"Why do we get sick?"
The question has plagued medical and public health officials for decades. The answer may seem trivial: an infectious disease enters the body and causes illness. But, as anyone who spends time among others knows, some people tend to be more susceptible than others.
Understanding this paradox has been a long standing goal for researchers although the numerous attempts have ended up in failure. The reason stems from the inability to directly focus on each individual leaving only a population-based alternative. While such models have been in use for centuries, their accuracy has been somewhat poor. But in the last two decades, researchers have developed a more reliable option that provides a better perspective on our relationship with pathogens.
The technique is known as quantitative risk assessment, or QRA. It was first developed in the 1970s to identify risks associated with nuclear power. But since then, it has been used in a vast array of fields.
In health, QRA is unlike traditional research in the lab and the clinical setting, all activities occur in the computer room. The process involves the development of mathematical models using real life situations of infectious disease outbreaks. The goal is to identify how a potential pathogen not only becomes introduced into the body but then manages to cause infection.
Normally, QRA studies are population-based and focus on groups rather than individuals. They have been performed effectively in the context of foodborne and travel health. Yet, the power of this analysis could help to understand the interaction between an individual and a pathogen. Unfortunately, those studies were few and far between. But, this past week, a team of researchers from the Netherlands provided what could be considered the first real examination of how our personal activities lead us to either fall prey to or resist infections.
As expected, the model was complex, taking into account several well-known factors, including immunity, the nature of the germs in question, and the environment in which someone lives. Eventually, a general equation was generated allowing the team to test it against specific real-life scenarios. To increase the relevance of the exercise, the authors chose the most common gastrointestinal bacterial pathogen, Campylobacter jejuni, and examined how infection might proceed in one of four different exposure scenarios common to the Dutch public:
After the data was plugged into the computer, they attempted to determine what risk, if any, a person had at becoming infected. What they found was truly remarkable.
The first run revealed contact with C. jejuni differed greatly among the test conditions. Swimmers were exposed to less than one bacterium per year; liver eaters would expect to find 300 bacteria; those having contact with farm or zoo animals had the most exposure between 830 and 1,200 per year. Not surprisingly, the greatest chance for infection happened with animal contact. For any disease hunter, this is fairly standard stuff.
But the real power of the model was revealed when the effects of immunity developed as a result of repeated low level exposure were incorporated into the model. This phenomenon is known as acquired immunity is the fundamental basis for vaccination; exposing a person to a pathogen without risk of infection trains the body to fight off natural attacks. The belief was lower levels of constant exposure would help prevent infections by training the immune system while higher levels seen rarely would lead to increased risks of infection.
Sure enough, the hypothesis was correct. The winners were the swimmers as they had continual low level exposure to the bacteria allowing for acquired immunity to develop. The biggest losers, however, were not those exposed to animals. Instead, the worst off were people who ate liver. The reason was due to three factors. First, they were rarely exposed to the pathogen and therefore would not develop immunity. Second, the dose would be high enough to cause infection. The third and most important factor was the route of entry: ingestion. As C. jejuni causes a foodborne illness, the exposure would allow for the full brunt of disease.
As for those in contact with animals at farms and zoos, the risk did not outweigh the benefit. Granted, they might have developed mild illness at the start but unlike the liver eaters, they would not have ingested the pathogen and not be subjected to the full course of disease. Over time, they would become resistant due to continued non-gastrointestinal exposure.
The most interesting aspect of the study came down to the realization of a natural vaccination process. While no vaccine currently exists for C. jejuni, those who came into constant, low level contact appeared to have acquired the immunity necessary to prevent infections in the future. In a similar vein, continual exposure at higher levels, such as those with direct animal contact or visited petting zoos, also developed a higher immune function. The difference was the incidence of illness upon initial exposure. The only problematic scenario appeared to be those who infrequently come into contact with the bacteria but do so in large numbers. This led only to disease.
The article reveals one of the most important aspects of our current understanding of why we get sick more today than we might have in the past. Our efforts to stay clean have hampered us, leaving us with no opportunity for continual exposure to those lower levels of bacteria. As a result, when we do come into contact with them -- such as eating contaminated food -- we tend to have an increased chance of becoming ill.
Granted, this study won't lead to the introduction of low levels of pathogens into our environment to promote natural vaccination. But it should help you realize the best way to stay healthy is to go outside into the wilds of nature and become acquainted with smaller doses of the germs out there. With the summer upon us, there is no better time than now to venture out and help gain some acquired immunity and hopefully some memories along the way.
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