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M Surdeanu

Publications and source records attributed to M Surdeanu.

At least 19 recordsLinked to original sources
PubMed2000

Comparison of serotyping, ribotyping and pulsed-field gel electrophoresis for distinguishing group A Streptococcus strains isolated in Albania.

Conventional serotyping for T antigens, rRNA gene restriction fragment length polymorphism analysis (ribotyping) and pulsed-field gel electrophoresis were compared for distinguishing among group A streptococci isolated in Albania between 1980-1982 and in 1995. A total of twelve serotypes were identified among seventy GAS strains. Ribotyping revealed eight and eleven distinct patterns after digestion with HindIII and PvuII, respectively. Twenty-three strains of serotype T12 were subdivided in 10 ribotypes and 11 strains of T2 serotype were differentiated in 5 ribotypes. By comparison, PFGE generated 37 patterns after SmaI digestion. The index of discrimination, using the Hunter-Gaston formula, was applied to assess the value of these methods for interpretation of the epidemiological data. For serotyping the value of index was 0.85. The ribotyping system revealed an ID of 0.83 when the combination HindIII and PvuII was used. This index reached 0.97 for PFGE. The methods used were useful to subtype the isolates of GAS.

Albania↗
PubMed1983

Isolation and complementation of temperature-sensitive replication mutants of Staphylococcus aureus plasmid pC194.

Temperature-sensitive replication (Tsr) mutants have been isolated from the Staphylococcus aureus plasmid pC194. For three of the four mutant plasmids tested (pSAO801, pSAO802, and pSAO804) the segregation kinetics suggested a complete block of plasmid replication at 43 degrees C. The replication defects of three mutant plasmids: pSAO802, pSAO803, and pSAO804 could be complemented by recombinant plasmids carrying a segment from either the wild type or the other mutant, pSAO801. There was no complementation when the segment carried by the recombinant plasmid was derived from one of the three complementable mutants. These data were taken as evidence for the involvement of a diffusible, plasmid-encoded product, RepH, in pC194 replication. The complementation of the fourth Tsr mutant, pSAO801, could not be tested due to an abnormal susceptibility of this mutant to the incompatibility expressed by recombinants carrying segments derived from pC194 or its mutants. A single mutation was found to be responsible for both pSAO801 instability and its altered incompatibility properties but the nature of the defect has not yet been elucidated.

DNA Replication↗
PubMed1976

Porphobilinogen-accumulating mutants of Salmonella typhimurium LT2.

Four independent porphobilinogen-accumulating mutants of Salmonella typhimurium LT2 were isolated by selecting for dwarf colony formation on neomycin agar media. Cell-free extracts of the parent strain, but not of the mutants, were able to convert 5-aminolaevulinic acid or porphobilinogen to porphyrins. The results indicated that the mutants were deficient in uroporphyrinogen I synthase (EC. 4.3.I. 8) activity: these are the first mutants of this type reported in S. typhimurium LT2. Mapping of the hemC locus (for uroporphyrinogen I synthase) by F-mediated conjugation and by P22-mediated transduction showed the gene sequence ilvEDAC-hemC-cya-metE.

Aminolevulinic Acid↗
PubMed1976

Two restriction and modification systems in Staphylococcus aureus NCTC8325.

The presence of two distinct host specificities in Staphylococcus aureus strain NCTC8325 was revealed by the isolation of restriction- and modification-deficient mutants. The two host specificity systems, designated S1 and S2, are both active on phage 80mualpha but are not additive in their restricting activity. Restriction-deficient, modification-proficient mutants were invariably affected in both restriction systems. The functional relationship between these two systems is discussed.

DNA, Bacterial↗
PubMed1970

Hemin-deficient mutants of Salmonella typhimurium.

Nine hemin-deficient mutants of Salmonella typhimurium LT2 were isolated as neomycin-resistant colonies. Five of these mutants could be stimulated by Delta-aminolevulinic acid (Delta-ALA), thus representing hemA mutants. Since S. typhimurium LT2 is not able to incorporate hemin, the identification of the mutants not stimulated by Delta-ALA was made on the basis of the simultaneous loss of catalase activity and cytochromes. The hemA gene was mapped by conjugation in the trp region, probably in the order purB-pyrD-hemA-trp; the episome FT(71)trp does not carry the hemA gene. Transductional intercrosses by phage P22 indicate that hemA 11, 12, 13, and 37 are at very closely linked sites, whereas hemA14 is at a more distant site in the same or an adjacent gene. No joint transduction was detected between hemA and trp or pyrF. The loci affected in the other hemin-deficient mutants were linked in conjugation to the pro(+) marker (frequency of linkage, 88 to 97%), but cotransduction of the two markers could not be obtained. The episome F lac hem purE, which originates from Escherichia coli K-12, could complement these hemin-deficient mutants of S. typhimurium LT2. As a result, the sequence of the markers on the chromosome of S. typhimurium LT2 is probably pro heme purE, analogous to the sequence found in E. coli K-12. Thus, the chromosome of S. typhimurium also possesses two hem regions, with a location similar to that described in E. coli K-12.

Amino Acids↗