SUMMARYFifty strains of Staphylococcus aureus resistant to penicillin or tetracycline or both were examined for loss of these two resistances as the result of growth a t 43-44'. Twelve strains showed a loss of penicillin resistance under the experimental conditions, and of these twelve, three showed a loss of tetracycline resistance. The two resistances were lost independently; in strains in which both resistances were lost most of the sensitive variants had lost one or other resistance but not both. However, penicillin resistance was lost only in strains that were also tetracycline-resistant and vice versa. All strains in which a loss of resistance occurred had similar phage-typing patterns and all belonged to the '52, 52A, 80, 81 complex' of strains. Not all strains in the complex, however, showed a loss of resistance. Both penicillin and tetracycline resistance were transduced into suitable sensitive recipients. The results showed that the heat-sensitivity of the transduced resistance was the same as in the donor in which the transducing phage was propagated. The results are consistent with the hypothesis that these two resistances are carried by two separate plasmids, a t least in certain strains of S. uureus.Nine multiply-resistant strains of Staphylococcw aureus were examined for loss of resistance to antibiotics other than penicillin and tetracycline as the result of growth at elevated temperatures. These other antibiotics included streptomycin, erythromycin, novobiocin, oleandomycin, neomycin and bacitracin. In no case was any loss of resistance observed.
SUMMARYPS 80 is a naturally occurring, penicillinase-producing strain of Staphylococcus aureus, which differs from the majority of such strains in that the genetic determinants for penicillinase production are located on the chromosome. The strain is also resistant to various metal ions and the genes controlling these resistances are located on a plasmid-the n plasmid. When the strain is maintained on nutrient agar slopes at room temperature, a change occurs in its genetic constitution in that these unlinked genetic elements become closely linked and co-transducible with a high frequency. The results described in this paper are consistent with the hypothesis that the change is due to a duplication of the penicillinase genes with one copy of the genes being retained in its original chromosomal location and the other copy being incorporated in the 7~ plasmid.
Eighty-one strains of Staphylococcus aureus that appeared to be tetracycline resistant on the basis of a preliminary disc-diffusion test were examined for resistance to tetracycline and to the semi-synthetic tetracycline, minocycline. Minimum inhibitory concentration (m.i.c.) values for both drugs were determined after induction of the strains by growth for 2 h in sub-inhibitory concentrations of tetracycline. Forty-seven strains (58 %) had m.i.c. values for minocycline of 12-5 pg/ml or greater, and were considered to be minocycline resistant. An additional ten strains had m.i.c. values for minocycline of 3-125 to 6-25 ,ug/ml and were classified as low-level resistant strains. It appears, therefore, that a fairly high proportion of tetracycline-resistant strains isolated at the present time are resistant to concentrations of minocycline unattainable in vivo with the recommended dosage for this antibiotic (Frisk & Tunevall, 1969).Transductional analysis of the genetic determinants for tetracycline resistance revealed the existence of two types of resistance to high concentrations of tetracycline. Strains in the first category (A) were inducibly resistant to tetracycline but sensitive to minocycline; in these strains the resistance determinant was plasmid-borne. Strains in the second category (B) were resistant to both tetracycline and minocycline and had low induction ratios for tetracycline resistance ; the genetic determinant for resistance in these strains was chromosomal. In addition, certain strains in category A were found to carry a chromosomal gene controlling low-level resistance to tetracycline and minocycline. This low-level resistance to tetracycline was masked in the presence of the tetracycline plasmid but could be demonstrated after loss of the plasmid. The results suggest that more than one mechanism of resistance to tetracyclines may exist in staphylococci.
SUMMARY : Three temperate phages isolated from lysogenic staphylococci of phage type 52/52A/80 were used to lysogenize strains of phage-type 80. Two of these phages belonged to serological group A and one to serological group F. Lysogenization of a strain of phage-type 80 with one of the phages (287') resulted in a change in the typing pattern from 80/81 to 52/52A/80. There was, therefore, a gain in sensitivity to phage 52 and 52A and a loss in sensitivity to phage 81. Lysogenization of type 80 strains with the second phage (581') caused a loss in sensitivity to phage 81, while lysogenization with phage 7287' caused a gain in sensitivity to phage 52 and 52A.Loss in sensitivity to phage 81 after lysogenization with phage 287' seems most probably due to specific prophage immunity since phages 287' and 81 belong to the same serological group (A) and may be closely related. Loss in sensitivity to phage 81 after lysogenization with phage 581' does not appear to be a case of specific prophage immunity since the two phages are serologically distinct and the phenomenon resembles examples of prophage interference observed in other organisms.Rountree & Freeman (1955) described a number of hospital epidemics in Australia caused by a strain of staphylococcus which was almost completely resistant to the routine typing phages then in use. However, the two group-I phages 52 and 52A produced a few plaques when applied undiluted to a lawn of the organisms, and phage 52A was 'adapted' to this new type of staphylococcus. The adapted phage is now known as phage 80 and strains lysed specifically by this phage as phage-type 80. A second phage known as 81 was isolated independently in Canada (Bynoe, Elder & Comtois, 1956); it is capable of lysing the majority of phage-type 80 strains. Such strains are therefore more accurately described as phage-type 80/81. Since, however, phage 81 is not included in the set of 21 basic phages used in Great Britain, the strains are usually reported simply as phage-type 80. The 81 reaction will be referred to in this paper only when relevant.Since the original description by Rountree & Freeman many epidemics caused by staphylococci of phage-type 80 have been described in different countries. During the past two or three years it has been noticed in this laboratory that, in some prolonged epidemics caused by phage-type 80, strains giving the typing pattern 52/52 A/80 were also isolated, particularly during the later part of the epidemic. The 'classical' phage-type 80 coccus is lysed only by phage 80 a t the routine test dilution (RTD), using the basic set of
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