Koch's Postulates

12/20/2017 Koch's postulates - Wikipedia
Koch'spostulates
Koch's postulates (/kx/)[2] are
four criteria designed to establish a
causative relationship between a
microbe and a disease. The postulates
were formulated by Robert Koch and
Friedrich Loeffler in 1884, based on
earlier concepts described by Jakob
Henle,[3] and refined and published by
Koch in 1890. Koch applied the
postulates to describe the etiology of
cholera and tuberculosis, but they have
been controversially generalized to
other diseases. These postulates were
generated prior to understanding of Robert Hermann Koch (11
modern concepts in microbial December 1843 27 May 1910)
pathogenesis that cannot be examined was a German physician who
developed Koch's postulates.[1]
using Koch's postulates, including
viruses (which are obligate cellular
parasites) or asymptomatic carriers. They have largely been supplanted by
other criteria such as the Bradford Hill criteria for infectious disease causality
in modern public health.
Contents
The postulates
History
For the 21st century
https://en.wikipedia.org/wiki/Koch%27s_postulates 1/8
References
Further reading
Thepostulates
Koch's postulates of disease.
Koch'spostulatesarethefollowing:
1. The microorganism must be found in abundance in all organisms suffering

from the disease, but should not be found in healthy organisms.
2. The microorganism must be isolated from a diseased organism and grown
in pure culture.
3. The cultured microorganism should cause disease when introduced into a
healthy organism.
4. The microorganism must be reisolated from the inoculated, diseased
experimental host and identied as being identical to the original specic
causative agent.
However, Koch abandoned the universalist requirement of the first postulate
altogether when he discovered asymptomatic carriers of cholera[4] and, later, of
typhoid fever. Asymptomatic or subclinical infection carriers are now known to
be a common feature of many infectious diseases, especially viruses such as
polio, herpes simplex, HIV, and hepatitis C. As a specific example, all doctors
and virologists agree that poliovirus causes paralysis in just a few infected
subjects, and the success of the polio vaccine in preventing disease supports
the conviction that the poliovirus is the causative agent.
The second postulate may also be suspended for certain microorganisms or

entities that cannot (at the present time) be grown in pure culture.[5] Viruses
also require host cells to grow and reproduce and therefore cannot be grown in
pure cultures.
The third postulate specifies "should", not "must", because as Koch himself
proved in regard to both tuberculosis and cholera,[6] not all organisms exposed
to an infectious agent will acquire the infection. Noninfection may be due to
such factors as general health and proper immune functioning; acquired
immunity from previous exposure or vaccination; or genetic immunity, as with
the resistance to malaria conferred by possessing at least one sickle cell allele.
There are a few other exceptions to Koch's postulates. A single pathogen can
cause several disease conditions. Additionally, a single disease condition can
be caused by several different microorganisms. Some pathogens can not be
cultured in the lab, and some pathogens only cause disease in the human
species. [7]
In summary, an infectious agent that satisfies Koch's postulates is necessary

but not necessarily sufficient to cause a specific illness.
History
Koch's postulates were developed in the 19th century as general guidelines to
identify pathogens that could be isolated with the techniques of the day.[8]
Even in Koch's time, it was recognized that some infectious agents were clearly
responsible for disease even though they did not fulfill all of the postulates.[4][6]
Attempts to rigidly apply Koch's postulates to the diagnosis of viral diseases in
the late 19th century, at a time when viruses could not be seen or isolated in
culture, may have impeded the early development of the field of virology.[9][10]
Koch's postulates have been recognized as largely obsolete by epidemiologists

since the 1950s.[11][12] Therefore, while Koch's postulates retain historical
importance and continue to inform the approach to microbiologic diagnosis,
they are not routinely used to demonstrate causality.
Koch's postulates have also influenced scientists who examine microbial

