Organisms such as Plasmo-
dium falciparum and herpes simplex virus or other viruses
cannot be grown alone, i.e., in cell-free culture, and hence
cannot fulfill Koch’s postulates, yet they are unequivocally
pathogenic. Similarly, certain microbes such as human immu-
nodeficiency virus (HIV) exhibit a host range that is restricted
to humans; they cannot produce typical disease in other hosts,
thereby making impossible or unethical the final fulfillment of
the third postulate. Furthermore, how does one meet criteria
for causation when a pathogenic microbe is also capable of a
carrier state (e.g., Neisseria meningitidis), causing disease in
one individual and not in another? In contrast to the beliefs of
Koch and those of his era, we are well aware today that mi-
crobial pathogens often cause subclinical infection. For exam-
ple, the vast majority of patients exposed to M. tuberculosis will
simply develop a silent infection accompanied by microscopic
forms of pathology, marked by the presence of a positive tu-
berculin skin test, and will not go on to develop active disease.
The presence of tubercle bacilli in healthy subjects or subjects
with an unrelated disease would seem to violate Koch’s second
postulate. What of the microbe that produces distant injury by
release of a toxin or injury that occurs via immune mechanisms
well after disappearance of the causative agent? What of the
microbe that can switch on or off disease-producing genes?
What of the bacteria that require coinfection with a bacterio-
phage or acquisition of extrachromosomal DNA to be able to
cause disease (e.g., Corynebacterium diphtheriae and entero-
toxigenic Escherichia coli) or the virus (hepatitis D virus) that
relies on a second virus (hepatitis B virus) to provide the
necessary structural components for reproduction in human
tissue (i.e., polymicrobial causation)? How does one incorpo-
rate host factors into the equation of causation, such as immu-
nological status, physiology, and genetic variability (42)? How
does one incorporate environmental factors (e.g., the roles of
vectors and reservoirs in virulence) into the equation of cau-
sation? These features of microbial pathogenesis and of mi-
crobial pathogens do not integrate well with the paradigm
provided by Koch’s postulates.
https://journals.asm.org/doi/epdf/10.1128/cmr.9.1.18
The U.S. Army's Typhoid Board, headed by Maj. Walter Reed, established that the house fly was a mechanical vector for the typhoid bacillus, Salmonella typhi ( Cirillo 2006 ). The board's evidence was so impressive that Leland O. Howard, chief of the U.S. Department of Agriculture's Bureau of Entomology, proposed renaming the house fly the “typhoid fly” to focus attention on its importance as a public health menace ( Howard 1911 )
https://academic.oup.com/ae/article-abstract/62/2/83/1751692
Another study reported in the same article, conducted in Rockford, Illinois, was
also inconclusive, because DDT spraying
did not commence until after the outbreak
had passed its peak (Melnick et al. 1947).
Thus, the riddle of the house fly’s role in
the spread of polio remained unanswered.
Cirillo, V. J. (2016). “I Am the Baby Killer!” House Flies and the Spread of Polio. American Entomologist, 62(2), 83–85. doi:10.1093/ae/tmw039
The polio epidemic that struck New Jersey,
Connecticut, Pennsylvania, and New York
State from May to October 1916 claimed
27,000 lives. New York City alone reported
8,900 cases and 2,400 deaths, 80 percent
of whom were children under five years
of age (Oshinsky 2005).
The etiologic agent of polio, poliovi-
rus (enterovirus C: Picornaviridae), was
discovered in 1908 by Viennese immu-
nologist—and future Nobel laureate—
Karl Landsteiner (1868-1943). At the
time, smallpox and rabies were the only
human diseases known to be caused by
viruses (Paul 1971). The implications of
this discovery cannot be overestimated,
for it meant that polio was an infectious, contagious disease with epidemic possi-
bilities. On the other hand, it also held
out hope that polio could be prevented
in the same fashion that typhoid fever
epidemics had recently been controlled
by a killed-bacteria vaccine (Wright 1900).
Revisiting Koch’s postulates: A tailored approach for clinical parasitology
In due course, the development of DNA technologies led to the discovery of virulence genes, which resulted in Molecular Koch’s postulates. Genetics and cloning technologies equipped scientists to isolate a putative virulence gene and evaluate its pathogenicity to fulfill Molecular Koch’s postulates. Pathogen and host continuously switch their genes on and off to achieve desirable phenotypes. Redundancy and robustness of effector and plant immunity genes explain that pathogen–host interaction results in various cross talks and counterattacks.
About a month later, Bill Gates suggested in his “Innovating to Zero” TED
talk in Long Beach, California on February 20, 2010 that reducing world popula-
tion growth could be done in part with “new vaccines” [71]. At 4 minutes and 29
seconds into the talk he says:The world today has 6.8 billion people. That’s headed up to about 9 billion
[here he is almost quoting Bryant
et al.]. Now, if we do a really great job on
new vaccines [our italics], health care, reproductive health services, we
could lower that by, perhaps, 10 or 15 percent∙∙∙ [71]
https://www.bbc.com/news/world-africa-29594091
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