The unprecedented increase of emerging infectious diseases in wild and domestic animals and humans does not follow predictable patterns. Disease outbreaks like influenza H5N2 in birds — especially recent incursions of the virus affecting turkeys in Central Canada and Midwestern U.S.; human Ebola in West Africa; equine herpes virus (EHV1) in North America, and five outbreaks of foot-and-mouth disease (FMD) in Korea between 2000 and 2011 leave little doubt that we do not understand how disease agents are transmitted within and between species. Often overlooked is the fact that not every individual within a given population contributes equally to disease transmission.
In 1896, Italian economist Vilfredo Pareto, described the 80-20 rule based on a simple observation: 20 per cent of pea pods in his garden contained 80 per cent of the peas. From this and other observations, science was handed the Pareto principle that states for many events, roughly 80 per cent of the effects come from 20 per cent of the causes.
Pareto’s principle has application to many viral and bacterial diseases affecting animals. The lack of uniformity in disease transmission within a population depends on how individual hosts respond to disease pathogens.
It is not uniform, due mainly to super-spreaders within every subset of a population. This is the 20 per cent of those infected that contribute to 80 per cent of the transmission. While super-spreading can be linked to the degree of contact between individuals and differences in pathogen load, other factors are at play.
Predicting the spread of a disease and changes in the number of infected individuals within a population is typically performed using epidemiological models that track numbers of susceptible, infected, and recovered individuals. One fault in many models is the assumption that populations of both animals and people are homogeneous, and that the “infected” are equally capable of spreading disease. We now know that is not the case. Individuals vary in their ability to maintain and shed infectious organisms. Some maintain average or low pathogen loads, while others support high pathogen loads and become super- shedders.
Super-shedding characterizes a wide range of bacterial and viral infections, and represents a major consideration in design of prevention and control strategies for animal diseases — both new and old, especially those that brood economic ruin for national industries. Adding to the implications for super-shedders in animals is the fact that nearly 60 per cent of animal diseases potentially involve humans.
Not everyone agrees on the definition and importance of super-spreaders (those who have more points of contact with others) and super-shedders (individuals who emit greater quantities of viruses or bacteria). Scientists also debate how frequently super-spreaders are likely to appear as asymptomatic carriers (infected but not showing clinical signs) in a population.
Super-spreaders typically amount to roughly 20 per cent of a given population, yet account for transmission of about 80 per cent of many infectious diseases. The phenomenon has been observed, among other contagions like the global SARS outbreak in 2002 and 2003 and as far back as Typhoid Mary, a cook in New York who infected dozens of people with typhoid fever in the early 1900s without falling ill herself.
Dr. Tony Goldberg, professor of epidemiology at the University of Wisconsin-Madison’s School of Veterinary Medicine provides two classic examples in support of the super-shedding phenomenon.
“Super-spreaders can be a big problem among farm animals. The virus causing bovine viral diarrhea can infect dairy cows early in life, causing them to shed large amounts of the virus without showing symptoms themselves. They become immunologically tolerant so don’t become sick, yet other infected cows produce less milk or suffer reproductive problems.”
In another example, Goldberg’s research has shown that American robins, as a species, seem to be super-spreaders for West Nile virus, a mosquito-borne disease. Robins are “able to maintain the viral infection without getting sick.”
Super-spreaders are known to exist for a number of diseases carried by animals that get spread to humans (zoonosis): E. coli, giardia, cryptosporidia, and campylobacter are examples. They also exist for animal diseases like BVD and persistently infected animals, Johne’s disease; and bovine leucosis. Swine are super-shedders of FMD virus.
Super-shedding is recognized as a significant contributor to the amount of E. coli O157:H7 that makes its way from pasture or feedlot pen and into packing houses. In the view of U.S. Agricultural Research Service microbiologist Terry Arthur, “Adding to our knowledge of super-shedding would help keep beef safe.” Although super-shedding of E. coli O157:H7 by cattle is relatively uncommon — about two per cent of the cattle population — super-shedding events contribute significantly to human risk.
Scientists are working to find the reasons why some animals spread disease more than others. Recent experiments suggest the immune system plays a role — not just in protecting against infection but also in the transmission of pathogens. Future research needs to examine: the relationship between super-shedding and super-spreading events; how contact rates and shedding events affect disease prevalence and its predictability; factors associated with development of pathogen load, and early detection of super-shedders; genetic or physiologic biomarkers that could be used for early detection of highly infectious individuals; the impact of environmental factors on shedding and whether super-shedding is a gene-controlled trait.
Detection of highly infectious individuals for many diseases is currently not possible because mechanisms behind super-shedding are largely unknown. Coupling the determinants of super-shedding and disease transmission is a missing component of effective control for many diseases. The contribution of super-shedders to epidemics can be disproportionate. The nub of success often sits with identifying the 20 per cent piece early.