Differentiation between Staphylococcus aureus and coagulase-negative Staphylococcus species by real-time PCR including detection of methicillin resistants in comparison to conventional microbiology testing.

BACKGROUND Staphylococcus aureus has long been recognized as a major pathogen. Methicillin-resistant strains of S. aureus (MRSA) and methicillin-resistant strains of S. epidermidis (MRSE) are among the most prevalent multiresistant pathogens worldwide, frequently causing nosocomial and community-acquired infections. METHODS In the present pilot study, we tested a polymerase chain reaction (PCR) method to quickly differentiate Staphylococci and identify the mecA gene in a clinical setting. RESULTS Compared to the conventional microbiology testing the real-time PCR assay had a higher detection rate for both S. aureus and coagulase-negative Staphylococci (CoNS; 55 vs. 32 for S. aureus and 63 vs. 24 for CoNS). Hands-on time preparing DNA, carrying out the PCR, and evaluating results was less than 5 h. CONCLUSIONS The assay is largely automated, easy to adapt, and has been shown to be rapid and reliable. Fast detection and differentiation of S. aureus, CoNS, and the mecA gene by means of this real-time PCR protocol may help expedite therapeutic decision-making and enable earlier adequate antibiotic treatment.

The Plasmodium Class XIV Myosin, MyoB, