Molecular characterization of methicillin-resistant Staphylococcus aureus clinical strains from the endotracheal tubes of patients with nosocomial pneumonia

Abstract

Background: Among all cases of nosocomial pneumonia, Staphylococcus aureus is the second most prevalent pathogen (17.8%). In Europe, 29.9% of the isolates are oxacillin-resistant. The changing epidemiology of methicillinresistant Staphylococcus aureus (MRSA) nosocomial infections and the decreasing susceptibility to first-line antibiotics leave clinicians with few therapeutic options. The objective of our study was to determine the antimicrobial susceptibility, the associated molecular mechanisms of resistance and the epidemiological relatedness of MRSA strains isolated from the endotracheal tubes (ETT) of intubated critically ill patients in the intensive care unit (ICU) with nosocomial pneumonia caused by Staphylococcus aureus. Methods: The antimicrobial susceptibility to vancomycin, linezolid, ciprofloxacin, clindamycin, erythromycin, chloramphenicol, fusidic acid, gentamicin, quinupristin-dalfopristin, rifampicin, sulfamethoxazole/trimethoprim, and tetracycline were measured. Resistance mechanisms were then analyzed by polymerase chain reaction and sequencing. Molecular epidemiology was carried out by multi-locus sequence typing. Results: S. aureus isolates were resistant to ciprofloxacin, erythromycin, gentamicin, tetracycline, clindamycin, and fusidic acid. The most frequent mutations in quinolone-resistant S. aureus strains were S84L in the gyrA gene, V511A in the gyrB gene, S144P in the grlA gene, and K401R/E in the grlB gene. Strains resistant to erythromycin carried the ermC, ermA, and msrA genes; the same ermC and ermA genes were detected in strains resistant to clindamycin. The aac(6′)-aph(2″) gene was related to gentamicin resistance, while resistance to tetracycline was related to tetK (efflux pump). The fusB gene was detected in the strain resistant to fusidic acid. The most frequent sequence types were ST22, ST8, and ST217, which were distributed in four clonal complexes (CC5, CC22, CC45, and CC59).

Mechanisms of Resistance to Macrolide Antibiotics among Staphylococcus aureus

“…Since each study group consisted of a different number of strains, and these strains differed in their resistance mechanisms, it is difficult to develop a good tool to track the spread of erm genes over the years. However, when analyzing the data presented in the Table 3, it can be concluded that the frequency of genes, especially ermA and ermC, increases with time [4,16,[20][21][22][23][24][25][26][27][28][29][30][31][32][33][34]36,37,[65][66][67][68][69][70][71]. -: no data, cMLS B : constitutive phenotype of resistance to macrolides, lincosamides and streptogramin B. iMLSB: inductive phenotype of resistance to macrolides, lincosamides, and streptogramin B. MS B : resistance to 14-and 15-membered macrolides and streptogramin B.…”

Methicillin-resistant Staphylococcus aureus colonization among healthcare workers in Oman

“…In dermal tissue, MRSA can cause skin, wound and burn infections [9]. Nosocomial pneumonia is an occasional form of MRSA infection [10]. Additionally, a study conducted in Russia showed that the MRSA was proved to cause a fatal community acquired pediatric pneumonia and intensive care unit associated bacteremia [11].…”

Molecular Epidemiology of Methicillin-Resistant Staphylococcus aureus in Hospitalized Patients in Eastern Heilongjiang Province, China

“… 32 There are also reports of MRSA strains extracted from the tracheal intubation of ICU patients. 33 Other researchers have suggested that the ICU admission history may be a risk factor for MRSA infection. 34 Therefore, active monitoring of MRSA in ICU patients is crucial and must be considered.…”