Anti-Staphylococcus Group B Polyclonal antibody

Background: Group B Streptococcus (S. agalactiae) is one of the colonizing bacteria in pregnant women which can be a causative agent of meningitis and neonatal sepsis. This organism has also been increasingly related to invasive infections in non-pregnant adults. Objective: In present study, we aimed to characterize the clonality of biofilm-producing S. agalactiae isolates from various sources from two different clinical laboratories in Tehran, Iran. Materials and Methods: S. agalactiae isolates were collected from community-acquired (CA) and hospital-acquired (HA) infections in pregnant and non-pregnant adults. The antimicrobial susceptibility patterns and biofilm formation ability were determined. In addition, pulse field gel electrophoresis (PFGE) was used to verify the clonal diversity of isolates. Results: Out of the 87 isolates, 15 (16.6%) formed biofilm. The antibiotic resistance rate was 98.85% for clindamycin, 98.85% for tetracycline, followed by 29.88% for erythromycin, 9.19% for moxifloxacin and 6.89% for levofloxacin. The PFGE patterns revealed a total of 16 different clusters consisting of 6 single types (STs). Conclusion: This study evaluated the biofilm formation of clinical S. agalactiae, which may be a step towards understanding its role in pathological processes. Biofilm formation was significant only in the hypervirulent ST-17 clone. Intraclonal spread of isolates indicates that a local lineage of isolates is responsible for infection by these bacteria.

Cholesterol-dependent cytolysins (CDCs) are key virulence factors involved in many lethal bacterial infections, including pneumonia, necrotizing soft tissue infections, bacterial meningitis, and miscarriage. Host responses to these diseases involve myeloid cells, especially macrophages. Macrophages use several systems to detect and respond to cholesterol-dependent cytolysins, including membrane repair, mitogen-activated protein (MAP) kinase signaling, phagocytosis, cytokine production, and activation of the adaptive immune system. However, CDCs also promote immune evasion by silencing and/or destroying myeloid cells. While there are many common themes between the various CDCs, each CDC also possesses specific features to optimally benefit the pathogen producing it. This review highlights host responses to CDC pathogenesis with a focus on macrophages. Due to their robust plasticity, macrophages play key roles in the outcome of bacterial infections. Understanding the unique features and differences within the common theme of CDCs bolsters new tools for research and therapy.