scholarly journals Failure of Clindamycin Treatment of Methicillin-Resistant Staphylococcus aureus Expressing Inducible Clindamycin Resistance In Vitro

2003 ◽  
Vol 37 (9) ◽  
pp. 1257-1260 ◽  
Author(s):  
G. K. Siberry ◽  
T. Tekle ◽  
K. Carroll ◽  
J. Dick
Keyword(s):  
Staphylococcus Aureus ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Methicillin Resistant ◽  
Inducible Clindamycin Resistance

scholarly journals Prevalence of inducible clindamycin resistance in methicillin-resistant Staphylococcus aureus: the first study in Jordan

2017 ◽  
Vol 11 (04) ◽  
pp. 350-354 ◽  
Author(s):  
Dua’a Jarajreh ◽  
Amin Aqel ◽  
Hamed Alzoubi ◽  
Wael Al-Zereini
Keyword(s):  
Staphylococcus Aureus ◽  
Polymerase Chain Reaction ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
High Rate ◽  
Chain Reaction ◽  
Methicillin Resistant ◽  
Inducible Clindamycin Resistance ◽  
Standard Procedures ◽  
Polymerase Chain

Introduction: A high rate of infections with methicillin-resistant Staphylococcus aureus (MRSA) has been documented, in both hospital- (HA-MRSA) and community-acquired (CA-MRSA) diseases in Jordan. Erythromycin and clindamycin are considered treatments of choice. However, resistance to erythromycin with false susceptibility to clindamycin in vitro may lead to therapeutic failure. Hence, it is mandatory to study the prevalence of inducible resistance to macrolide-lincosamide-streptogramin B (iMLSB) antibiotics conferred by erm genes in those bacteria. Methodology: S. aureus isolates were identified morphologically and biochemically, and MRSA were appraised using standard procedures. Induction in resistance to MLSB antibiotics among MRSA isolates was detected phenotypically using the D-test, and the presence of erm genes was revealed by polymerase chain reaction (PCR). Results: Of 126 collected Staphylococcus isolates, 71 (56.3%) isolates were S. aureus, of which 55 (77.5%) were MRSA. A total of 43 (78.2%) MRSA-discordant isolates were resistant to erythromycin, of which 33 (76.7%) exhibited the iMLSB (D-test positive), 2 (4.7%) the MSB (D-test negative), and 8 (18.6%) the constitutive resistant (cMLSB) phenotypes. Induction of clindamycin resistance was 1.6 times greater in CA-MRSA than in HA-MRSA. Furthermore, ermA and ermC were significantly prevalent in HA-MRSA and CA-MRSA, respectively. Conclusions: Continuous surveillance of the MLSB resistance is important and required before the prescription of clindamycin to treat MRSA infections.

scholarly journals Group V Phospholipase A2 Mediates Endothelial Dysfunction and Acute Lung Injury Caused by Methicillin-Resistant Staphylococcus aureus

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1731
Author(s):  
Yu Maw Htwe ◽  
Huashan Wang ◽  
Patrick Belvitch ◽  
Lucille Meliton ◽  
Mounica Bandela ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Acute Lung Injury ◽  
Endothelial Dysfunction ◽  
Lung Injury ◽  
Phospholipase A2 ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Group V ◽  
Methicillin Resistant

Lung endothelial dysfunction is a key feature of acute lung injury (ALI) and clinical acute respiratory distress syndrome (ARDS). Previous studies have identified the lipid-generating enzyme, group V phospholipase A2 (gVPLA2), as a mediator of lung endothelial barrier disruption and inflammation. The current study aimed to determine the role of gVPLA2 in mediating lung endothelial responses to methicillin-resistant Staphylococcus aureus (MRSA, USA300 strain), a major cause of ALI/ARDS. In vitro studies assessed the effects of gVPLA2 inhibition on lung endothelial cell (EC) permeability after exposure to heat-killed (HK) MRSA. In vivo studies assessed the effects of intratracheal live or HK-MRSA on multiple indices of ALI in wild-type (WT) and gVPLA2-deficient (KO) mice. In vitro, HK-MRSA increased gVPLA2 expression and permeability in human lung EC. Inhibition of gVPLA2 with either the PLA2 inhibitor, LY311727, or with a specific monoclonal antibody, attenuated the barrier disruption caused by HK-MRSA. LY311727 also reduced HK-MRSA-induced permeability in mouse lung EC isolated from WT but not gVPLA2-KO mice. In vivo, live MRSA caused significantly less ALI in gVPLA2 KO mice compared to WT, findings confirmed by intravital microscopy assessment in HK-MRSA-treated mice. After targeted delivery of gVPLA2 plasmid to lung endothelium using ACE antibody-conjugated liposomes, MRSA-induced ALI was significantly increased in gVPLA2-KO mice, indicating that lung endothelial expression of gVPLA2 is critical in vivo. In summary, these results demonstrate an important role for gVPLA2 in mediating MRSA-induced lung EC permeability and ALI. Thus, gVPLA2 may represent a novel therapeutic target in ALI/ARDS caused by bacterial infection.

In vitro infectability of prosthetic mesh by methicillin-resistant Staphylococcus aureus

Hernia ◽  
2006 ◽  
Vol 10 (2) ◽  
pp. 120-124 ◽  
Author(s):  
A. G. Harrell ◽  
Y. W. Novitsky ◽  
K. W. Kercher ◽  
M. Foster ◽  
J. M. Burns ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Prosthetic Mesh ◽  
Methicillin Resistant
Sign in / Sign up

Export Citation Format

Share Document