The Acquired Resistance of Staphylococcus aureus to Bacteriophage

Lowbury, E. J. L.; Hood, A. M.

doi:10.1099/00221287-9-3-524

Cited by 39 publications

(23 citation statements)

References 4 publications

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“…For this reason, we first examined the effect of simultaneous injection of the phage and its host routinely. The possibility of bacterial resistance to phage is unquestionably an obstacle in the development of an effective phage therapy system (18). Indeed, we noted the emergence of mutants of P. aeruginosa D4 that were resistant to phage strain KPP10 in vitro (data not shown).…”

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confidence: 89%

Efficacy of Bacteriophage Therapy against Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice

Watanabe

Matsumoto

Sano

et al. 2007

Antimicrob Agents Chemother

192

130

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We evaluated the efficacy of bacteriophage (phage) therapy by using a murine model of gut-derived sepsis caused by Pseudomonas aeruginosa that closely resembles the clinical pathophysiology of septicemia in humans. Oral administration of a newly isolated lytic phage strain (KPP10) significantly protected mice against mortality (survival rates, 66.7% for the phage-treated group versus 0% for the saline-treated control group; P < 0.01). Mice treated with phage also had lower numbers of viable P. aeruginosa cells in their blood, liver, and spleen. The levels of inflammatory cytokines (tumor necrosis factor alpha TNF-␣, interleukin-1␤ [IL-1␤], and IL-6) in blood and liver were significantly lower in phage-treated mice than in phage-untreated mice. The number of viable P. aeruginosa cells in fecal matter in the gastrointestinal tract was significantly lower in phage-treated mice than in the saline-treated control mice. We also studied the efficacy of phage treatment for intraperitoneal infection caused by P. aeruginosa and found that phage treatment significantly improved the survival of mice, but only under limited experimental conditions. In conclusion, our findings suggest that oral administration of phage may be effective against gut-derived sepsis caused by P. aeruginosa.

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mentioning

confidence: 89%

Efficacy of Bacteriophage Therapy against Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice

Watanabe

Matsumoto

Sano

et al. 2007

Antimicrob Agents Chemother

192

130

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“…They found differences between members of these sets of cultures which indicated that some change in typing pattern occurred from day to day. It was shown previously [2,15] that changes in phage typing pattern in staphylococci resulted from artificial lysogenization. It was reported by Asheshov and Rippon [1] and by Rountree [32] that certain changes in phage typing patterns which follow artificial lysogenization are the results of serologically specific prophage immunity.…”

Section: Genetic Features Of Drug Resistance and Phage Type In S Aureusmentioning

confidence: 99%

Epidemiological and Genetical Study of Drug Resistance in Staphylococcus aureus

Mitsuhashi

1967

Japanese Journal of Microbiology

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Surveys of staphylococcal strains, isolated from clinical sources in geographically scattered hospitals in Japan, disclosed the following facts: 1) Triple (TC·SM·SA, TC·PC· SA, PC·SM·SA) and quadruple (TC·SM·PC·SA) resistant strains with reference to TC, SM, PC and SA, were manifest and they were restricted to specific phage group. 2) There is a maximum population of resistant strains (M.P.R.) in a restricted area, which is governed by the amount and period of use of a drug and by genetic characters of the bacteria such as the mutation rate to resistance, and character which governs infectivity and ability for successful parasitism. 3) There are two types of resistant strains: the first becomes resistant easily and consequently multiple resistant when a new drug is introduced, and consists largely of strains in phage group I containing phage type 80/81. The second type remains single (SA) or double (PC·SA; SM·SA) resistant, and consists primarily of strains in group II and III From the facts that all of the tested staphylococcal strains from clinical sources carry prophages and their drug resistance can be transduced to other strains by their prophages, the present author presents the hypothesis that transduction of drug resistance by prophage is mainly responsible for the acquisition of multiple resistance and wide distribution of multiple resistant strains in phage type or phage group.Genetic studies of drug resistance in staphylococci have disclosed the following facts: 1) Resistance to TC is easily transduced at high frequencies by prophages obtained from multiple resistant strains, and in various combinations of donors and recipients. Resistance to SA and SM is jointly transduced with TC, and vice donors and recipients. Resistance to SA and SM is jointly transduced with TC, and vice versa. Resistance to PC, the ability to form penicillinase (PCase), and chloramphenicol (CM) resistance is not transduced jointly with resistance to TC, SM, and SA. 2) Resistance to macrolide (Mac) antibiotics (EM, OM, LM, SP) is eliminated jointly and irreversibly by acriflavine treatment or by ultraviolet irradiation, and is transduced jointly by phages obtained from donor strains. From these results it can be concluded that Mac resistance is located on an extrachromosomal plasmid. 3) Because of the genetic character of PCase formation (PCase+) and irreversible elimination of PCase+, it was concluded that the gene which governs PCase formation is located on a plasmid. And there are two types of plasmid; one which carries the genetic characters of resistance to macrolide antibiotics (Macr) and of the penicillinase formation (PCase+) and the other carries only PCase+. A genetic model for the genes which govern resistance to TC, SM, SA and for the plasmids is presented. 4) The genetic character which governs resistance to CM is irreversibly eliminated during storage of stock culture or by treatment with acriflavine. This fact and results from transductional analysis suggest that the gene responsible for CM resistance may be located on a plasmid, probably different from the plasmids which govern (Macr. PCase+) or (PCase+). The findings that CM resistant strains of S. aureus inactivated CM in the presence of acetylcoenzyme A strongly suggest that CM resistance in strains from clinical sources is accounted for by inactivation of CM through acetylation of the drug molecule.

