What makes a Super-Spreader?

Parameters that should be theoretically equal often aren’t so in the real world. Ideally everyone should have the same potential to transmit an infection during a given outbreak, but it has long been observed that this isn’t true. Super-spreaders play an extraordinary role in driving outbreaks of infectious disease. A super-spreader is a person who transmits an infection to a significantly greater number of other people than the average infected person. The occurrence of a super spreader early in an outbreak can be the difference between a local outbreak that fizzles out and a regional epidemic.

Super-spreaders have been known since infamous Typhoid Mary spread typhoid fever to 51 people over seven years with just an asymptomatic infection [1]. For much of the time since then, they have been treated as oddities, puzzles that could be cracked as if there was necessarily something intrinsically wrong with them. It turns out that its a lot more complicated than personal immunity or genetics. Eventually new models arose like the “20/80″ rule that says that 20% of cases are responsible for 80% of the transmission and formed a core ‘high risk’ group [2,3]. This model works well for some diseases but not all.

For pathogens that do rely on super-spreaders, the majority of cases will not transmit the infection to anyone [3]. This can lead to a sense of false security because it seems poorly communicated. As Galvani and May assert, “heterogeneously infectious emerging disease will be less likely to generate an epidemic, but if sustained, the resulting epidemic is more likely to be explosive”[3].  Super-spreaders tend to beget more super-spreaders, although most of the cases they generate will still not transmit the infection to anyone. For example, a super-spreader begets 30 cases, 3 (10%) of which become new super spreaders.  The rest may transmit to 0-1 people.  Even with super-spreaders it superficially doesn’t look very efficient but it can create an explosive epidemic.

Super-spreading has been documented for HIV, SARS (Sudden Acute Respiratory Syndrome), measles, malaria, smallpox and monkeypox, pneumonic plague, tuberculosis, Staphylococcus aureus, typhoid fever, and a variety bacterial sexually transmitted diseases [1,2,3]. For the sexually transmitted diseases (STDs) we tend to talk more about risk groups than super-spreaders but this still what they are. Case studies are easily found for most of the diseases listed above, including measles super-spreaders who infect known vaccinated children [1].

So what makes a super-spreader? Richard Stein recently summarized what we know so far. Some pathogens have virulence factors that have been associated with super-spreading. I am not aware of many pathogen genes or genotypes associated with super-spreading. So far predominantly extra-pathogen factors have been associated with super-spreading.

Co-infection is turning out to be the most interesting factor in producing super-spreaders. Consider Typhoid Mary, her normal flora may have kept her both asymptomatic and promoted her super-spreader activity. Its been known for some time that co-infection with another sexually transmitted disease increases transmission of HIV. There are less obvious co-infections. It has been shown that a rhinovirus, a common cold virus, infection dramatically increases the airborne spread of Staphylococcus aureus, producing ‘cloud-adults’ or ‘cloud-babies’ [1].

Immunological factors are often suspected in super-spreaders. People with a decreased immunity for any reason may carry a higher pathogen load that can increase environmental pathogen shedding. It has also been suspected that conditions that cause sneezing like seasonal allergies could spread pathogens colonizing the respiratory system[1].

Host behavior is a known factor in some super-spreading events. Transmission of STDs depends on contact rates and so contact frequency and length matters, [1]. People who ignore instructions like wearing a condom or not working in food service can become super-spreaders.  Education aimed at high risk groups (potential super-spreaders) seeks to alleviate this risk. There are also a number of laws that have been on the books many years that make it illegal to intentionally spread disease and force compliance with some public health mandates. These laws and mandates work pretty well considering people with life threatening infections are not too concerned with trouble in the seemingly distant future, or who like Typhoid Mary simply don’t believe they are a threat.

Last but not least, the environment can be a key factor in super-spreading events. Crowding, poor ventilation, improper isolation procedures, unnecessary movement of the infectious, and misdiagnosis have all been identified as factors during the SARS pandemic [1]. For fairly unusual diseases like plague, misdiagnosis is likely to happen frequently in the early phase of an outbreak. Crowding and ventilation are probably significant reasons why ships have been so frequently associated with explosive historic epidemics.  A super-spreading event has already happened before the ship pulls into the dock releasing a new set of super-spreaders in the port. The same could be said for clustering together in buildings during cold weather.

To make things even more complicated, super-spreading goes down the animal chain for zoonotic diseases.  Mosquitoes infected with West Nile Virus preferentially feed on the American Robin, 17 times more likely than by chance in one study [1]. The super-spreading phenomenon could extend to transmission of the pathogen by vectors and among reservoir hosts. Cattle have been documented as being super-spreaders of brucellosis and E. coli O157. In one UK study, 9% of cattle accounted for 96% all bacteria detected in fecal specimens and were high shedders of E. coli O157 [1].

The super-spreading phenomenon is not new but it is only now that our epidemiological models are beginning to seriously wrestle with its implications. These events introduce more uncertainty into our predictions and analyses than we are often comfortable with. We crave certainty in an uncertain world. As difficult as super-spreaders will make the lives of public health professionals preparing for future threats and coping with ongoing outbreaks, they may be the key to understanding many historical mysteries.


[1] Stein RA (2011). Super-spreaders in infectious diseases. International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases, 15 (8) PMID: 21737332

[2] Lloyd-Smith JO, Schreiber SJ, Kopp PE, & Getz WM (2005). Superspreading and the effect of individual variation on disease emergence. Nature, 438 (7066), 355-9 PMID: 16292310

[3] Galvani AP, & May RM (2005). Epidemiology: dimensions of superspreading. Nature, 438 (7066), 293-5 PMID: 16292292


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5 thoughts on “What makes a Super-Spreader?

  1. Very interesting! One thing which has always confused me about viruses: So many of the negative reactions (fever, vomiting, sneezing ect) are our body trying to fight AGAINST the virus, so what does the virus actually do? besides try turning our cells into more viruses.

    1. Viruses exist to make more viruses. They take over our cells, consume the cellular contents to make new viruses and kill the cell. People can die of viral infections.

      1. People do die of viral infections. People with weak immunology can die of the vaccination to them. But others seem to be able to acquire the infection and are still able to live their life, circulate in the population, and spread virulent disease without displaying any symptoms (that they would notice) at all. Typhoid Mary lived in the era when things like public sanitation and personal hygiene were just being proved to be important. She was identified and eventually isolated.
        Take a virus, any virus. I’ll use herpes simplex II. It seems that anyone exposed catches it, almost all present obvious symptoms, and there isn,t any debate about what it is. Patients with antibody titers greater than zero but less than five see the doctor with great ga-ga symptoms. Others, who are greater than fifty, don’t have a clue. There’s virus in there somewhere, but what,s it doing? And why is it transmissible? I think most other viruses can exploit this same phenomenon. From your pox viruses to the common cold. Subclinical measles. But Y Pestis? I dunno.

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