The pathogenesis of cardiac microlesion formation during severe bacteremic infection

ABSTRACT Immunological and epidemiological evidence suggests that the development of natural immunity to meningococcal disease results from colonization of the nasopharynx by commensal Neisseria spp., particularly with N. lactamica. We report here that immunization with N. lactamica killed whole cells, outer membrane vesicles, or outer membrane protein (OMP) pools and protected mice against lethal challenge by a number of diverse serogroup B and C meningococcal isolates in a model of bacteremic infection. Sera raised to N. lactamica killed whole cells, OMPs, or protein pools were found to cross-react with meningococcal isolates of a diverse range of genotypes and phenotypes. The results confirm the potential of N. lactamica to form the basis of a vaccine against meningococcal disease.

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Trends in Bacteremic Infection Due to Streptococcus pyogenes (Group A Streptococcus), 1986-1995

Emerging Infectious Diseases ◽

10.3201/eid0201.960107 ◽

1996 ◽

Vol 2 (1) ◽

pp. 54-56 ◽

Cited By ~ 14

Author(s):

Daniel Musher

Keyword(s):

Streptococcus Pyogenes ◽

Group A Streptococcus ◽

Group A ◽

Bacteremic Infection

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Pulmonary sequestration of polymorphonuclear leukocytes released from bone marrow in bacteremic infection

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1998.275.2.l255 ◽

1998 ◽

Vol 275 (2) ◽

pp. L255-L261 ◽

Cited By ~ 3

Author(s):

Yukio Sato ◽

Stephan F. Van Eeden ◽

Dean English ◽

James C. Hogg

Keyword(s):

Bone Marrow ◽

Streptococcus Pneumoniae ◽

Polymorphonuclear Leukocytes ◽

Pulmonary Sequestration ◽

Infection Model ◽

Subcutaneous Infection ◽

Thymidine Analog ◽

Bacteremic Infection

We examined the bone marrow response and the sequestration of polymorphonuclear leukocytes (PMNs) in lung using a bacteremic infection model in rabbits. PMNs were labeled with the thymidine analog 5-bromo-2′-deoxyuridine (BrdU) in the bone marrow, and the bone marrow release and the sequestration of BrdU-labeled PMNs were measured using immunohistochemistry. A focal subcutaneous infection (S) was induced, and the bacteremia (B) was produced 4 h later with Streptococcus pneumoniae (S+B). This S+B group was compared with other groups with only subcutaneous infection or only bacteremia. The S+B group developed a profound leukopenia after the bacteremia that was associated with an increase in circulating BrdU-labeled PMNs. Morphometric studies showed more PMN sequestration in the lung of the S+B group compared with the others ( P < 0.05). Compared with unlabeled PMNs, BrdU-labeled PMNs, which represent newly released PMNs, preferentially sequestered in lung ( P< 0.05) and were slow to migrate into the infected tissues ( P < 0.05). We conclude that bacteremic infection is associated with an accelerated release of PMNs from the bone marrow and that these newly released PMNs preferentially sequester in lung and are slow to migrate into infected tissues.

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