TY - JOUR
T1 - Infectious Spondylitis-Associated Staphylococcus aureus with Virulence Gene pvl or tst Causes More Necrosis than Apoptosis in Human Alveolar Basal Epithelial Cell Line A549
AU - Huang, Tsung-Jen
AU - Lee, Chi-Han
AU - Wu, Meng-Huang
AU - Li, Yen Yao
AU - Yang, Tsung Han
AU - Cheng, Chin Chang
AU - Lee, Ching-Yu
AU - Lu, Chih Cheng
AU - Chu, Chishih
PY - 2016/6
Y1 - 2016/6
N2 - Methicillin-sensitive and resistant Staphylococcus aureus (MSSA and MRSA, respectively) can cause non-tuberculosis infectious spondylitis. In 43 cases of bacterial infectious spondylitis, Mycobacterium tuberculosis and S. aureus were the two major causative pathogens. MRSA caused more anterior operations and thoracic infections, while MSSA caused more posterior infections and lumbar infections. Differences between six S. aureus isolates from infectious spondylitis were characterized. MLST and staphylococcal cassette chromosome mec (SCCmec) analysis identified MSSA ST959 and ST30 isolates, MRSA ST239/SCCmec IIIA isolates 2 and 3, ST59/SCCmec IIIA-like isolate 6, and ST30/SCCmec IV isolate 5. While all of the isolates were resistant to penicillin and ampicillin, the MRSA isolates were more resistant than the MSSA isolates. Carbapenem-resistant MRSA ST239/SCCmec IIIA and ST59/SCCmec IIIA-like isolates of the agr1 type were also resistant to clindamycin and erythromycin. Leukocidin genes (pvl or lukED) and hemolysin genes (hla, hld and hlg) were present in all of the isolates. All six isolates caused more necrosis than apoptosis in the human alveolar basal epithelial cell line A549; however, ST59/SCCmec IIIA-like isolate 6, ST30/ SCCmec IV isolate 5 with pvl genes, and MSSA ST30 isolates with tst caused greater than 40% cell death after the 4-h incubation. Regardless of the MRSA isolate and its SCCmec type or the MSSA isolate, the infectious spondylitis-associated S. aureus isolates differed genetically, and the pvl and tst genes may be important genes for cell necrosis.
AB - Methicillin-sensitive and resistant Staphylococcus aureus (MSSA and MRSA, respectively) can cause non-tuberculosis infectious spondylitis. In 43 cases of bacterial infectious spondylitis, Mycobacterium tuberculosis and S. aureus were the two major causative pathogens. MRSA caused more anterior operations and thoracic infections, while MSSA caused more posterior infections and lumbar infections. Differences between six S. aureus isolates from infectious spondylitis were characterized. MLST and staphylococcal cassette chromosome mec (SCCmec) analysis identified MSSA ST959 and ST30 isolates, MRSA ST239/SCCmec IIIA isolates 2 and 3, ST59/SCCmec IIIA-like isolate 6, and ST30/SCCmec IV isolate 5. While all of the isolates were resistant to penicillin and ampicillin, the MRSA isolates were more resistant than the MSSA isolates. Carbapenem-resistant MRSA ST239/SCCmec IIIA and ST59/SCCmec IIIA-like isolates of the agr1 type were also resistant to clindamycin and erythromycin. Leukocidin genes (pvl or lukED) and hemolysin genes (hla, hld and hlg) were present in all of the isolates. All six isolates caused more necrosis than apoptosis in the human alveolar basal epithelial cell line A549; however, ST59/SCCmec IIIA-like isolate 6, ST30/ SCCmec IV isolate 5 with pvl genes, and MSSA ST30 isolates with tst caused greater than 40% cell death after the 4-h incubation. Regardless of the MRSA isolate and its SCCmec type or the MSSA isolate, the infectious spondylitis-associated S. aureus isolates differed genetically, and the pvl and tst genes may be important genes for cell necrosis.
M3 - Article
SP - 479
EP - 488
JO - Advances in Microbiology
JF - Advances in Microbiology
ER -