Loss of the genetic determinant for pesticin I in Pasteurella pestis results in concomitant loss of the plague coagulase and fibrinolytic factor. The median lethal dose for mice of an isolate lacking only these activities is increased by factors of about 10 1 , 10 4 , and 10 7 cells when administered by the intravenous, intraperitoneal, and subcutaneous routes, respectively. Virulence of the aforesaid strain can be enhanced in mice treated with 40 μg of ferrous iron. This response resembles that of Pasteurella pseudotuberculosis , a closely related species that normally lacks pesticin I.

No abstract

Mutational loss of pesticin I, a bacteriocin-like substance produced by Pasteurella pestis, is known to result in concomitant loss of a coagulase and fibrinolytic factor. No relationship was detected between pesticinogeny and other tested properties either associated with virulence or peculiar to P. pestis. Pesticin I was distinguished from the coagulase and fibrinolytic activities on the basis of anatomical distribution, behavior during gel filtration, and sensitivity to heat. Coagulase and the fibrinolytic factor were not differentiated by these criteria. Spontaneous suppressor mutations causing reversion to pesticinogeny were not detected, nor were such mutants obtained by treatment with ultraviolet light or 2-aminopurine. Attempts to demonstrate a common activator of pesticin I, coagulase, or the fibrinolytic factor in extracts of pesticinogenic cells were not successful. These results are in accord with the hypothesis that at least two structural genes for the three activities reside on a replicon distinct from the chromosome proper. Fibrinolytic activity was significantly reduced in the presence of 0.003 M e-aminocaproic acid and was nonexistent on fibrin films freed from endogenous plasminogen by treatment with heat. Fibrinolytic activity on heated films could be restored by addition of plasma or serum from six mammalian species. Accordingly, the plague fibrinolytic factor, like staphylokinase or urokinase, promotes the conversion of plasminogen to plasmin.

Ability to detect pigmented and nonpigmented Pasteurella pestis is essential in plague research, and is currently dependent on use of the synthetic hemin-agar of Jackson and Burrows. We have devised a new differential medium for this purpose, containing Congo red dye and common, commercially available laboratory media. The ease and simplicity of preparation make the Congo red-agar a practical routine laboratory tool in plague research. These findings, possibly indicating a common binding site for hematin and Congo red, should be useful in efforts to determine the chemical nature of a bacterial component associated with high virulence in P. pestis .

Current methods of identifying Pasteurella pestis rely heavily on tests specific for detecting fraction I, the envelope antigen. Pesticin I, a bacteriocin inhibitory for P. pseudotuberculosis, has been demonstrated in nearly all tested strains isolated from human infections. The results of using this characteristic as an identifying trait for P. pestis were compared with results reported for detecting fraction I by fluorescent-antibody and antiserum-agar techniques. Data indicate that, although certain atypical strains of P. pestis fail to react in one system or the other, a combination of these tests provides positive identification in all cases. Detection of P. pestis in contaminated materials is greatly facilitated, and the simplicity of this test makes it a valuable tool in the study of plague infections and an important adjunct to methods currently in use. The use of the pesticin I assay is not intended to replace other accepted techniques, but rather to supplement them and increase the effectiveness of plague investigation.