In vitro ability of Staphylococcus aureus isolates from bacteraemic patients with and without metastatic complications to invade vascular endothelial cells.
Invasion of vascular endothelial cells is thought to be a critical step in the development of metastatic infections in patients with Staphylococcus aureus bacteraemia. This study was designed to evaluate the association between the ability to invade endothelial cells and metastatic infection by S. aureus. Patients with metastatic infection were identified among those with community-acquired S. aureus bacteraemia in a tertiary referral hospital. Patients with simple bacteraemia caused by S. aureus over the same period served as the control group. The ability of each clinical isolate to invade endothelial cells was evaluated by counting the number of intracellular organisms 1 h after inoculation onto human umbilical vein endothelial cells in vitro. The cytotoxic activity of intracellular S. aureus was determined 24 h after internalization, and expressed as the percentage of cells killed. The clinical isolates varied in invasiveness and cytotoxicity. The median invasiveness, relative to S. aureus reference strain ATCC 29213, was 145 % in the cases (n=10) [interquartile range (IQR) 103-160] and 153 % (IQR 111-173) in the controls (n=11; P=0.44). The median cytotoxicity was 59.4 % (IQR 47-68) in the cases and 65.2 % (IQR 50-74) in the controls (P=0.44). Differences in the ability of S. aureus to invade and destroy vascular endothelial cells in vitro were not associated with the development of metastatic complications in patients with S. aureus bacteraemia. This implies that the invasiveness and toxicity of S. aureus for endothelial cells may not be major determinants of metastatic infection.
Park
Wan Beom
WB
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Kim
Sung Han
SH
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Kang
Cheol-In
CI
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Cho
Jae Hyun
JH
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Bang
Ji Whan
JW
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Park
Kyoung Wha
KW
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Lee
Yeong Seon
YS
National Institute of Health, Korea Center for Diseases Control and Prevention, Seoul 122-701, Republic of Korea.
Kim
Nam Joong
NJ
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Oh
Myoung-Don
MD
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Kim
Hong Bin
HB
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
Won Choe
Kang
K
Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.
D000328:Adult; D000368:Aged; D016470:Bacteremia / Q000382:microbiology*; D015169:Colony Count, Microbial; D017714:Community-Acquired Infections / Q000382:microbiology; D003593:Cytoplasm / Q000382:microbiology; D042783:Endothelial Cells / Q000382:microbiology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D013203:Staphylococcal Infections / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000302:isolation & purification / Q000472:pathogenicity*