Koch’s & Evan’s Postulates ( of cause of disease) Presented by: Noreen Majeed 2017-ag-5368 Institute of IOM,UAF
Robert Koch German physician and one of the founders of bacteriology. Discovered the anthrax disease cycle (1876) and the bacteria responsible for tuberculosis (1882) and cholera (1883). For his discoveries in regard to tuberculosis, he received the Nobel Prize for Physiology or Medicine in 1905. 1843-1910
Koch’s Postulates: A set of 4 criteria to be met before the relationship between a particular infectious agent and a particular disease is accepted as causal. These postulates enabled the germ theory of disease to achieve dominance in medicine over other theories.
HENLE-KOCH’S POSTULATES Koch determined guidelines to prove that a disease is caused by a specific organism. These four basic criteria , called Koch’s postulates, are: A specific microorganism is always associated with a given disease.
The microorganism can be isolated from the diseased animal and grown in pure culture in the laboratory. The cultured microbe will cause disease when transferred to a healthy animal. The same type of microorganism can be isolated from the newly infected animal.
KOCH’S hypothesis Koch’s proposed that anthrax bacillus, gram positive, was causative agent of anthrax disease. He proved his hypothesis correct by infecting mice with the bacillus strains taken from the spleens of the animals who died from the disease. He grew the bacilli in pure cultures over several generations, and find out the they could still cause anthrax in later generations. Koch’s Invented the method of cultivating bacteria on nutrient medium, using potatoes as his source of nutrients for bacteria
Hill-Evan’s Postulates A set of 9 or 10 criteria (depending on interpretation of original papers) that each contribute a different amount of strength to the likelihood that a relationship between a potential risk factor and a disease is causal. The entire set constitutes very strong evidence of causality when fulfilled.
Hill-Evans Postulates Prevalence of the disease should be significantly higher in those exposed to the risk factor than those not. Exposure to the risk factor should be more frequent among those with the disease than those without. In prospective studies, the incidence of the disease should be higher in those exposed to the risk factor than those not.
The disease should follow exposure to the risk factor with a normal or log-normal distribution of incubation periods. A spectrum of host responses along a logical biological gradient from mild to severe should follow exposure to the risk factor. A measurable host response should follow exposure to the risk factor in those lacking this response before exposure or should increase in those with this response before exposure. This response should be infrequent in those not exposed to the risk factor.
In experiments, the disease should occur more frequently in those exposed to the risk factor than in controls not exposed. Reduction or elimination of the risk factor should reduce the risk of the disease. Modifying or preventing the host response should decrease or eliminate the disease. All findings should make biological and epidemiological sense.