Disease relevance of SAB1892c

• The deduced sequence of the 488-amino-acid protein (MsrA) revealed the presence of two ATP-binding motifs homologous to those of a family of transport-related proteins from Gram-negative bacteria and eukaryotic cells, including the P-glycoprotein responsible for multidrug resistance [1].
• Its in vitro activity was assessed against 472 gram-positive cocci, largely selected as epidemiologically unrelated isolates with multidrug resistance [2].
• GG918, a synthetic inhibitor of P-glycoprotein-mediated mammalian tumour multidrug resistance, was found to be equipotent to reserpine in enhancing the in vitro activity of norfloxacin and ciprofloxacin against strains of Staphylococcus aureus expressing distinct efflux-related multidrug resistance pumps [3].
• Enterobacteriaceae and Pseudomonas species proved to have high but variable rates of multidrug resistance [4].
• Phage therapy will compensate for unavoidable complications of chemotherapy such as the appearance of multidrug resistance or substituted microbism [5].

High impact information on SAB1892c

• All S. aureus isolates (54.2% oxacillin resistant) were susceptible to linezolid (MIC90 = 2 microg/ml); MIC distributions were consistent, regardless of oxacillin or multidrug resistance status [6].
• The Portuguese and Spanish clones also had a common heterogeneous class 3 phenotype and identical multidrug resistance patterns [7].
• RESULTS: Although the antibiograms of isolates from 2 obstetrics clinics differed, no strain showed multidrug resistance to antimicrobials [8].
• Outpatient MRSA exhibited 26 different resistance phenotypes; the 4 most common were resistance to erythromycin only (40.8%), multidrug resistance to erythromycin, clindamycin, and levofloxacin (21.5%), double drug resistance to erythromycin and levofloxacin (11.3%), and double drug resistance to clindamycin and erythromycin (5.1%) [9].
• The emergence of strains with multidrug resistance, including resistance to vancomycin, the antibiotic of last resort, presents the medical community with a major public health problem [10].

Biological context of SAB1892c

• Multidrug resistance plasmid pSK108 from coagulase-negative staphylococci; relationships to Staphylococcus aureus qacC plasmids [11].

Associations of SAB1892c with chemical compounds

• These phenotypes were also the most common among inpatient MRSA (n = 946), but multidrug resistance to erythromycin, clindamycin, and levofloxacin (43.7%) was most common [9].
• Isolates from this clonal cluster exhibited multidrug resistance but were susceptible to linezolid and glycopeptides [12].

References