30, 2020, and will
likely change rapidly, as has most everything since the pandemic was declared on March 11, 2020.
Click here to read part 1 of the COVID-19 Q&A.
Q: Is the SARS-CoV-2 virus a cold virus or something else altogether? If it is a cold virus, is there a difference between an influenza virus and a cold virus? If so, what is the main difference?
DR. PARFITT AND DR. FENTON: This is a great question and a concept we often teach to medical students. A “cold” is a syndrome — a collection of symptoms usually including a runny nose, maybe a sore throat. “Colds” can be caused by a number of different viruses, such as rhinoviruses, adenoviruses and other coronaviruses that have been circulating for a long time. Similarly, “flu” is a syndrome where we see fever, cough and muscle aches, and it is usually caused by the influenza virus.
But other viruses can also cause these symptoms — but not to be confused with “stomach flu,” which is what some people call nausea and vomiting. We call this “gastroenteritis” and it can be caused by viruses such as norovirus or bacteria such as e.coli or salmonella.
A coronavirus is a virus, an infectious agent that can create a number of different symptoms and, therefore, syndromes. Coronaviruses can cause both “cold” and “flu” syndromes. This is why the list for compatible symptoms may seem long and vague, but it is important to get tested for COVID-19 if you have these symptoms. COVID-19 can cause a wide range of symptoms and can cause both “cold” and “flu” syndromes, so doctors, nurses and patients cannot really distinguish what they have based on symptoms.
One of the reasons testing has become such a critical pillar of our response to COVID is the fact that it can cause a wide range of symptoms and can cause both “cold” and “flu” syndromes, so doctors, nurses and patients cannot really distinguish what they have based on symptoms. There are some symptoms that make it more likely, such as changes in smell/taste, and, of course, it's more likely if you live in a higher prevalence area or have had contact with someone knowingly, but otherwise, we just need to test.
This is nothing new to us in medicine — people can come in with “flu-like” symptoms and be diagnosed with a bacterial infection or a medication reaction.
Ultimately, with the question, we would say SARS-CoV-2 is a “respiratory” virus, based on its mechanism of spread. However, once in the human host, it can cause myriad symptoms and, therefore, syndromes, including some unusual post-infectious phenomena.
Q: The last great pandemic was the Spanish Flu of 1918-1920. There was no vaccine back then and tens of millions of people died. But, eventually, the pandemic ended and life did return to normal. How did the pandemic end with no vaccine and what happened to the virus? I heard it remains alive and can be found as part of current flu viruses. Is that true?
DR. PARFITT: Corona-
viruses and influenza viruses are different viruses.The 1918 pandemic was worse than COVID-19 for a number of reasons. An example is the lower risk of severe complications from COVID-19 in children and younger adults versus influenza, for which we are all grateful. Rather, poor outcomes with COVID-19 are strongly associated with increasing age. And, yes, the 1918 influenza strain is still, in essence, “with us,” although it will have changed over time. Life likely went back to normal with a combination of herd or community immunity through natural infection and through weakening of the virus over time as it changed genetically, as influenza viruses do.
But it is difficult to compare to the current pandemic for a number of reasons:
• The population structure was different in 1918. There were less elderly and people with chronic health conditions. We have come to expect a longer life expectancy and for medical interventions to enable us to live longer despite disease.
• Our ability to provide supportive care, such as ventilators and other forms of life support, antibiotics for bacterial infections, kidney dialysis and many other expectations of modern-day medical care in a high-income country is different. It is difficult to compare mortality to 1918 because many of those people might have survived with modern medical care, rather than succumb to illness. It is well described that many in 1918 likely died of bacterial pneumonia that complicated their influenza, rather than from the virus itself.
• Our ability to intervene with a vaccine is a potential reality in 2020 that did not exist in 1918, changing the ethical framework of how to respond and prevent — as opposed to living with — the virus. The “best we can do” is better now that it was then.
DR. FENTON: What we think happened during and after the pandemic a hundred years ago was that without vaccination to protect them and prevent the spread, the influenza virus strain that caused the 1918-1920 pandemic continued to circulate for two years and the people who became severely ill once infected died. The people who survived infection produced antibodies that gave them protection when they encountered the virus again after that.
