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M J SURGALLA

Publications and source records attributed to M J SURGALLA.

At least 19 recordsLinked to original sources
PubMed1964

EFFECTS OF BICARBONATE ON GROWTH OF PASTEURELLA PESTIS. I. DIFFERENTIAL RESPONSE OF VIRULENT AND AVIRULENT CELLS.

Surgalla, M. J. (Fort Detrick, Frederick, Md.), A. W. Andrews, and C. L. Baugh. Effects of bicarbonate on growth of Pasteurella pestis. I. Differential response of virulent and avirulent cells. J. Bacteriol. 88:269-272. 1964.-Virulent Pasteurella pestis and the avirulent mutants always present in a virulent inoculum have been demonstrated to give growth responses in opposite directions upon addition of bicarbonate to broth cultures under certain conditions. The effect of supplemental bicarbonate on initiation of growth from a virulent inoculum was found to be either stimulation of both virulent and avirulent cells at low levels of added bicarbonate, depression of both virulent and avirulent cells at higher initial concentrations, or depression of avirulent mutants with simultaneous stimulation of virulent cells at a narrow range of intermediate levels.

Animals↗
PubMed1964

EFFECTS OF BICARBONATE ON GROWTH OF PASTEURELLA PESTIS. II. CARBON DIOXIDE FIXATION INTO OXALACETATE BY CELL-FREE EXTRACTS.

Baugh, C. L. (Fort Detrick, Frederick, Md.), J. W. Lanham, and M. J. Surgalla. Effects of bicarbonate on growth of Pasteurella pestis. II. Carbon dioxide fixation into oxalacetate by cell-free extracts. J. Bacteriol. 88:553-558. 1964.-Enzyme preparations from Pasteurella pestis will carboxylate phosphoenolpyruvate to form oxalacetate by two distinct reactions. The reactions are similar to those catalyzed by the enzymes, phosphoenolpyruvic carboxylase and phosphoenolpyruvate carboxykinase. No significant differences in enzyme characteristics or enzyme content were found when virulent cells were compared with avirulent under the conditions of our experiments. The carboxykinase of P. pestis differs from that of animal origin, because it is dependent upon adenine derivatives rather than inosine or guanosine nucleotides. The latter two nucleotides can act indirectly by way of adenosine nucleotides, because nucleoside diphosphokinase and myokinase are present in the extract.

Acetates↗
PubMed1962

Pesticins. II. Production of pesticin I and II.

Brubaker, Robert R. (Fort Detrick, Frederick, Md.) and Michael J. Surgalla. Pesticins. II. Production of pesticin I and II. J. Bacteriol. 84:539-545. 1962.-Pesticin I was separated from pesticin I inhibitor by ion-exchange chromatography of cell-free culture supernatant fluids and by acid precipitation of soluble preparations obtained from mechanically disrupted cells. The latter procedure resulted in formation of an insoluble pesticin I complex which, upon removal by centrifugation and subsequent dissolution in neutral buffer, exhibited a 100- to 1,000-fold increase in antibacterial activity over that originally observed. However, activity returned to the former level upon addition of the acid-soluble fraction, which contained pesticin I inhibitor. Since the presence of pesticin I inhibitor leads to serious errors in the determination of pesticin I, an assay medium containing ethylenediaminetetraacetic acid in excess Ca(++) was developed; this medium eliminated the effect of the inhibitor. By use of the above medium, sufficient pesticin I was found to be contained within 500 nonirradiated cells to inhibit growth of a suitable indicator strain; at least 10(7) cells were required to effect a corresponding inhibition by pesticin II. Although both pesticins are located primarily within the cell during growth, pesticin I may arise extracellularly during storage of static cells. Slightly higher activity of pesticin I inhibitor was found in culture supernatant fluids than occurred in corresponding cell extracts of equal volume. The differences and similarities between pesticin I and some known bacteriocins are discussed.

Anti-Bacterial Agents↗
PubMed1962

Genotypic alterations associated with avirulence in streptomycin-resistant Pasteurella pestis.

Brubaker, Robert R. (Fort Detrick, Frederick, Md.) and Michael J. Surgalla. Genotypic alterations associated with avirulence in streptomycin-resistant Pasteurella pestis. J. Bacteriol. 84:615-624. 1962.-Avirulence in Pasteurella pestis, as indicated by the existence of a new genotype, was associated with the genetic loss of Ca(++) dependence rather than with the usual concomitant loss of ability to produce virulence antigens. Strains of the new type exhibited all four of the known virulence factors of P. pestis but were avirulent for mice and guinea pigs (ld(50) > 10(8) cells). In addition to producing virulence antigens, the new strains formed rough colonies at 37 C when grown on Ca(++)-deficient medium, as opposed to typical avirulent strains which formed smooth colonies on this medium and failed to produce virulence antigens. Growth of the new strains in a corresponding Ca(++)-deficient broth medium was slow, as compared with that of typical avirulent strains, but was more rapid than that of virulent strains. The new strains were obtained (i) at 26 C by selecting for resistance to streptomycin or (ii) at 37 C by isolation from rough colonies growing on a Ca(++)-deficient agar medium plated with either a virulent streptomycin-sensitive or -resistant culture. Usually, isolates obtained at 26 C exhibited a marked reduction in ability to form colonies upon primary plating at 37 C. Of 108 streptomycin-resistant isolates obtained from six virulent strains, 20% were of the new type. In addition, five isolates were of reduced virulence (mouse ld(50) approximately 10(4) cells) but differed in being Ca(++)-dependent; they possessed all of the known virulence properties. Certain streptomycin-resistant strains failed to give rise to avirulent colonies when plated on a Ca(++)-deficient agar medium containing streptomycin. The significance of this phenomenon, which was not exhibited by the five strains of reduced virulence, is discussed, as are some apparent differences between isolates from a glycerol-fermenting strain and similar isolates obtained from five nonglycerol-fermenting strains.

Animals↗
PubMed1961

Pesticins. I. Pesticinbacterium interrelationships, and environmental factors influencing activity.

Brubaker, Robert R. (U. S. Army Biological Laboratories, Fort Detrick, Frederick, Md.) and Michael J. Surgalla. Pesticins. I. Pesticin-bacterium interrelationships, and environmental factors influencing activity. J. Bacteriol. 82: 940-949. 1961-A second bacteriocin-like substance produced by all tested strains of Pasteurella pestis and P. pseudotuberculosis is described. This activity, termed pesticin II, is active against the two avirulent P. pestis strains, A12 and Java. These strains do not produce pesticin I, which inhibits the growth of type I strains of P. pseudotuberculosis. Pesticin I was also found to be active against certain strains of Escherichia coli, strain A12, but not strain Java, and some P. pestis isolates which also produce pesticin I. A number of E. coli strains produce a substance which also inhibits the growth of strains A12 and Java; the activity of this substance is dependent upon the presence of high concentrations of Ca(++). The activity of both pesticins is inhibited under anaerobic conditions or in the presence of antiserum. The activity of pesticin I, but not pesticin II, is suppressed by Fe(+++), hemin, certain hemin-containing proteins, Mg(++), and inorganic phosphate. Suppression of pesticin I activity by Fe(+++) can be reversed by the addition of either Ca(++) or Sr(++) or by metal chelating agents. All tested strains of P. pestis and P. pseudotuberculosis produce a metabolite which suppresses the activity of pesticin I. The activity of this substance, termed pesticin I inhibitor, is enhanced by Fe(+++), and to a lesser extent by Mg(++) or by inorganic phosphate; its activity is suppressed by Mn(++) and by protamine sulfate.

Bacteriocins↗