What Even is Infectious?
Ryan Argetsinger, 8/4/24
Ryan Argetsinger, 8/4/24
There was a point in world history, just after the invention of penicillin, when it was thought that infectious and viral diseases were going to be on the way out. So much so, that in 1967, the United States Surgeon General stated, “It’s time to close the book on infectious diseases. We have basically wiped out infection in the United States.”
Although this was wishful thinking, this statement was far from the truth that could even be described. Within the past half-century of this statement being made, the world had seen outbreaks of Ebola, Sars, and COVID-19, to name a few, but most importantly, the infectious disease that arguably changed the paradigm and perspective of infectious disease is peptic ulcer disease.
Dr. Robert Koch put forth initial postulates to determine the causation of infectious diseases, ranging from (1) the causative organisms can be isolated and experimentally transmitted, and (2) symptoms that occur soon after the onset of infection in a high proportion of infected individuals. Although these serve as a general rule for how we may think about infectious disease and their effect on individual and population health, the greater issue is that Koch’s postulates were useful because they could generate conclusive evidence of infectious causation, particularly when (1) the causative organisms could be isolated and experimentally transmitted, and (2) symptoms occurred soon after the onset of infection in a high proportion of infected individuals. While guiding researchers down one path, however, the postulates directed them away from alternative paths: researchers attempting to document infectious causation were guided away from diseases that had little chance of fulfilling the postulates, even though they had the potential to be caused by infectious agents. In the 1970s peptic ulcer disease was thought to be a chronic disease, influenced by lifestyle effects on the acidity of the stomach lining. Factors like smoking, excessive coffee, and stress. Most medical practitioners at the time considered this to be the main and only cause, however, when looking further into physiological biopsies of peptic ulcer patients, the bacteria Helicobacter pylori was found to be the culprit that adjusted the interior environment of the stomach to produce the chronic symptoms of peptic ulcers.
This initial finding was questioned and also rejected when initially provided to medical journals, but is now accepted after further study. This finding may not completely break the postulates Koch presented, but it forces a reevaluation of perspective. The understanding of current infectious diseases (more importantly, documented infectious diseases) provides an understanding of the potential of infectious agents and their mechanisms. But, they also provide some understanding of how researchers and physicians may approach current medical investigations. Now it’s thought that other chronic diseases may be caused due to infection, such as atherosclerosis. Evidence from the 1980s showed that the strain of bacteria Chlamydia pneumoniae was correlated to atherosclerosis as an infectious agent. Chlamydia pneumoniae has also been found to be linked as a suspect to Alzheimer’s disease, too; however, the difficulty in making these claims for causation, and transitioning the status of chronic or genetic, to infectious, is the difficulty in examining serological samples. Since most sites of infection are internal, like peptic ulcer disease, it’s difficult to claim or macroscopically find evidence to support claims of infection. But, as more research surfaces with a paradigm shift to re-evaluating what infectious diseases actually may pertain to, evidence continues to grow to show how several chronic diseases may more than likely be initiated by factors on infectious agents.
Several factors play into the further difficulty in assessing claims of infection, especially in the realm of genetics and lifestyle. Some people may have lived as smokers well into older age, only to succumb to the COVID-19 virus, rather than being extremely at risk for lung cancer. Although this is only an allegory in stating that there are factors of genetics and lifestyle that can provide improved routes to infection for diseases, it goes to show for example how factors must be considered in the investigation. For individuals that have the epsilon 4 allele of the human apolipoprotein E gene, risk factors for atherosclerosis, stroke, and Alzheimer’s disease are all raised, while also appearing to increase susceptibility to Chlamydia pneumoniae infection.
The realm of infectious disease, unlike suggested by the previous Surgeon General of the United States, speaking from a wishful point of view in the 1960s, is far from being closed. We now know that more than 15% of human cancers are attributable to infectious agents, which is also affected by genetic predispositions, and lifestyle factors. In breast tumors, infectious causation is suspected because of the presence of oncogenic retroviruses present in breast tumors for Epstein-Barr virus. Although efforts are at an all-time high in the realm of biomedical research, what if our change of thinking about infection and chronic disease were to slightly pivot? Medicine treated patients of peptic ulcer disease by means of a chronic illness, resulting in no alleviation of symptoms, while accepting that patients had to continue managing the pain of their ailments. But, honestly, who would have thought that all it would take is the right antibiotics and maybe some pepto bismol?
References
Ethics and Infectious Disease
Infectious Causation of Disease: An Evolutionary Perspective