A doctor would not listen to a patient and cited Koch’s postulates as the reason the patient was mistaken. Actually, the patient, not the doctor, was more informed. Koch’s Postulates are problematic.
Nature gives us many counter-examples to Koch’s method of linking a single microbe to a disease or condition. Our bodies are far from sterile; they are riddled with parasitic microbes. There are many problems with Koch’s 19th century simple rules. Persistent microbes are pathogenic in varying ways. The bacteria are polymorphic---changing their forms. The invaders live part of their lives inside our cells. The target cell-types include blood cells, immune cells and epithelial cells everywhere in the body. The invaded target cells make disrupting bioactive molecules and stop making others. Energy balance is disrupted, along with mitochondria chemistry. Long term infections have gradual subclinical pathologies lasting for years. Because many persistent microbes are ubiquitous, infecting close to 100% of the herd, their slow working pathologies are mistaken for aging.
To understand chronic disease we need to understand each of the many immune-stimulation/suppression cofactors, not just one. We find in our microbiome, multiple-microbe-complexes (biofilm & plaque colonies) associated with: COPD, Rheumatoid Arthritis, IBS, Interstitial cystitis, CFIDS, Fibromyalgia, Heart/Artery Disease, Brain Plaques, Ear aches, GERD, Cancer, etc.
Polymorphic microbe complexes require multiple antibiotic types plus other modes of medical attack. Koch’s postulates represent a compelling intellectual simplicity: one bug = one disease = one medicine. This kind of thinking is inadequate to characterize the complex natural world.
To prove causality of a disease by a microbe, Koch's postulates require:
· Postulate #1 Counter example: Asymptomatic carriers of cholera, typhoid fever, etc. Sub-clinical infection carriers are common: polio, herpes simplex, HIV and hepatitis C. Many examples.
· Postulate #2 Discussion: Fastidious, intracellular microbes that live only in living host cells may be impossible or slow to culture; prions.
· Postulate #3 Discussion: "should", not "must", because some hosts exposed to an infectious agent will not acquire the infection. Non-infection causes: Genetic, diet, ascorbate intake level, better immune functioning, prior infection history not pre-disposing: prior vaccination or exposure.
· Postulate #4 Discussion: Some microbes are pleomorphic and mutate, some pleomorphic forms are not pathogenic; Some forms require restart from seed or cyst form. It is hard to differentiate different strains, except by genome sequencing or special pathologic results. Gut environment is hyper polymicrobial with good and bad genetic recipes and recipe interchange via plasmids. Gut ecology is diet dependent. Atkins ketosis (fats, proteins, no carbs) induces a different gut ecology. High levels of vitamin C inhibit microbial proliferation in vivo.
8. ^ Jacomo V, Kelly P, Raoult D (2002). "Natural history of Bartonella infections (an exception to Koch's postulate)". Clin Diagn Lab Immunol 9 (1): 8–18. doi:10.1128/CDLI.9.1.8-18.2002. PMC 119901. PMID 11777823.
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