Catálogo de publicaciones - libros

We humans are being attacked by minute killer germs that silently, stealthily, invade and clog our arteries, causing heart attacks, strokes, and other major arterial problems of pandemic proportions.

Let me introduce myself. I could best be described as a type of germ, or more precisely a bacterium, related to the family, which has been around for many generations.

Heart attacks, strokes, and other vascular problems are among the most common diseases in the world today. They are the result of buildup of fatty gruel deposits that clog the arteries. The name of the obstructive disease is atherosclerosis, and the actual deposits are called atheroma. It is such a common disease that it would not be amiss to state that almost every person, whether old, young, male, female, the very wealthy, or the very poor, has these lesions in their arteries, to a lesser or greater extent.

My involvement with study of atheroma lesions came about in the following manner. As a pathologist, my work entailed examination of large numbers of arterial specimens, which had been removed at surgical bypass operations and autopsies and then referred for further specialized study. Atheroma lesions were very common, being present in nearly every case, and very few arteries indeed were entirely free of the disease.

Looking through the literature, I came across some articles on electron microscopic findings of human atherosclerotic lesions. The various structures described bore some similarity to what I had noted in atheroma.

Germs in atheroma show common features to organisms, but there are some differences.

Now here was a major problem. ? There had to be some type of confirmatory evidence, and fairly convincing evidence at that, if anyone was to take the concept of atheroma containing germs seriously. Everyone accepts that the structures which make up atheroma are inert lipid droplets. They even call it a lipid-rich pool. Any suggestion of a germ would be seen as a major heretical deviation in the accepted knowledge of the disease. Introducing such a new concept is not an easy task. Not only would it be necessary to prove that the lipid of atheroma is in fact a germ, but also the exact species or strain would have to be identified. For precise identification, microbiologists rely on methods such as culture, immunocytochemistry, and genetic studies, in addition to morphology.

A discovery is meaningless if the findings are not published in a scientific or medical journal. Publishing in a journal is not an easy process. There are a limited number of medical journals, and the number of the many articles submitted for consideration for publication far exceeds the journal space available. It has been stated that less than 5% of articles submitted are published and more than 95% are rejected. There is just not enough space to accommodate all the articles that are submitted. On the other hand, there is tremendous pressure to publish. Publish or perish is a well-known fact. Unfortunately, a substantial amount of research just does not get published.

Positivity rates for finding germs in atheroma depending on the methods used for detection vary from 0% to 100% (mean, 60%), with a few studies failing to detect the organisms by polymerase chain reaction (PCR). The many reviews on the subject of detection indicate increasing acceptance of the presence of organisms in human atherosclerotic lesions, but there are suggestions for a need to improve and standardize the diagnostic techniques.

The first part of the story concerns the discovery of in atheroma. Actually, to be more precise, the discovery that many of the fat structures in atheroma are overlooked germs. We now have to examine another aspect: whether this germ is the actual cause of the atheroma lesion.