Abstract

It is important to note that according to Koch's Postulate, before a clear causative relationship between a pathogen and a certain disease can be established, three conditions should be fulfilled: (1) the pathogen should be present in individuals with the disease, (2) it should cause the disease when isolated and introduced in a healthy subject, and (3) it should be possible to identify the agent in the subject that has contracted the disease. When atherosclerosis is concerned, it is clear that these postulates are not unequivocally fulfilled in atherosclerosis, and infection as a cause of atherosclerosis or cardiovascular disease (CVD) is therefore an unproven albeit interesting possibility from a more orthodox point of view. Taken together, several different infectious agents may in principle contribute to atherosclerosis and CVD, and for at least C Pneumonae, the evidence is relatively compelling though clear-cut evidence remains to be demonstrated. Likewise, evidence of oral pathogens is also interesting; however, for other infectious agents, including cytomegalovirus (CMV), the evidence of any relation to atherosclerosis or CVD is scarce, except the fact that for CMV, there may be an association with transplantation atherosclerosis. Infections may still contribute to atherosclerosis in an indirect way, involving general systemic inflammation and its relation to established risk factors like dyslipidemia and emerging ones like C-reactive protein (CRP). However, it does not seem that infections are a prerequisite of this disease process.

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