The first known lectures on the subject were delivered by Professor August Friedrich Hecker [de] at the University of Erfurt in 1790, and in 1791, he published the first textbook on pathophysiology, Grundriss der Physiologia pathologica,[2] spanning 770 pages.
[4] Virchow’s influence extended to his student Julius Cohnheim, who pioneered experimental pathology and the usage of intravital microscopy, further advancing the study of pathophysiology.
[4] By 1863, motivated by Louis Pasteur's report on fermentation to butyric acid, fellow Frenchman Casimir Davaine identified a microorganism as the crucial causal agent of the cattle disease anthrax, but its routinely vanishing from blood left other scientists inferring it a mere byproduct of putrefaction.
[5] In 1876, upon Ferdinand Cohn's report of a tiny spore stage of a bacterial species, the fellow German Robert Koch isolated Davaine's bacterides in pure culture —a pivotal step that would establish bacteriology as a distinct discipline— identified a spore stage, applied Jakob Henle's postulates, and confirmed Davaine's conclusion, a major feat for experimental pathology.
In London, pathologist with the Ministry of Health, Fred Griffith in 1928 reported pneumococcal transformation from virulent to avirulent and between antigenic types —nearly a switch in species— challenging pneumonia's specific causation.
[10][11] The laboratory of Rockefeller Institute's Oswald Avery, America's leading pneumococcal expert, was so troubled by the report that they refused to attempt repetition.
[12] When Avery was away on summer vacation, Martin Dawson, British-Canadian, convinced that anything from England must be correct, repeated Griffith's results, then achieved transformation in vitro, too, opening it to precise investigation.
In 1944, Avery, Colin MacLeod, and Maclyn McCarty reported the transformation factor as DNA, widely doubted amid estimations that something must act with it.
In the late 1930s, Rockefeller Foundation had spearheaded and funded the molecular biology research program —seeking fundamental explanation of organisms and life— led largely by physicist Max Delbrück at Caltech and Vanderbilt University.
[15] Mindful of Griffith and Avery, Joshua Lederberg confirmed bacterial conjugation —reported decades earlier but controversial— and was awarded the 1958 Nobel Prize in Physiology or Medicine.
[17] At Cold Spring Harbor Laboratory in Long Island, New York, Delbrück and Salvador Luria led the Phage Group —hosting Watson— discovering details of cell physiology by tracking changes to bacteria upon infection with their viruses, the process transduction.
[18] In the late 1970s, as president of Memorial Sloan–Kettering Cancer Center, Thomas collaborated with Lederberg, soon to become president of Rockefeller University, to redirect the funding focus of the US National Institutes of Health toward basic research into the mechanisms operating during disease processes, which at the time medical scientists were all but wholly ignorant of, as biologists had scarcely taken interest in disease mechanisms.
Five proposed major mechanisms for neuronal death in Parkinson's Disease include protein aggregation in Lewy bodies, disruption of autophagy, changes in cell metabolism or mitochondrial function, neuroinflammation, and blood–brain barrier (BBB) breakdown resulting in vascular leakiness.
The pathophysiology of multiple sclerosis is that of an inflammatory demyelinating disease of the CNS in which activated immune cells invade the central nervous system and cause inflammation, neurodegeneration and tissue damage.
When the CD4 lymphocyte count falls below 200 cells/ml of blood, the HIV host has progressed to AIDS,[27] a condition characterized by deficiency in cell-mediated immunity and the resulting increased susceptibility to opportunistic infections and certain forms of cancer.