scholarly journals The Effect of Whole Honey Bee Venom (Apismellifera) on Reducing Skin Infection of Rabbits Caused by Methicillin Resistant Staphylococcus aureus: An In vivo Study

2018 ◽  
Vol 12 (4) ◽  
pp. 2111-2116 ◽  
Author(s):  
Lamyaa Kadhim Baqer ◽  
Raed Taha Yaseen
Keyword(s):  
Staphylococcus Aureus ◽  
Honey Bee ◽  
Skin Infection ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Bee Venom ◽  
In Vivo Study ◽  
Methicillin Resistant

scholarly journals In vitro and in vivo study of fosfomycin in methicillin-resistant Staphylococcus aureus septicaemia

1986 ◽  
Vol 96 (3) ◽  
pp. 419-423 ◽  
Author(s):  
W. Y. Lau ◽  
C. H. Teoh-Chan ◽  
S. T. Fan ◽  
K. F. Lau
Keyword(s):  
Staphylococcus Aureus ◽  
Fusidic Acid ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
In Vivo Study ◽  
Methicillin Resistant ◽  
Drug Of Choice

SUMMARYFive hundred strains of methicillin-resistant Staphylococcus aureus were tested against various anti-staphylococcal agents. Vancomycin, fusidic acid and fosfomycin were found to be the most effective. Only 1 strain out of 500 was resistant to fosfomycin. Three patients with methicillin-resistant Staphylococcus aureus septicaemia were successfully treated by fosfomycin. We conclude that fosfomycin could be the drug of choice for methicillin-resistant Staphylococcus aureus infection.

scholarly journals In Vivo Activity of a Novel Polymeric Guanidine in Experimental Skin Infection with Methicillin-Resistant Staphylococcus aureus

2007 ◽  
Vol 51 (9) ◽  
pp. 3437-3439 ◽  
Author(s):  
Christina Kratzer ◽  
Selma Tobudic ◽  
Karin Macfelda ◽  
Wolfgang Graninger ◽  
Apostolos Georgopoulos
Keyword(s):  
Staphylococcus Aureus ◽  
Guinea Pig ◽  
Skin Infection ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
The Novel ◽  
In Vivo Efficacy ◽  
Methicillin Resistant ◽  
Superficial Skin ◽  
Guinea Pig Model

ABSTRACT The in vivo efficacy of the novel polymeric guanidine AKACID Plus was evaluated in a guinea pig model of experimental skin infection with methicillin-resistant Staphylococcus aureus (MRSA). Topical application of AKACID Plus at concentrations of ≥0.5% was as effective as mupirocin 2% cream in the treatment of superficial skin infection with MRSA.

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.

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