Influenza viruses mutate over time, so similar influenza viruses continue to circulate and, depending on how much mutation occurred, they are able to cause sickness in enough members of the population to continue to spread. The only way to stop the pandemic before it kills all the people that it would if allowed to circulate naturally is with vaccination. Vaccines give the body the information to make protective antibodies without having to risk infection from the live virus.
Q: Dr. Bonnie Henry has said a vaccination rate of 60 to 70 per cent is needed to achieve herd immunity. How does herd immunity work and how do doctors and scientists arrive at a required percentage of the population?
DR. RAATH: If we think of a sick person spreading a virus, we can imagine there are a circle of people around him/her that could possibly get infected. Not everyone gets infected. Some people are just lucky, some may be immune, some people fight off the virus without many symptoms and may or may not spread it, some people get ill and some get very ill.
Each of these people in turn are in contact with more people and the pattern continues in a rapid pattern, travelling outwards through the individuals that get infected, but hitting dead ends at the individuals that don’t. What we ideally want is to create more dead ends and less contacts. We do this by decreasing the contact circles, using barriers like masks and distance and then, eventually, by immunity.
With COVID, we have a virus with extremely low community immunity rates (at last report, we were still only around one per cent in B.C.). It’s a new virus. So, trying to get to immunity for the population is a hard and long road. Herd immunity is the term that we use to describe when enough people in that circle of contact are immune that the virus just can’t find a way to spread beyond it. You might still see outbreaks occur in subsets of the population that have lower rates of immunization than the average.
There are two main ways that immunity occurs: through natural infection or through vaccination. Many people hope we can reach natural herd immunity by just letting the virus run its course, but there are significant barriers to this:
1. People will die or develop adverse changes to their health status during natural infections. This infection is more lethal than the flu and not everyone gets the flu every year because of pre-existing immunity and immunization.
2. We can’t predict who will get the sickest, although we can use probabilities, based on age, for example. When there is a high burden of the disease in the population, it ultimately gets into those portions of the population who are at increased risk of dying (i.e. shielding “only the vulnerable” is very difficult when there is a lot of the virus around).
3. We don’t know how long natural immunity lasts. We expect immunity to fade within months to years from our experience with other coronaviruses and we have seen some reinfections already.
4. Our medical system cannot handle the large influx of patients that would result in allowing COVID to spread completely unchecked. It’s not only the numbers, it’s the length of stay. With severe COVID, patients are needing extended time in hospital.
In terms of estimating what percentage of immunity we need to get to herd immunity, it’s unfortunately largely an educated estimate and a modeling challenge. That percentage is something we really only know after the fact, when we look back at data. It’s based on the reproductive number (the average number of people a sick person goes on to infect) and how effective the vaccine is.
For example, measles, a highly contagious virus, requires more than 90 per cent vaccination coverage for herd immunity. Most experts are saying we need around 70 per cent for COVID. But through targeted vaccination of high-risk individuals and their contacts, we might see a significant reduction in hospitalizations and deaths well before reaching herd immunity, since those events are concentrated in older individuals.
If you want a deeper dive on herd immunity and the math of it, click here.
DR. FENTON: It’s great that the public is interested in these public health terms as we navigate the pandemic together.
Herd immunity is when enough of the population is immune to a communicable disease that it is no longer passing through. This works because if one person is infected, they do not encounter enough people who are susceptible to infect anyone and it stops transmitting. The calculation for herd immunity for a vaccine is based on a few numbers: the vaccine effectiveness, the number of people vaccinated and the likelihood for transmission.
That last point, likelihood of transmission, can change easily in the population depending on many things. Right now, we are keeping it as low as possible with prevention measures such as staying home when sick, wearing a mask, washing our hands and keeping our number of contacts as low as possible. If we continue these practices, we won’t need as much vaccine to stop the virus as we would if we weren’t doing these things. What I am hoping is that we continue these prevention measures as we roll out the vaccine, so hopefully we can stop this virus even before we can get everyone vaccinated. We we can save lives this way.