By doing so we can drive the selection of nonvirulent strains.
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To his amazement, he discovered that if he injected a heat-killed, virulent strain of Streptococcus pneumoniae, followed by a live, nonvirulent strain, bacteria that were normally innocuous would somehow become pathogenic.
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NDV strains can be categorised as velogenic (highly virulent), mesogenic (intermediate virulence), or lentogenic (nonvirulent). Velogenic strains produce severe nervous and respiratory signs, spread rapidly, and cause up to 90% mortality. Mesogenic strains cause coughing, affect egg quality and production, and result in up to 10% mortality. Lentogenic strains produce mild signs with negligible mortality.
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Griffith used two strains of pneumococcus (Streptococcus pneumoniae) bacteria which infect mice – a type III-S (smooth) which was virulent, and a type II-R (rough) strain which was nonvirulent. The III-S strain synthesized a polysaccharide capsule that protected itself from the host's immune system, resulting in the death of the host, while the II-R strain did not have that protective capsule and was defeated by the host's immune system. A German bacteriologist, Fred Neufeld, had discovered the three pneumococcal types (Types I, II, and III) and discovered the quellung reaction to identify them in vitro.Lehrer, Steven.
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Testable outlines exist for the origin of each of the three motility systems, and avenues for further research are clear; for prokaryotes, these avenues include the study of secretion systems in free-living, nonvirulent prokaryotes. In eukaryotes, the mechanisms of both mitosis and cilial construction, including the key role of the centriole, need to be much better understood. A detailed survey of the various nonmotile appendages found in eukaryotes is also necessary. Finally, the study of the origin of all of these systems would benefit greatly from a resolution of the questions surrounding deep phylogeny, as to what are the most deeply branching organisms in each domain, and what are the interrelationships between the domains.
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The possibility of bacteriophage involvement in speA production was first introduced in 1926 when Cantacuzene and Boncieu reported that nonvirulent strains of S. pyogenes were transformed to virulent strains through some transferable element. Frobisher and Brown reported similar results in 1927, and in 1949, the reports were confirmed by Bingel Later, in 1964, Zabriskie reported that phage T12 could cause speA production by lysogeny in strains that it became a part of. In 1980, Johnson, Schlievert and Watson were able to confirm this and show that the gene for speA production was transferred from toxigenic strains of bacteria to non-toxigenic strains through lysogeny. In their experiment, every transformed, toxin-producing bacterial colony was lysogenic, i.e. contained the T12 gene.
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There McCarty developed a special interest in infectious diseases — in particular, antibacterial sulfonamide drug treatments that were just entering medicine — which he subsequently pursued by moving to New York University to work with William Tillett. A National Research Council Fellowship in the medical sciences and an opening in Oswald T. Avery's laboratory spurred his move to Rockefeller University in 1941. At that time, research in the Avery laboratory was focused on the pneumococcal transformation, the heritable alteration of a pneumococcal strain from a nonvirulent rough form to a virulent smooth encapsulated form. McCarty's arrival at the Rockefeller Institute in September 1941 marked 13 years since this discovery, also known as the Griffith phenomenon. Prior to this discovery, the 1920s had been marked by a medley of disparate observations on Streptococcus pneumoniae that seemed to involve an exchange of receptors among diverse bacteria either grown together in liquid media or exposed to various kinds of extracts and supernatants.
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