HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cavanaugh, D. C. Articles by Randall, R. Search for Related Content PubMed PubMed Citation Articles by Cavanaugh, D. C. Articles by Randall, R.

The Role of Multiplication of Pasteurella Pestis in Mononuclear Phagocytes in the Pathogenesis of Flea-Borne Plague

From the Walter Reed Army Institute of Research, Washington, D. C., and the Department of Medicine, School of Medicine, University of Maryland, Baltimore, Maryland

Abstract

The result of experiments conducted in this laboratory to determine the fate of virulent strains of Pasteurella pestis inoculated into an animal host by a blocked flea led to an examination and extension of the observations of Burrows (3) and Burrows and Bacon (4). These workers found that virulent strains of the plague bacillus, in contrast to avirulent strains, can occur in three forms or types: a) phagocytosis-sensitive (S-type), b) nonencapsulated phagocytosis-resistant (R-type), and c) (M-type), which is visibly well encapsulated, rich in Fraction I and is highly resistant to phagocytosis. Further, they found that polymorphonuclear leukocytes could phagocytize and destroy a large percentage of the phagocytosis-sensitive (S-type) organisms.

Our findings agreed with their observations that the R- and M-forms that occur only in virulent strains of the plague bacillus were resistant to phagocytosis by polymorphonuclear leukocytes. We confirmed their findings that polymorphonuclear leukocytes could readily phagocytize and destroy the phagocytosis-sensitive S-form of both virulent and avirulent strains of P. pestis.

On the other hand we have demonstrated that the phagocytosis-sensitive S-type of virulent P. pestis is ingested by and multiplies within mononuclear leukocytes of normal mice and guinea pigs. On release from the damaged monocytes the bacilli are of the encapsulated M-type and are highly resistant to phagocytosis by either neutrophils or monocytes.

Our results also show that the plague blocked flca inoculates its host with the phagocytosis-sensitive S-type of virulent P. pestis which is readily phagocytized and destroyed in great numbers by the polymorphonuclear leukocytes. By contrast, those bacilli that are ingested by the monocytes in vivo rapidly multiply, and on release from the damaged cells are of the M-type and are resistant to phagocytosis by both polymorphs and monocytes, a condition that permits the establishment of bubonic plague in a susceptible host.

This article has been cited by other articles:

				J. L. Spinner, J. A. Cundiff, and S. D. Kobayashi Yersinia pestis Type III Secretion System-Dependent Inhibition of Human Polymorphonuclear Leukocyte Function Infect. Immun., August 1, 2008; 76(8): 3754 - 3760. [Abstract] [Full Text] [PDF]

				J. Sha, S. L. Agar, W. B. Baze, J. P. Olano, A. A. Fadl, T. E. Erova, S. Wang, S. M. Foltz, G. Suarez, V. L. Motin, et al. Braun Lipoprotein (Lpp) Contributes to Virulence of Yersiniae: Potential Role of Lpp in Inducing Bubonic and Pneumonic Plague Infect. Immun., April 1, 2008; 76(4): 1390 - 1409. [Abstract] [Full Text] [PDF]

				X. Yang, B. J. Hinnebusch, T. Trunkle, C. M. Bosio, Z. Suo, M. Tighe, A. Harmsen, T. Becker, K. Crist, N. Walters, et al. Oral Vaccination with Salmonella Simultaneously Expressing Yersinia pestis F1 and V Antigens Protects against Bubonic and Pneumonic Plague J. Immunol., January 15, 2007; 178(2): 1059 - 1067. [Abstract] [Full Text] [PDF]

				M. L. Fisher, C. Castillo, and J. Mecsas Intranasal Inoculation of Mice with Yersinia pseudotuberculosis Causes a Lethal Lung Infection That Is Dependent on Yersinia Outer Proteins and PhoP Infect. Immun., January 1, 2007; 75(1): 429 - 442. [Abstract] [Full Text] [PDF]

				B. Velan, E. Bar-Haim, A. Zauberman, E. Mamroud, A. Shafferman, and S. Cohen Discordance in the Effects of Yersinia pestis on the Dendritic Cell Functions Manifested by Induction of Maturation and Paralysis of Migration Infect. Immun., November 1, 2006; 74(11): 6365 - 6376. [Abstract] [Full Text] [PDF]

				A. P. Anisimov and K. K. Amoako Treatment of plague: promising alternatives to antibiotics. J. Med. Microbiol., November 1, 2006; 55(Pt 11): 1461 - 1475. [Abstract] [Full Text] [PDF]

				F. Liu, H. Chen, E. M. Galvan, M. A. Lasaro, and D. M. Schifferli Effects of Psa and F1 on the Adhesive and Invasive Interactions of Yersinia pestis with Human Respiratory Tract Epithelial Cells. Infect. Immun., October 1, 2006; 74(10): 5636 - 5644. [Abstract] [Full Text] [PDF]

				A. Zauberman, S. Cohen, E. Mamroud, Y. Flashner, A. Tidhar, R. Ber, E. Elhanany, A. Shafferman, and B. Velan Interaction of Yersinia pestis with Macrophages: Limitations in YopJ-Dependent Apoptosis. Infect. Immun., June 1, 2006; 74(6): 3239 - 3250. [Abstract] [Full Text] [PDF]

				M. A. Parent, L. B. Wilhelm, L. W. Kummer, F. M. Szaba, I. K. Mullarky, and S. T. Smiley Gamma Interferon, Tumor Necrosis Factor Alpha, and Nitric Oxide Synthase 2, Key Elements of Cellular Immunity, Perform Critical Protective Functions during Humoral Defense against Lethal Pulmonary Yersinia pestis Infection. Infect. Immun., June 1, 2006; 74(6): 3381 - 3386. [Abstract] [Full Text] [PDF]

				R. Rebeil, R. K. Ernst, C. O. Jarrett, K. N. Adams, S. I. Miller, and B. J. Hinnebusch Characterization of Late Acyltransferase Genes of Yersinia pestis and Their Role in Temperature-Dependent Lipid A Variation J. Bacteriol., February 15, 2006; 188(4): 1381 - 1388. [Abstract] [Full Text] [PDF]

				W. A. Janssen and M. J. Surgalla Plague Bacillus: Survival within Host Phagocytes Science, February 28, 1969; 163(3870): 950 - 952. [Abstract] [PDF]