pathogenesis from a molecular point of view. In the 1980s, a molecular version
of Koch's postulates was developed to guide the identification of microbial
genes encoding virulence factors.[13]
That HIV causes AIDS does not follow from Koch's postulates[14], which may
have supported HIV/AIDS denialism. Also Oncoviruses causing cancers does
not follow Koch's postulates.[15]
Forthe21stcentury
Kochs postulates have played an important role in microbiology, yet they have
major limitations. For example, Koch was well aware that in the case of
cholera, the causal agent, Vibrio cholerae, could be found in both sick and
healthy people, invalidating his first postulate. Furthermore, viral diseases
were not yet discovered when Koch formulated his postulates, and there are
many viruses that do not cause illness in all infected individuals, a requirement
of the first postulate. Additionally, it was known through experimentation that
H. pylori caused mild inflammation of the gastric lining when ingested. As
evident as the inflammation was, it still did not immediately convince skeptics
that H. pylori was associated with ulcers. Eventually, skeptics were silenced
when a newly developed antibiotic treatment eliminated the bacteria and
ultimately cured the disease. Contradictions and occurrences such as these
have led many to believe that a fifth postulate may be required. If enacted, this
postulate would state that sufficient microbial data should allow scientists to
treat, cure, or prevent the particular disease.
More recently, modern nucleic acid-based microbial detection methods have

made Kochs original postulates even less relevant. These nucleic acid-based
methods make it possible to identify microbes that are associated with a
disease, but in many cases the microbes are uncultivable. Also, nucleic acid-
based detection methods are very sensitive, and they can often detect the very
low levels of viruses that are found in healthy people without disease.
The use of these new methods has led to revised versions of Kochs postulates:
Fredricks and Relman[16] have suggested the following set of Kochs postulates
for the 21st century:
1. A nucleic acid sequence belonging to a putative pathogen should be

present in most cases of an infectious disease. Microbial nucleic acids
should be found preferentially in those organs or gross anatomic sites
known to be diseased, and not in those organs that lack pathology.
2. Fewer, or no, copies of pathogen-associated nucleic acid sequences
should occur in hosts or tissues without disease.
3. With resolution of disease, the copy number of pathogen-associated
nucleic acid sequences should decrease or become undetectable. With
clinical relapse, the opposite should occur.
4. When sequence detection predates disease, or sequence copy number
correlates with severity of disease or pathology, the sequence-disease
association is more likely to be a causal relationship.
5. The nature of the microorganism inferred from the available sequence
should be consistent with the known biological characteristics of that
group of organisms.
6. Tissue-sequence correlates should be sought at the cellular level: efforts
should be made to demonstrate specic in situ hybridization of microbial
sequence to areas of tissue pathology and to visible microorganisms or to
areas where microorganisms are presumed to be located.
7. These sequence-based forms of evidence for microbial causation should
be reproducible.
These modifications are still controversial in that they do not account well for
established disease associations, such as papillomavirus and cervical cancer,
nor do they take into account prion diseases, which have no nucleic acid
sequences of their own.
References
1. Koch, R. (1876). "Untersuchungen ber Bakterien: V. Die tiologie der
Milzbrand-Krankheit, begrndet auf die Entwicklungsgeschichte des
Bacillus anthracis" (http://edoc.rki.de/documents/rk/508-5-26/PDF/5-26.pd
f) [Investigations into bacteria: V. The etiology of anthrax, based on the
ontogenesis of Bacillus anthracis] (PDF). Cohns Beitrage zur Biologie der
Panzen (in German). 2 (2): 277310.
2. "Koch" (http://dictionary.reference.com/browse/koch). Random House
Webster's Unabridged Dictionary.
3. Evans AS (October 1978). "Causation and disease: a chronological
journey. The Thomas Parran Lecture" (http://aje.oxfordjournals.org/cgi/pmi
dlookup?view=long&pmid=727194). American Journal of Epidemiology.
108 (4): 24958. PMID727194 (https://www.ncbi.nlm.nih.gov/pubmed/727
194).
4. Koch, R. (1893). "Ueber den augenblicklichen Stand der bakteriologischen
Choleradiagnose" [About the instantaneous state of the bacteriological
diagnosis of cholera]. Zeitschrift fr Hygiene und Infektionskrankheiten (in
German). 14: 31938. doi:10.1007/BF02284324 (https://doi.org/10.1007%
2FBF02284324).
5. Inglis TJ (November 2007). "Principia aetiologica: taking causality beyond
Koch's postulates"
(http://jmm.sgmjournals.org/cgi/content/full/56/11/1419). Journal of
Medical Microbiology. 56 (Pt 11): 141922. doi:10.1099/jmm.0.47179-0 (ht
tps://doi.org/10.1099%2Fjmm.0.47179-0). PMID17965339 (https://www.n
cbi.nlm.nih.gov/pubmed/17965339).
6. Koch Robert (1884). "2 Die Aetiologie der Tuberkulose". Mitt Kaiser
Gesundh. pp.188.
7. Slonczewski, Joan; Foster, John (2011). Microbiology An Evolving Science
Second Edition. New York, N.Y.: W. W. Norton & Company, Inc. pp.2022.
ISBN978-0-393-93447-2.
8. Walker L, Levine H, Jucker M (2006). "Koch's postulates and infectious
proteins". Acta Neuropathol. 112 (1): 14. doi:10.1007/s00401-006-0072-x
(https://doi.org/10.1007%2Fs00401-006-0072-x). PMID16703338 (https://
www.ncbi.nlm.nih.gov/pubmed/16703338).
9. Brock TD (1999). Robert Koch: a life in medicine and bacteriology.
Washington DC: American Society of Microbiology Press. ISBN1-55581-
143-4.
10. Evans AS (May 1976). "Causation and disease: the Henle-Koch
postulates revisited" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2595
276). Yale J Biol Med. 49 (2): 17595. PMC2595276 (https://www.ncbi.nl
m.nih.gov/pmc/articles/PMC2595276) . PMID782050 (https://www.ncbi.n
lm.nih.gov/pubmed/782050).
11. Huebner, Robert J. (April 1957). "Criteria for etiologic association of

