Comparison of the activities of coumermycin, ciprofloxacin, teicoplanin, and other non-beta-lactam antibiotics against clinical isolates of methicillin-resistant Staphylococcus aureus from various geographical locations.

Emerging infections represent an enormous challenge to both human and veterinary medicine. Identification of Methicillin-Resistant Staphylococcus aureus (MRSA) in various species and in food has raised concerns about the roles of animals in the epidemiology of MRSA. MRSA are a group of gram-positive bacteria, distinct from other strains of S. aureus in that this pathogen is resistant to methicillin, oxacillin, and all beta-lactam antibiotics. The severity of infections caused by MRSA depends on the strain responsible for the infection and can vary from soft tissue infections to bacteremia and sometimes pneumonia. MRSA strains are divided into clones, based on their genetic makeup. According to the setting of infection, MRSA are divided into three epidemiological types: hospital acquired (HA-MRSA), community acquired (CA-MRSA), and livestock acquired (LA-MRSA) (ie. Transmitted from animal carriers). The epidemiology of HA-MRSA, CA-MRSA, and LA-MRSA is blurred as different recent genetic studies have revealed significant overlap of identical clones between HA-MRSA and CA-MRSA, and the significant increase of human infection caused by LA-MRSA. Furthermore, the animal-human and animal-animal transmission of LA-MRSA has prompted further investigation to study the origin of this epidemiological type and the transmission dynamics. The genetic and virulence profiles of different types of MRSA vary widely, where community acquired and livestock acquired strains are more virulent than hospital acquired strains. This review sheds light on three epidemiological groups of MRSA (HA-MRSA, CA-MRSA, and LA-MRSA), and their most prevalent clonal clusters, that can consequently allow better understanding of their evolution, emergence, transmission, and global dissemination.

Download Full-text

Molecular Study of Immune Evasion Cluster Genes in Clinical Isolates of Staphylococcus aureus

Current Biotechnology ◽

10.2174/2211550110666211029123127 ◽

2021 ◽

Vol 10 ◽

Author(s):

Maysaa El Sayed Zaki ◽

Samah Sabry El-Kazzaz

Keyword(s):

Staphylococcus Aureus ◽

Immune Evasion ◽

Clinical Isolates ◽

Diffusion Method ◽

Beta Lactam ◽

Sensitivity Testing ◽

Cross Sectional ◽

Methicillin Resistant ◽

Beta Lactam Antibiotics ◽

Immune Evasion Cluster

Aims: The aim of the present research was to highlight the prevalence of immune evasion cluster genes (IEC) sak, chp, scn, sea, sep among Staphylococcus aureus (S. aureus) clinical isolates. Background: The present study was a cross-sectional retrospective study, included one hundred isolates of S. aureus that were isolated from patients with nosocomial infections. S. aureus isolates were subjected to full microbiological identification and antibiotics sensitivity testing by the disc diffusion method. The presence of IEC genes scn, sea, sak, sep, chp was determined by polymerase chain reaction (PCR). Methods: The current study included 100 S. aureus isolates; 40% were classified as methicillin resistant. The isolates exhibited marked resistance to beta lactams antibiotics, the lowest resistance was to erythromycin, ciprofloxacin and vancomycin. The presence of one or more IEC was determined in 89 isolates. The prevalence of chp, sak, sea, sep and scn was 54%, 53%, 8%, 7% and 30%, respectively. Results: S. aureus isolates with IEC genes had increased resistance rates to the studied antibiotics; however, this increase was statistically insignificant either to beta-lactam antibiotics, such as amoxacillin/clavulinic acid (P=0.794), ampicillin (P=0.561), cefotaxim (P=0.271), ceftazidime (P=0.145), imipenem (P=0.589) or non beta-lactam antibiotics, such as amikacin (P=0.955) and trimethoprim/sulfamethoxazale (P=0.974). From 40 methicillin resistant Staphylococcus aureus (MRSA) strains, 37 isolates harbor one or more immune evasion cluster genes. Conclusion: The high prevalence of these genes among MRSA may explain its pathogenesis. There is a need for studies with a high number of isolates to verify the present findings.

Download Full-text