Persistence of Group A Streptococci Labeled with Fluorescein Isothiocyanate in Inflammatory Sites in the Heart and Muscle of Mice and Rabbits

Streptococcal Rheumatic Carditis.

“…This pattern of localization was similar to that seen in the mouse muscle injected with fluorescence-labeled streptococci (215). Localization of the cell wall components was also found to occur in the reticuloendothelial system, as expected for a particulate substance (50,131,188).…”

“…Some of these components include somatic antigens such as M-protein (13-16, 19-22, 37, 45, 57, 68-70, 83, 102, 110, 114, 116, 119, 135, 145, 172, 198, 201, 205, 222, 230, 242, 285, 287, 288, 299, 301), C-polysaccharide complexes of mucopeptide and polysaccharide (6, 27, 37, 50, 63, 131, 135, 188, 215, 216, 233-235, 237, 240, 245), mucopeptide (1,84,132,167,223,224,236,302), cell wall components (2,50,82,85,86,148,238,244,271), and antigens cross-reactive with tissues (118, 119, 126, 129, 210, 249, 273, 2%, 298,299). Others include the cell membrane (43,71,84,274) and L-forms (19,43,91,103,113,166,215,244,263,297,298). Of these various antigens, the ones with the most convincing experimental evidence are the: (i) Mprotein; (ii) complexes of mucopeptide and polysaccharide; (iii) mucopeptide; (iv) persisting, degraded streptococci; and (v) streptococcal antigens cross-reactive with tissues.…”

Persistence in Mice of the L-Phase of Three Streptococcal Strains Adapted to Physiological Osmotic Conditions

“…This is indicated by the fact that, in the experiments described above, there is no difference in survival between the GL-8 low-salt L-strain and the VB lowsalt L-strain upon intraperitoneal or intravenous injection. In this respect it is interesting that fluorescein labelled GL-8 membranes have been found to disappear within 72 h. after intramuscular injection of mice (Rickles et al 1969). …”

Is Bacteriolysis In vivo a Friend or a Foe? Relation to Sepsis, Chronic Granulomatous Inflammation and to Oral Disorders: an Overview Hypothesis

“…At this point, it should also bring us back to the late eighteen nineties and early nineteen twenties, when the hotly-debated "focus of infection theory" and its relation to oral and systemic manifestations, had been proposed [60][61][62][63][64][65][66]. Accordingly, oral microorganisms, involving no less than 500 species, but mainly cariogenic streptococci, staphylococci, strict anaerobes causing periodontal disease, and fungal cells may lodge in injured heart valves (endocarditis), traumatized joints (arthritis) and in additional damaged tissue sites [37,38,[62][63][64][65][66].…”

“…Accordingly, oral microorganisms, involving no less than 500 species, but mainly cariogenic streptococci, staphylococci, strict anaerobes causing periodontal disease, and fungal cells may lodge in injured heart valves (endocarditis), traumatized joints (arthritis) and in additional damaged tissue sites [37,38,[62][63][64][65][66]. This phenomenon also led to the proposition that pulling out teeth infested with microbiota might be a proper way to prevent the translocation of bacteria from the oral cavity to remote tissue sites.…”