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Antimicrobial Agents and Chemotherapy, December 1998, p. 3169-3172, Vol. 42, No. 12
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
In Vitro Resistance to Thrombin-Induced Platelet Microbicidal
Protein among Clinical Bacteremic Isolates of Staphylococcus
aureus Correlates with an Endovascular Infectious
Source
Arnold S.
Bayer,1,2,*
Darwin
Cheng,1
Michael R.
Yeaman,1,2
G. Ralph
Corey,3
R. Scott
McClelland,3
Lizzie J.
Harrel,4 and
Vance G.
Fowler Jr.3
The St. John's Cardiovascular Research
Center and the Division of Infectious Diseases, Harbor-UCLA Medical
Center, Torrance, California 905091;
the
UCLA School of Medicine, Los Angeles, California
900242; and
the Departments of Internal
Medicine3 and
Microbiology,4 Duke University Medical
Center, Durham, North Carolina 27705
Received 1 June 1998/Returned for modification 2 September
1998/Accepted 16 September 1998
Platelet microbicidal proteins (PMPs), small cationic peptides
released at sites of endovascular damage, kill common bloodstream pathogens in vitro. Our group previously showed that in vitro resistance of clinical staphylococcal and viridans group streptococcal bacteremic strains to PMPs correlated with the diagnosis of infective endocarditis (IE) (Wu et al., Antimicrob. Agents Chemother.
38:729-732, 1994). However, that study was limited by (i) the small
number of Staphylococcus aureus isolates from IE patients,
(ii) the retrospective nature of the case definitions, and (iii) the
diverse geographic sources of strains. The present study evaluated the
in vitro PMP susceptibility phenotype of a large number of
staphylococcemic isolates (n = 60), collected at a
single medical center and categorized by defined and validated clinical
criteria. A significantly higher proportion of staphylococcemic strains
from patients with IE was PMP resistant in vitro than the proportion of
strains from patients with soft tissue sepsis (83% and 33%,
respectively; P < 0.01). Moreover, the levels of PMP
resistance (mean percent survival of strains after 2-h exposure to PMP
in vitro) were significantly higher for isolates from patients with IE
and with vascular catheter sepsis than for strains from patients with
abscess sepsis (P < 0.005 and P < 0.01, respectively). These data further support the concept that
bloodstream pathogens that exhibit innate or acquired PMP resistance
have a survival advantage with respect to either the induction or
progression of endovascular infections.
*
Corresponding author. Mailing address: Division of
Infectious Diseases, Harbor-UCLA Medical Center, Bldg RB2/Room 225, 1000 West Carson St., Torrance, CA 90509. Phone: (310) 222-6422. Fax: (310) 782-2016. E-mail: Bayer{at}HUMC.EDU.
Antimicrobial Agents and Chemotherapy, December 1998, p. 3169-3172, Vol. 42, No. 12
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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