Previous work: I accept credit for pioneering many important ideas and concepts in the study of microbial dysbiosis; I published these ideas in the first edition of my Integrative Rheumatology in 2006 and also in several articles around that same time, including “Nutritional and Botanical Treatments against ‘Silent Infections’ and Gastrointestinal Dysbiosis, Commonly Overlooked Causes of Neuromusculoskeletal Inflammation and Chronic Health Problems”, Nutritional Perspectives 2006 which is available at https://www.academia.edu/3862817/ and http://inflammationmastery.com/reprints/vasquez_part6_2006_dysbiosis.pdf.
In 2015, I updated my information on dysbiosis and published the work as a small monograph titled Human Microbiome and Dysbiosis in Clinical Disease, and in 2016 the work was contextualized in Inflammation Mastery, 4th Edition and replicated in Volume 1 of Textbook of Clinical Nutrition and Functional Medicine. In 2015-2016, I created a video series detailing the pathophysiology, assessment, and treatment of various types and locations of dysbiosis—more accurately: multifocal polydysbiosis—and an introduction to that series is available here: https://vimeo.com/ondemand/ichnfmmicrobiome1/135280606
Reasonable and practical definitions of key terminology:
Colonization: Basically, all of us humans are covered with bacteria on our skin and also within our oral cavity (mouth), sinuses and respiratory tract, intestinal tract, and throughout the genitourinary tract as well. Generally, these bacteria cause no harm and often they provide benefit by low-grade stimulation of the immune system which can be said to mature and prepare the immune system for proper performance. Also, because colonizing bacteria are benign, they defend us from invasive and pathogenic bacteria by producing defensive/antimicrobial substances and otherwise blocking the presence of potentially pathogenic bacteria.
Infection: We all know about the classic bacterial infections such as pneumonia (infection in the lung’s air spaces), sepsis (life-threatening systemic blood-borne infection) and other types and locations of infections such as wound infectionsin the skin. True infections are typically caused by pathogenic “aggressive” bacteria taking advantage of some type of weakness or breach in immune and physical defenses, such as due to immune impairment (eg, advanced age, alcoholism, diabetes, HIV/AIDS), nutritional deficiencies (eg, deficiencies of zinc, or vitamins A or D), or break in the skin barrier due to an open wound or placement of a needle (eg, such as in a hospital setting or with intravenous drug use) or feeding tube. True infections tend to cause redness and swelling of the affected area (due to increased local blood flow), fever, pain due to the elaboration of inflammatory mediators that increase nerve sensitivity, and the characteristic pus—the white/yellow/green gel-like substance that is a collection of dead immune cells, dead bacteria, and various proteins and enzymes.
Dysbiosis (bacterial): Intermediate between benign colonization and invasive infection is the category of dysbiosis. With dysbiosis, tissue damage is mild or nonexistent, and patients generally have no manifestations of redness, swelling, or fever. Dysbiosis is generally best thought of as non-infectious colonization with pathogenic bacteria, or—in the absence of pathogenic bacteria—many times what we find is an overgrowth of normal/benign bacteria (eg, small intestine bacterial overgrowth, SIBO) or an excessive inflammatory/immune response directed against the benign bacteria. Starting at minute #12 of the introductory video linked above, you can see that my definition of dysbiosis is that it is a “relationship of nonacute noninfectious host-microorganism interaction that adversely affects the host.” Generally, when we talk about dysbiosis, we are implying “bacterial dysbiosis.” I have extended this concept to apply to viruses as well.
Dysbiosis (viral): Just as we all have many millions of bacteria in us and on us, we also have many viruses living within us. Some viruses come and go; they make us sick for a while (eg, common cold viruses or influenza virus) or they cause a local infection which is (generally) cleared by the immune system (eg, human papilloma virus). However, some viruses cause acute infection which soon subsides, but the virus never truly leaves the body; it remains in a dormant or “sleeping” or “hibernating” state via active suppression by the immune system. For example, this is true for all of the viruses in the herpes family, including herpes simplex 1 and 2 (HSV1/HSV2), cytomegalovirus (CMV), and Epstein-Barr virus (EBV). With stress, immunosuppression due to age or drugs, or an excess of inflammation from another cause or a different infection, these dormant viruses can be re-awoken or “re-activated.” In between dormancy and infection is an intermediate state of existence, wherein the virus is not causing a tissue-damaging infection and is likewise not eliciting a suppressive or effective immune reponse; in this condition of “semi-activation”, “silent infection”, possibly "viral persistence" or what I call “viral dysbiosis”, the virus is provoking adverse metabolic and inflammatory effects, but doing so in a way that is clinically invisible until and unless we perform investigative laboratory tests and/or appreciate the long-term clinical consequences. Examples compatible with viral semiactivation or viral dysbiosis include the promotion of Alzheimer’s dementia by herpes simplex virus type-1 and also by human colonization/infection with the algal virus. Many autoimmune and rheumatic diseases—especially SLE/lupus, Sjogren’s syndrome, and scleroderma—have viral contributions, such as from CMV, EBV, and parvovirus B19. As such, we as patients and clinicians need to consider—and often search for and treat—the viral components of many long-term diseases, not simply the overt and obvious acute and classic infections.
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