Recent advances in understanding the molecular basis of group BStreptococcusvirulence

Abstract

Group B Streptococcus commonly colonises healthy adults without symptoms, yet under certain circumstances displays the ability to invade host tissues, evade immune detection and cause serious invasive disease. Consequently, Group B Streptococcus remains a leading cause of neonatal pneumonia, sepsis and meningitis. Here we review recent information on the bacterial factors and mechanisms that direct host-pathogen interactions involved in the pathogenesis of Group B Streptococcus infection. New research on host signalling and inflammatory responses to Group B Streptococcus infection is summarised. An understanding of the complex interplay between Group B Streptococcus and host provides valuable insight into pathogen evolution and highlights molecular targets for therapeutic intervention.GBS (Group B Streptococcus/-cocci) is a leading agent of severe, invasive bacterial infection in human newborns. Neonatal infection with this opportunistic pathogen can present as earlyonset or late-onset disease. In early-onset cases, bacteria are transferred from the mother to the infant in utero, following ascending infection of the placental membranes, or during passage through the birth canal, by aspiration of infected vaginal fluids. Early-onset neonatal infection manifests within the first few hours or days of life, often presenting as pneumonia and respiratory failure, which can quickly progress to bacteraemia and septic shock. By contrast, late-onset GBS disease can occur in infants up to several months old, and is distinguished by bloodstream infection with a high rate (40-60%) of progression to meningitis (Ref. 1). Infants that survive GBS meningitis can suffer serious long-term neurological consequences, such as seizures, hearing loss and cognitive impairment. Serious GBS infections are increasingly recognised in adult populations, particularly in the elderly and individuals compromised by underlying medical conditions. More than 40% of all invasive GBS cases in the USA occur past infancy (Ref. 2).The development of GBS disease reflects successful bacterial colonisation of the vaginal epithelium, penetration of placental or epithelial barriers, resistance to immune clearance allowing bloodstream survival and, in cases of meningitis, the ability to breach the endothelial blood-brain barrier (BBB). In overcoming these obstacles, GBS expresses a diverse array of surface-associated and secreted virulence factors that mediate specific host-cell interactions and interfere with innate immune clearance mechanisms. The present review explores

Molecular characterization and virulence gene profiling of pathogenic Streptococcus agalactiae populations from tilapia (Oreochromis sp.) farms in Thailand

“…13 To confirm whether suspected isolates were GBS, bacterial DNA was extracted by standard phenol-chloroform extraction, 2 and a polymerase chain reaction (PCR) using species-specific primers targeting the16S ribosomal RNA (rRNA) gene of GBS was carried out as previously described. 19 Group B streptococci A909 (serotype Ia) was included as a positive control for the PCR assays. The relative percent isolation (RPI) of streptococcus from tilapia farms was calculated using the following formula: RPI = [(number of streptococci-positive pond)/(total sampling ponds)] × 100.…”

Small RNAs in streptococci

“…In a few cases, streptococci can cause significant infections in both man and animals. 22,23 Three species, Streptococcus pyogenes (also called Group A streptococcus), 24,25 Streptococcus pneumoniae (also known as pneumococcus), [26][27][28] and also Streptococcus agalactiae (also called Group B streptococcus), 29,30 are notable human pathogens, responsible for serious acute infections.…”

Neonatal brain infections

“…By contrast, infants with late-onset disease usually have diffuse purulent arachnoiditis [7]. These differences reflect the immaturity of the immunological response in the immediate neonatal period [13]. Subdural or subarachnoid serous effusions may result from increased permeability of capillaries and veins of the dura mater, but these are uncommon in neonates, as are purulent collections [14].…”