Hospital-Related Lineage of USA300 Methicillin-Resistant Staphylococcus aureus (MRSA) to Cause Bacteremia in Iran.

Staphylococcus aureus is an important pathogen that causes bloodstream infections. This study is aimed at assessing the genotypic characteristics of S. aureus strains responsible for bloodstream infections. An epidemiological study was conducted using 85 S. aureus strains isolated from bloodstream infections. Susceptibility was tested using the broth microdilution method and disk diffusion. All detected methicillin-resistant S. aureus (MRSA) isolates were confirmed by mecA PCR assays. S. aureus isolated from bacteremia were characterized using SCCmec, spa, and multilocus sequence typing methods. The prevalence of S. aureus strains responsible for bloodstream infections was 38.8%. All isolates were MRSA. Multidrug resistance (MDR) was present in 84.7% of isolates. MRSA isolated categorized within six clonal complexes including CC8 (60%), CC22 (22.4%), CC5 (5.9%), CC30 (4.7%), CC45 (4.7%), and CC59 (2.3%). The main lineages found were USA300/CC8-MRSA-IV/t008 (41.2%), followed by ST22-SCCmecIV/t790 (9.4%), ST239-SCCmecIII/t037 (7.1%), ST22-SCCmecIV/t032 (7.1%), ST239-SCCmecIII/t631 (5.9%), ST239-SCCmecIII/t860 (5.9%), ST22-SCCmecIV/t852 (5.9%), ST5-SCCmecIV/t002 (4.7%), ST45-SCCmecIV/t038 (4.7%), ST30-SCCmecIV/t318 (4.7%), ST59-SCCmecIV/t437 (2.3%), and ST225-SCCmecII/t045 (1.1%). Resistance to vancomycin amounted to 5.9% of isolates that belonged to ST239-SCCmecIII/t037 (80%) and ST8-SCCmecIV/t008 (20%). The emergence of USA300 strains in bloodstream infections in our country is a serious alarm and highlights the significant invasion of this lineage into the healthcare system. MDR patterns among these strains appear to be becoming the biggest problem in healthcare treatment.

Emerging Challenges in Staphylococcus aureus Bloodstream Infections: Insights from Coagulase Typing, Toxin Genes, and Antibiotic Resistance Patterns.

Background: The incidence of complications and mortality associated with Staphylococcus aureus (S. aureus) bloodstream infections has been increasing significantly, particularly in developing countries where control strategies against this virulent pathogen and its resistance to antibacterial agents are insufficient. The aim of this study was to investigate coagulase typing, the prevalence of toxin genes, and the antibiotic resistance profile of S. aureus isolated from bloodstream infections. Methods: Antibiotic susceptibility of the isolates was determined by the disk diffusion method. The prevalence of toxin genes was determined using the polymerase chain reaction (PCR) method. Genetic variability of isolates was determined using multiplex PCR based on coagulase gene polymorphism. Results: Out of 120 strains, 55 (46%) were methicillin-resistant S. aureus (MRSA) and 65 (54%) were methicillin-sensitive S. aureus (MSSA). All isolates were susceptible to linezolid and teicoplanin but showed varying levels of resistance to other antibiotics. The highest resistance was observed for ampicillin (92.5%), gentamicin (69.2%), and amikacin (68.3%). Multidrug resistance was observed in all isolates. PCR analysis revealed a higher prevalence of toxin genes in MRSA (tst: 38%, pvl: 29.1%, eta: 10%, and etb: 4.1%) than that in MSSA. According to the coa typing, the most prevalent types were coa III (29.2%), coa II (26.7%), and coa VI (10%). Conclusion: The presence of genetic variability and widespread multidrug resistance in our hospitals emphasizes the circulation of various coa types. Therefore, it is crucial to implement antimicrobial stewardship and infection control measures to prevent and control the spread of these strains.

Mupirocin-Resistant Staphylococcus aureus in Iran: A Biofilm Production and Genetic Characteristics.

The spread of mupirocin-resistant Staphylococcus aureus strains in hospitals and communities is a universal challenge. Limited data is available on the genetic features of high-level mupirocin resistant- (HLMUPR-) S. aureus isolates in Tehran. In the present research, we investigated 48 high-level mupirocin resistance S. aureus by antimicrobial activity, virulence analysis, biofilm formation, multilocus sequence typing (MLST), and staphylocoagulase (SC) typing. All the HLMUPR strains were positive for mupA gene. The frequency of multidrug resistance was 97.9%. Twenty-one (43.8%) were toxinogenic with 14 producing pvl (29.2%), 5 tst (10.4%), and two eta (4.2%). Among the HLMUPR isolates, biofilm production was detected in 45 (89.6%) isolates with complete dominance clfB, clfA genes, and a noticeably high frequency fnbA (95.8%), followed by fnbB (93.8%), eno and icaD (each 83.3%), sdrC (81.3%), ebps (79.2%), icaA (75%), sdrD (66.7%), fib (60.4%), sdrE (50%), cna (41.7%), and bap (4.2%). Coagulase typing distinguished isolates into four genotypic patterns including III (50%), II (27.1%), and type IVa (22.9%). A total of three clonal complexes (CCs) and 4 sequence types (STs) including CC/ST22 as the most prevalent (52.1%), CC8/ST239 (20.8%), CC/ST8 (16.7%), and CC/ST5 (10.4%) were identified in current work. According to our analysis, nonbiofilm producer isolates belonged to CC8/ST239 (6.3%) and CC/ST8 (4.2%). Fusidic acid-resistant isolates belonged to CC/ST45 (n = 3) and CC8/ST239 (n = 1). Observations highlighted the circulation of the CC/ST22 HLMUPR S. aureus strains with strong biofilm-production ability in our hospitals, indicating the possibility of transmission of this type between community and hospital.

