The thrust of the experimental data presented here is that small air ions are biologically active. There is convincing evidence that both negative and positive ions (i) inhibit growth of bacteria and fungi on solid media; (ii) exert a lethal effect on vegetative forms of bacteria suspended in water when opportunity is provided for contact of cells and ions; and (iii) reduce the viable count of bacterial aerosols. Through physical action, ions of either charge upset the stability of aerolosized bacterial suspensions and, in addition, have a direct lethal effect which is more prominent with negative ions than with positive ions. With regard to the serotonin hypothesis of air ions action, the situation is more complex. The essential fact is that mice and rats display a charge-related metabolic response to air ions and this phenomenon also occurs in humans. Because serotonin is such a potent hormone, the ultimate functional changes incident to air ion action are impressive and account for the signs of symptoms of the sharav syndrome. Alterations in the cumulative mortality rate with three experimental respiratory disease in the mouse also are charge-dependent, positive ions routinely exercising a detrimental effect. Further, in the case of mice infected with influenza virus, ion-deprivation increases the cumulative mortality rate. Since ion depletion is a constant concomitant of modern urban life, one reasonably may speculate about comparable inimical effects on humans.
Abstract. The emergence of antibiotic-resistant bacterial strains still remains a significant problem for antimicrobial chemotherapy in the clinic. Bacterial viruses (bacteriophages or phages) have been suggested to be used as alternative therapeutic agents for bacterial infections. However, the efficacy of phage therapy in treating drug-resistant infections in humans is uncertain. Therefore in the present study, we examined the effectiveness of phages in the treatment of imipenem-resistant Pseudomonas aeruginosa (IMPR-Pa) infection in an experimental mouse model. Twenty-nine strains of phage were isolated from our hospital sewage, and phage ØA392 was representatively used for all testing because it has lytic activity against a wide range of clinical isolates of IMPR-Pa. We found that intraperitoneal (i.p.) injections of one IMPR-Pa strain (3x10 7 CFU) caused bacteremia and all mice died within 24 h. A single i.p. inoculation of the phage strain (MOI ≥0.01) at up to 60 min after the bacterial challenge was sufficient to rescue 100% of the animals. This lifesaving effect coincided with the rapid appearance of ØA392 in the circulation (within 2 h after i.p. injection), which remained at substantially higher levels for up to 48 h until the bacteria were eradicated. However, the survival rates of the mice dropped to approximately 50% and 20% when the same dose of this purified phage preparation was administered at 180 min and 360 min, respectively, after IMPR-Pa infections. In addition, we demonstrated that the ability of this phage to rescue bacteremic animals was due to the functional capabilities of the phage and not to a nonspecific immune effect. The protection from death occurred only in animals inoculated with bacteria-specific virulent phage strains. When the heat-inactivated phages were used, the survival rate of the infected mice was dramatically reduced to 20% or lower. Moreover, the levels of the antibody against the phage were not significantly changed at the time when the bacteremic animals were protected by the active phages. Finally, our observations revealed that the inoculation of the mice with high-doses of ØA392 alone produced no adverse effects attributable to the phage. These data indicate that phages can save animals from pernicious P. aeruginosa infections and suggest that phage therapy may be potentially used as a stand-alone therapy for patients with IMPR-Pa infections.
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