One in five 'super-spreaders' responsible for the majority of viral infections
This phenomenon occurs not only in human populations but also in animal populations, and involves both viral and bacterial infections.
A notable recent example was the Severe Acute Respiratory Syndrome (SARS) pandemic in 2003 where up to 75% of infections from Hong Kong and Singapore were linked to super-spreaders. Other infectious diseases where this phenomenon has been observed worldwide include outbreaks of tuberculosis, measles, cholera, as well as Ebola viral haemorrhagic fever.
What makes a super-spreader?
Why such individuals become super-spreaders is less clear. Reasons that have been put forward include immune system deficiencies in these individuals and possibly a greater virulence of the pathogen. Co-infection with another pathogen can also push the spread of disease, as has been observed with HIV and other sexually-transmitted infections.
Overcrowding and group settings such as nurseries, schools, prisons and barracks, are also known to facilitate the spread of diseases such as norovirus, Hepatitis A and influenza. In healthcare settings, delays in diagnosing infected persons and higher frequency of staff and patient transfers between wards and hospitals are other recognised risk factors.
Resistance versus tolerance
The answer may lie in how the super-spreading individual’s immune system handles infection. One “resistance” mechanism involves the body’s immune system fighting off infection to control, if not eliminate, the pathogen. In the ensuing battle between host and pathogen, organ and tissue damage often occurs and these individuals often show symptoms.
The other way the body deals with infection is to “tolerate” the infection and limit the damage it causes. In doing so, this allows the pathogen to survive and thrive in the affected individual with no or minimal ill effects to either the host or the pathogen.
New research suggests that this “immune tolerant” second group may explain how some individuals become super-spreaders. The researchers were able to create mice with a super-spreader condition using antibiotics that eliminated much of their gut flora – this allowed a population of antibiotic-resistant pathogenic bacteria to flourish in the gut.
However, while these artificially created super-spreader mice were able to shed considerable numbers of the pathogenic bacteria as a consequence of antibiotic therapy, they also experienced considerable ill health. By comparison, mice that were natural super-spreaders suffered no apparent ill health from the use of antibiotics that disrupted their gut flora.
Unlike the artificially created super-spreader mice, these natural super-spreaders were found to have a dampened immune response that probably explains their lack of ill health. They also found that by suppressing the immune system response of the non-super-spreader mice, this alleviated their symptoms of ill health.
A hidden threat
So what are the implications of this research for public health? Perhaps what is most worrying is that super-spreaders, by virtue of their “immune tolerance”, may show little if any signs of ill health.
Such individuals are a hidden threat who would continue to live and move freely within their communities where they could unwittingly transmit infection on to others. They present a real challenge for infectious disease control as they would be less likely to seek medical attention and even if they were to do so it would be difficult to identify them.
Antibiotics – a risk to human health?
Another issue related to this research is about the role of antibiotics. Antibiotics are often seen as the solution to the present and growing threat of infectious diseases. However, they may be the root cause of the problem of super-spreaders. Some individuals may have the innate ability to become super-spreaders, which only becomes apparent when they are infected with a pathogen. But the use of antibiotics could lead to the creation of their super-spreader state.
Antibiotic over-use, even with the best of therapeutic intent, both in human and animal populations, may therefore worsen this situation. This re-affirms the urgent need for judicious and controlled use of antibiotics.
Current infectious disease-control measures such as mass screening, contact tracing and isolation of infected individuals tends to be laborious and not always effective. This is partly due to the fact that there are limited public health options available and disease-control responses tend to be reactive. If super-spreaders can be identified early in an outbreak, this may allow for a more finessed and effective approach to disease control.
Put it this way: if the 20% of infected individuals who spread 80% of infections are identified early and managed appropriately, 80% of onward infections within the community could be avoided – a tantalising prize for public health.