No abstract
SUMMARYTwo nocardiophages were isolated from soil samples: one, called #C, was specific for the Nocardia canicruria mating type; the other, called +EC, proliferated in N. canicruria and N. erythropolis mating types. Inactivation of phage q5C was rapid in NaCl solutions, with chloroform, 0.3% hydrogen peroxide and 30% (v/v) ethanol in water. Phage q5EC behaved similarly but was less labile in NaCl solutions. Both phages were resistant to diethyl ether. Phage q5C could be propagated to titres of 1010 plaque-forming units/ml. on a medium containing peptone, yeast extract and calcium nitrate ; the highest observed titres of phage q5EC were also produced in this medium. A chemically defined medium for proliferation of phage q5C consisted of inorganic salts, valine, isoleucine, leucine, nicotinamide, glycerol. Other variables which affected the growth of these phages were the amount of phage and host inocula and the age of the host before infection. Phage q5C was distinct from other nocardiophages in its ability to attach quickly and efficiently to its host; 95 % of the phage attached, and attachment was time and temperature dependent. Attachment of phage $EC was slow and inefficient, reaching only 34%. The latent period for phage q5C was about 25 min., the increase period was 35 min. and the burst size about 60 particles/infective centre. The latent period of phage q5EC was 180 min. and the burst size about 20 particles. Both these nocardiophages possessed the typical actinophage morphology.
The segregation of unselected genes expressing resistance or susceptibility to acriflavine, erythromycin, streptomycin, and tetracycline was analyzed in selected prototrophic recombinants resulting from matings of Nocardia erythropolis and N. canicruria. The organisms were shown to be functionally haploid and appeared to contain not more than one genome. It was postulated that all observed genes were present in a linear linkage group. The ordering of the genes in N. erythropolis was: tetB10 eryB9 his-3 purAl acr-2 strAl (respectively, resistance to tetracycline and erythromycin, deficiency for histidine and for purine, and resistance to acriflavine and streptomycin). The ordering of the genes in N. canicruria was: purB2 tetA9 eryA7 acr-11 strB2 (respectively, deficiency for purine, and resistance to tetracycline, erythromycin, acriflavine, and streptomycin). Excluding the genes for acriflavine resistance, acr-2 and acr-J1, resistance loci in N. erythropolis were not allelic to and showed lateral displacement from genes controlling phenotypically similar resistance in N. canicruria. Evidence for some lack of homology between N. erythropolis and N. canicruria genomes was found. Recombination phenomena between the nocardial species was postulated to occur as a result of formation of a heterogenomic zygote in which new combinations were produced. Production of selectable, haploid recombinants was ascribed to subsequent haploidization of the zygote.
Three clinical isolates of Staphylococcus aureus, which were previously shown to contain a 50S plasmid conferring resistance to several aminoglycosides, were examined for modifying enzymes. Both the wild-type and heat-cured derivatives of the isolates were screened for acetyl-, adenylyl-, and phosphotransferase activities. The substrates were ntamicin, amikacin and ilniieir the results indicated that even though all three activites were present, the phosphotransferase reaction was most respo i otice-es_eantibiotics. The absence of any of the modifying activites in cured derivatives of the three isolates supports the conclusion that aminoglycoside resistance in these strains is conferred by a plasmid.Gentamicin resistance in clinical isolates of Staphylococcus aureus has been reported in Europe (4, 7, 9, 10) and the United States (11). Recent studies in this laboratory identified a 50S plasmid in two strains as the genetic element responsible for this resistance (11). The organisms studied were recovered from an outbreak of infections in our neonatal intensive care unit (Talmadge Memorial Hospital, Augusta, Ga.) and were of different phage types. Speller et al. (10) reported an outbreak in three hospitals by a single strain of gentamicin-resistant S. aureus. In France, Le Goffic et al. (7) have studied a gentamicin-resistant strain isolated from a blood culture.Since gentamicin resistance in S. aureus has only recently been noted in clinical isolates, we undertook the biochemical characterization of our strains in an effort to determine which of several possible modifying enzymes could be involved in this resistance. We now describe the relative susceptibility of gentamicin, amikacin, and netilmicin to acetyltransferase (AAC) adenylyltransferase (ANT), and phosphotransferase (APT) modification by crude cell-free extracts of our S. aureus strains.
Recombinants obtained from matings of Nocardia erythropolis x N. canicruria were tested for their genetic stability by comparing phenotypes from direct selection with the same population after unselected growth. Contraselective loci were employed in various combinations in order that all of the mapped characters might be subjected to unselected analysis. Some recombinant class types appeared as stable haploids, whereas others behaved as heterozygous diploids, segregating out new phenotypes. All regions of the parental genomes were found to be involved in segregation, implying that the entire mapped region can become merozygotic under standard mating conditions. On the basis of segregating phenotypes, the genetic potentials of these compatible nocardiae were ascertained as follows: the formation of a diploid with subsequent segregation of parental or haploid recombinant genomes or both; persistence of the diploid through many generations; continuing reassort
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