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“…The single-clone origin (b) is improbable for the following reasons: the properties of the strains harbouring the plasmid seem to be too variable (table I) to be accounted for by evolution from a single clone, in particular their variety of phage-typing patterns. The susceptibility of staphylococci to lysis by phages can be altered by changes in prophage carriage, in vitro and probably under natural conditions (Lowbury and Hood, 1953 ;Rountree, 1959;Asheshov and Rippon, 1959;Rosendal and Bulow, 1965;Jevons, John and Parker, 1966;Jessen et al, 1969). These changes can be summarised as either a restriction or widening in the phage susceptibility within phage-group I or a progressive restriction in the susceptibility within group 111.…”

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confidence: 99%

An Unusual "Penicillinase Plasmid" In Staphylococcus Aureus; Evidence for its Transfer Under Natural Conditions

Lacey

Rosdahl

1974

Journal of Medical Microbiology

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E XTRACHROMOSOMAL elements that determine production of penicillinase can undergo experimentally a variety of changes within the staphylococcal cell : irreversible loss of the entire element (Novick, 1963) or loss of a fragment from the plasmid (Lacey and Grinsted, 1972), recombination between two of these plasmids (Richmond, 1969), reversible integration of part of the plasmid into the chromosome Richmond and Johnson, 1969), and acquisition of chromosomal genes (Asheshov, 1969). The occurrence of these events under natural conditions, with transfer of the plasmids between cells, could produce re-assortment of many of the available genes; this might occur despite the capacity of transduction to transfer only a small part of the cell genome at any one time. Although the " penicillinase plasmids " may be transferred in the laboratory between cultures of different strains (Novick and Morse, 1967;Lacey, 1972), the extent of this type of transfer between staphylococci in their natural environment is uncertain. Studies on the possible epidemiology of the " penicillinase plasmids " are complicated by the high proportion of strains that produce penicillinase.In this paper, we describe an uncommon " penicillinase plasmid", designated PF because it also carries the genes for resistance to fusidic acid, that occurs in Staphylococcus aureus of phage-groups I, 11, and I11 and in some non-typable strains. Most of these strains have probably acquired the PF plasmid by transfer from other strains. MATERIALS AND METHODSStrains no. FAR 1 to 3 were isolated in Birmingham during 1971 and were supplied by Dr G. A. J. Ayliffe; strains no. FAR7 and 9 (Colindale nos. 1701 and 5487 respectively) were supplied by Dr E. H. Asheshov; strains no. FAR4, 5, 9, and 11 were isolated in Bristol during 1971 and 1972; strains no. FAR24 Fusidic-acid-resistant Staphylococcus aureus.

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The Acquired Resistance of Staphylococcus aureus to Bacteriophage

Cited by 39 publications

References 4 publications

Efficacy of Bacteriophage Therapy against Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice

Efficacy of Bacteriophage Therapy against Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice

Epidemiological and Genetical Study of Drug Resistance in Staphylococcus aureus

An Unusual "Penicillinase Plasmid" In Staphylococcus Aureus; Evidence for its Transfer Under Natural Conditions

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