When one infects many
We need to beware the unsuspecting superspreader, who has the ability to infect many more people than the average Covid-19-positive person.
DURING the Covid-19 pandemic, several medical terms have been used in the public domain, especially on social media.
Some of these terms in the pandemic lexicon have given rise to misperceptions.
One such term is superspreader.
Highly infectious people
A typical person with Covid-19 will usually infect about two to three other people.
However, a superspreader is a someone who infects more than this number.
Most superspreaders, who are highly infectious, are unaware of their infection and spread the virus unknowingly.
Superspreaders were reported during the SARS (Severe Acute Respiratory Syndrome) outbreak in 2003 in China, Hong Kong and Singapore.
An example of a superspreader during that outbreak was a hospitalised patient in Beijing, China, who became the source of four generations of spread to 76 patients, visitors and healthcare staff in that hospital.
During the MERS (Middle Eastern Respiratory Syndrome) outbreak in South Korea in 2015, about nine out of 10 cases did not spread the infection at all.
But five patients alone spread it to 154 others, with the index patient spreading it to 28 others, and three of these secondary cases infecting 84, 23 and seven others respectively.
During the Ebola outbreak in West Africa in 2014-2015, 3% of patients were estimated to be responsible for 61% of the infections.
Ground zero events
The term “superspreading event” is used for a gathering in which one or more individuals infect an unusually large number of secondary cases.
It was initially used in a 2005 paper published in the Nature journal.
With the SARS-COV-2 virus that causes Covid-19, 60-75% of cases infect no one, but 10-20% cause 80% of secondary infections, propelled by superspreading events.
These events can be societal or isolated.
A study from Hong Kong that used contact-tracing data from 1,038 Covid-19 patients found that 19% of cases had caused 80% of infections.
The researchers identified between four and seven superspreading events that resulted in 51 clusters.
These events took place at family gatherings, bars, live music settings, weddings and other social events, as well as at a temple.
The researchers did not find that reducing the time between symptom onset and confirming a positive diagnosis, reduced the rate of transmission.
Other super-spreading events causing Covid-19 include:
> A religious gathering in February 2020 in Daegu, South Korea, where one individual led to more than 5,000 people becoming infected.
> A pharmaceutical company’s executives conference in February 2020, in Boston, United States, which initially saw 97 people infected.
The viral strains at the meeting then spread to other US states, Australia, Sweden and Slovakia, infecting about 245,000 Americans, and potentially 300,000 by the end of October 2020. One worker in a fish-processing factory in Ghana reportedly infected 533 fellow workers in May 2020.
Those who are superspreaders
Superspreaders have certain features.
Firstly, superspreaders infect large numbers of people.
The spread of infectious diseases is characterised by the basic reproductive number (Ro or R-naught) and the dispersion parameter (K).
Ro describes how many individuals in a susceptible population will be infected by someone with that infection, and K details the variation in individual infectiousness.
The smaller the K value, the greater the variation.
This means that fewer cases cause most of the infections, and a greater proportion of infections tend to be linked to large clusters via superspreading events.
Where there is great variability in the number of people who are infected, the K number gets closer to zero. Covid-19 is thought to have a K number of 0.19.
It is currently not possible to identify the superspreader in advance.
This is because people are most infectious before symptoms develop and 44% of new cases are due to asymptomatic spread.
However, superspreaders are known to spread the virus in crowded and/or closed places where there is poor ventilation and where people are breathing heavily, singing or shouting.
Secondly, SARS-COV-2 viral variants of concern may increase the risk of spread.
The variants of concern, i.e. Alpha, Beta, Gamma and Delta, spread faster.
The Delta variant in particular is becoming dominant in most countries – probably due to its ability to spread much faster than the other variants and its high viral load, which is 1,200 times that of the original virus reported at the pandemic’s beginning.
If the new variants, including Delta, are spread by superspreaders, pandemic control will be problematic.
Fortunately, the current Covid19 vaccines are effective against the Delta variant, albeit with lesser effectiveness.
Thirdly, superspreaders may have a higher viral load.
The viral load is the number of viral particles in one millilitre of blood.
A high viral load indicates large numbers of viruses are replicating, thus, increasing viral shedding and infectivity.
The viral load is more likely to be high if the recipient is infected by another superspreader who has a high viral load.
High viral loads are usually associated with severe infections.
Concomitantly, it often leads to a stronger immune response compared to someone infected with lower viral loads.
Those with high viral loads are more likely to be hospitalised.
Although this stops them from spreading the virus in the community, there is higher risk of infecting other patients and hospital staff.
Fourthly, the environment impacts on viral spread.
A study in São Paolo, Brazil, on the environmental and social factors associated with Covid-19 spread, reported that higher infection rates were associated with increased population density.
Lower infection rates were associated with social isolation, increasing air temperature, increasing wind speed and higher amounts of ultraviolet (UV) light.
These findings confirm the advice to stay at home and to avoid crowds, closed spaces and close contacts.
Fifthly, individual genetic factors may affect viral spread.
Genetic differences in the quality and quantity of saliva and mucous may facilitate or hinder viral spread.
For example, sneezing with a blocked nose can increase the distance of mucous spray by 60%.
Individual genetic variations may increase viral infection or spread, e.g.:
> Differences in the ACE-2 gene alter the ability of the coronavirus to attach to the receptor and invade the cell
> Human leukocyte antigens (HLA) A, B and C have been reported in more severe infections, and > The TMPRSS2 gene, associated with prostate cancer, has been linked to more severe infection. Finally, non-pharmaceutical interventions protect against superspreading.
A Swiss study estimated that a superspreader’s cough rapidly fills a room with 7.4 million viruses for every cubic metre of air.
Heavy breathing, shouting or singing increases the viral load further.
A review in The Lancet journal reported that viral spread was lower with physical distancing of one metre or more, with protection increasing with further distance.
Face mask use substantially reduced infection risk, more so when N95 or similar respirators were used, compared with disposable surgical masks.
Eye protection was also associated with less infection.
Only in hindsight
The superspreader is often unaware that (s)he is infected and spreading Covid-19 in most instances.
Anyone could be a superspreader.
Control of Covid-19 depends on not allowing ourselves to become a superspreader and protecting ourselves from the undetectable superspreaders already in the community.
Identifying a superspreader is a retrospective finding, as it requires studies of epidemiological and clinical characteristics, contact-tracing, environmental surveys, and laboratory investigations, including genome sequencing.
Public health messages have to be science-based, lest they lead to loss of public trust.
Similar to a patient-doctor relationship, it will be challenging to regain trust when it is lost.
As such, it is incumbent that all public health messages be conveyed professionally.
Dr Milton Lum is a past president of the Federation of Private Medical Practitioners Associations and the Malaysian Medical Association. For more information, email starhealth @thestar.com.my. The views expressed do not represent that of organisations that the writer is associated with. The information provided is for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care. The Star disclaims all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.