Koch's Postulates:  We should not let their simplicity restrict our thinking:  (Oct 2011)

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. 

Nature gives us many counter-examples to Koch’s method of linking a single microbe to a disease or condition. There are many problems with Koch’s 19th century simple rules.  Many pathogenic microbes are persistent. The bacteria are polymorphic---changing their forms.  The invaders live part of their lives inside our cells. The target multiple cell-types include immune cells and epithelial cells everywhere in the body. The invaded target cells make disrupting bioactive molecules and stop making others.

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, CFIDS, Fibromyalgia, Heart/Artery Disease, Brain Plaques, ear aches, 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.

Koch’s Postulates Update

Koch's postulates are:

  1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms. [ “…should not be found…”  not   “…. MUST not be found…”]
  2. The microorganism must be isolated from a diseased organism and grown in pure culture. [If you cannot conventionally culture it, it cannot be in a causal category. Fastidious microbes that live inside our cells are problematic]
  3. The cultured [isolated] microorganism should cause disease when introduced into a healthy organism. [cultures may attenuate the strain, some target hosts may be immune]
  4. The microorganism must be re-isolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.  [Pleomorphic alternate forms do not fit this model.]
Refutation

·        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.

Natural History of Bartonella Infections (an Exception to Koch’s Postulate)

Causation and Disease: The Henle-Koch Postulates Revisited,  ALFRED S. EVANS, World Health Organization Serum Reference Bank
 
 Very good update based on modern technology:  http://cmr.asm.org/cgi/reprint/9/1/18 

http://en.wikipedia.org/wiki/Koch%27s_postulates

References

1.      ^ Koch Robert (1893). "Über den augenblicklichen Stand der bakteriologischen Choleradiagnose" (in German). Zeitschrift für Hygiene und Infectionskrankheiten 14: 319–333. doi:10.1007/BF02284324.

2.      ^ a b Koch Robert (1884). "2 Die Aetiologie der Tuberkulose". Mitt Kaiser Gesundh. pp. 1–88.

3.      ^ Inglis TJ (November 2007). "Principia aetiologica: taking causality beyond Koch's postulates". J. Med. Microbiol. 56 (Pt 11): 1419–22. doi:10.1099/jmm.0.47179-0. PMID 17965339.

4.      ^ Walker L, Levine H, Jucker M (2006). "Koch's postulates and infectious proteins.". Acta Neuropathol (Berl) 112 (1): 1–4. doi:10.1007/s00401-006-0072-x. PMID 16703338.

5.      ^ Koch R (1893). "Ueber den augenblicklichen Stand der bakteriologischen Choleradiagnose". J. Hyg. Inf. 14: 319–33. doi:10.1007/BF02284324.

6.      ^ Brock TD (1999). Robert Koch: a life in medicine and bacteriology. Washington DC: American Society of Microbiology Press. ISBN 1555811434.

7.      ^ Evans AS (May 1976). "Causation and disease: the Henle-Koch postulates revisited". Yale J Biol Med 49 (2): 175–95. PMC 2595276. PMID 782050.

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.

9.      ^ Falkow S (1988). "Molecular Koch's postulates applied to microbial pathogenicity". Rev. Infect. Dis. 10 (Suppl 2): S274–6. PMID 3055197.

10.  ^ Fredericks DN, Relman DA (1996). "Sequence-based identification of microbial pathogens: a reconsideration of Koch's postulates". Clin Microbiol Rev 9 (1): 18–33. PMC 172879. PMID 8665474.

Further reading:  http://ocp.hul.harvard.edu/contagion/koch.html

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