The global prevalence of fusidic acid resistance in clinical isolates of Staphylococcus aureus: a systematic review and meta-analysis.

BACKGROUND AND AIM: Staphylococcus aureus (S. aureus) is one of the most common pathogens causing nosocomial and community-acquired infections with high morbidity and mortality rates. Fusidic acid has been increasingly used for the treatment of infections due to methicillin-susceptible S. aureus (MSSA) and methicillin-resistant S. aureus (MRSA). The present study aimed to determine the precise prevalence of fusidic acid resistant MRSA (FRMRSA), fusidic acid resistant MSSA (FRMSSA), and total fusidic acid resistant S. aureus (FRSA) on a global scale. METHODS: Several international databases including Medline, Embase, and the Web of Sciences were searched (2000-2020) to discern studies addressing the prevalence of FRSA, FRMRSA, and FRMSSA. STATA (version14) software was used to interpret the data. RESULTS: Of the 1446 records identified from the databases, 215 studies fulfilled the eligibility criteria for the detection of FRSA (208 studies), FRMRSA (143 studies), and FRMSSA (71 studies). The analyses manifested that the global prevalence of FRSA, FRMRSA, and FRMSSA was 0.5%, 2.6% and 6.7%, respectively. CONCLUSION: This meta-analysis describes an increasing incidence of FRSA, FRMSSA, and FRMRSA. These results indicate the need for prudent prescription of fusidic acid to stop or diminish the incidence of fusidic acid resistance as well as the development of strategies for monitoring the efficacy of fusidic acid use.

Active integrins regulate white adipose tissue insulin sensitivity and brown fat thermogenesis.

OBJECTIVE: Reorganization of the extracellular matrix is a prerequisite for healthy adipose tissue expansion, whereas fibrosis is a key feature of adipose dysfunction and inflammation. However, very little is known about the direct effects of impaired cell-matrix interaction in adipocyte function and insulin sensitivity. The objective of this study was to determine whether integrin activity can regulate insulin sensitivity in adipocytes and thereby systemic metabolism. METHODS: We characterized integrin activity in adipose tissue and its consequences on whole-body metabolism using adipose-selective deletion of ß1 integrin (Itgb1adipo-cre) and Kindlin-2 (Kind2adipo-cre) in mice. RESULTS: We demonstrate that integrin signaling regulates white adipocyte insulin action and systemic metabolism. Consequently, loss of adipose integrin activity, similar to loss of adipose insulin receptors, results in a lipodystrophy-like phenotype and systemic insulin resistance. However, brown adipose tissue of Kind2adipo-cre and Itgb1adipo-cre mice is chronically hyperactivated and has increased substrate delivery, reduced endothelial basement membrane thickness, and increased endothelial vesicular transport. CONCLUSIONS: Thus, we establish integrin-extracellular matrix interactions as key regulators of white and brown adipose tissue function and whole-body metabolism.

Carnosine ameliorates cognitive deficits in streptozotocin-induced diabetic rats: Possible involved mechanisms.

Diabetic patients are at increased risk to develop cognitive deficit and senile dementia. This study was planned to assess the benefits of chronic carnosine administration on prevention of learning and memory deterioration in streptozotocin (STZ)-diabetic rats and to explore some of the involved mechanisms. Rats were divided into 5 groups: i.e., control, carnosine100-treated control, diabetic, and carnosine-treated diabetics (50 and 100mg/kg). Carnosine was injected i.p. at doses of 50 or 100mg/kg for 7 weeks, started 1 week after induction of diabetes using streptozotocin. Treatment of diabetic rats with carnosine at a dose of 100mg/kg at the end of the study lowered serum glucose, improved spatial recognition memory in Y maze, improved retention and recall in elevated plus maze, and prevented reduction of step-through latency in passive avoidance task. Furthermore, carnosine at a dose of 100mg/kg reduced hippocampal acetylcholinesterase (AChE) activity, lowered lipid peroxidation, and improved superoxide dismutase (SOD) activity and non-enzymatic antioxidant defense element glutathione (GSH), but not activity of catalase. Meanwhile, hippocampal level of nuclear factor-kappaB (NF-κB), tumor necrosis factor α (TNF-α), and glial fibrillary acidic protein (GFAP) decreased and level of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase 1 (HO-1) increased upon treatment of diabetic group with carnosine at a dose of 100mg/kg. Taken together, chronic carnosine treatment could ameliorate learning and memory disturbances in STZ-diabetic rats through intonation of NF-κB/Nrf2/HO-1 signaling cascade, attenuation of astrogliosis, possible improvement of cholinergic function, and amelioration of oxidative stress and neuroinflammation.