Digalactoside expression in the lipopolysaccharide of Haemophilus influenzae and its role in intravascular survival.

Digalactoside (galalpha-1-4 galbeta) structures of the lipopolysaccharide (LPS) of Haemophilus influenzae are implicated in virulence. A confounding factor is that tetranucleotide repeats within the lic2A, lgtC, and lex2 genes mediate phase-variable expression of the digalactosides. By deleting these repeats, we constructed recombinant strains of RM153 constitutively expressing either one or two LPS digalactosides.

Genetic islands of Streptococcus agalactiae strains NEM316 and 2603VR and their presence in other Group B streptococcal strains.

Background: Streptococcus agalactiae (Group B Streptococcus; GBS) is a major contributor to obstetric and neonatal bacterial sepsis. Serotype III strains cause the majority of late-onset sepsis and meningitis in babies, and thus appear to have an enhanced invasive capacity compared with the other serotypes that cause disease predominantly in immunocompromised pregnant women. We compared the serotype III and V whole genome sequences, strains NEM316 and 2603VR respectively, in an attempt to identify genetic attributes of strain NEM316 that might explain the propensity of strain NEM316 to cause late-onset disease in babies.

Bacterial virulence factors in neonatal sepsis: group B streptococcus.

Purpose Of Review: Group B streptococcus is a leading cause of neonatal pneumonia, septicaemia and meningitis. Up to one quarter of women in labour are now given intravenous antibiotics to prevent early-onset disease by the organism, a situation that will remain constant until a successful vaccine is available. From a molecular understanding of the pathogenicity of group B streptococcus we may be able to devise novel means for controlling disease, such as identifying inhibitors of key metabolic pathways or regulatory networks.

Evidence for extensive transmission distortion in the human genome.

It is a basic principle of genetics that each chromosome is transmitted from parent to offspring with a probability that is given by Mendel's laws. However, several known biological processes lead to skewed transmission probabilities among surviving offspring and, therefore, to excess genetic sharing among relatives. Examples include in utero selection against deleterious mutations, meiotic drive, and maternal-fetal incompatibility.