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Infection and Immunity, December 2005, p. 7932-7937, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.7932-7937.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Capsule-Negative Staphylococcus aureus Induces Chronic Experimental Mastitis in Mice

Lorena P. N. Tuchscherr,1 Fernanda R. Buzzola,1 Lucía P. Alvarez,1 Roberto L. Caccuri,1 Jean C. Lee,2 and Daniel O. Sordelli1*

Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina,1 Channing Laboratory, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts2

Received 5 May 2005/ Returned for modification 2 August 2005/ Accepted 21 September 2005

Staphylococcus aureus capsular polysaccharides (CP) have been shown to enhance staphylococcal virulence in numerous animal models of infection. Although serotype 5 CP (CP5) and CP8 predominate among S. aureus isolates from humans, most staphylococcal isolates from bovines with mastitis in Argentina are capsule negative. This study was designed to evaluate the effects of CP5 and CP8 expression on the pathogenesis of experimental murine mastitis. Lactating mice were challenged by the intramammary route with one of three isogenic S. aureus strains producing CP5, CP8, or no capsule. Significantly greater numbers of acapsular mutant cells were recovered from the infected glands 12 days after bacterial challenge compared with the encapsulated strains. Histopathological analyses revealed greater polymorphonuclear and mononuclear leukocyte infiltration and congestion in the mammary glands of mice infected with the encapsulated strains compared with the acapsular mutant, and the serotype 5 strain elicited more inflammation than the serotype 8 strain. In vitro experiments revealed that the acapsular S. aureus strain was internalized by MAC-T bovine epithelial cells in significantly greater numbers than the CP5- or CP8-producing strain. Taken together, the results suggest that S. aureus lacking a capsule was able to persist in the murine mammary gland, whereas encapsulated strains elicited more inflammation and were eliminated faster. Loss of CP5 or CP8 expression may enhance the persistence of staphylococci in the mammary glands of chronically infected hosts.

* Corresponding author. Mailing address: Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155 P-12, (C 1121 ABG) Buenos Aires, Argentina. Phone: 5411 5950 9618. Fax: 5411 4964 2554. E-mail: sordelli{at}fmed.uba.ar.

Editor: V. J. DiRita

Infection and Immunity, December 2005, p. 7932-7937, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.7932-7937.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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