prevalent viruses with prevalent diseases; the virologist's dilemma".
Annals of the New York Academy of Sciences. 67 (8): 4308.
Bibcode:1957NYASA..67..430H (http://adsabs.harvard.edu/abs/1957NYA
SA..67..430H). doi:10.1111/j.1749-6632.1957.tb46066.x (https://doi.org/10.
1111%2Fj.1749-6632.1957.tb46066.x). PMID13411978 (https://www.ncbi.
nlm.nih.gov/pubmed/13411978).
12. Evans AS (December 1995). "Causation and disease: a chronological
journey. The Thomas Parran Lecture. 1978" (http://aje.oxfordjournals.org/c
gi/pmidlookup?view=long&pmid=7485059). American Journal of
Epidemiology. 142 (11): 112635; discussion 1125. PMID7485059 (http
s://www.ncbi.nlm.nih.gov/pubmed/7485059).
13. Falkow S (1988). "Molecular Koch's postulates applied to microbial
pathogenicity". Rev. Infect. Dis. 10 (Suppl 2): S2746.
doi:10.1093/cid/10.Supplement_2.S274 (https://doi.org/10.1093%2Fcid%2
F10.Supplement_2.S274). PMID3055197 (https://www.ncbi.nlm.nih.gov/p
ubmed/3055197).
14. Weiss, Robin A.; Jaffe, Harold W. (1990). "Duesberg, HIV and AIDS".
Nature. 345 (6277): 65960. Bibcode:1990Natur.345..659W (http://adsab
s.harvard.edu/abs/1990Natur.345..659W). doi:10.1038/345659a0 (https://
doi.org/10.1038%2F345659a0). PMID2163025 (https://www.ncbi.nlm.nih.
gov/pubmed/2163025).
15. Moore, Patrick S.; Chang, Yuan (2013). "The conundrum of causality in
tumor virology: The cases of KSHV and MCV". Seminars in Cancer
Biology. doi:10.1016/j.semcancer.2013.11.001 (https://doi.org/10.1016%2
Fj.semcancer.2013.11.001).
16. Fredericks DN, Relman DA (1996). "Sequence-based identication of
microbial pathogens: a reconsideration of Koch's postulates" (http://cmr.as
m.org/cgi/reprint/9/1/18). Clin Microbiol Rev. 9 (1): 1833. PMC172879 (h
ttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC172879) . PMID8665474
(https://www.ncbi.nlm.nih.gov/pubmed/8665474).
Furtherreading
http://ocp.hul.harvard.edu/contagion/koch.html
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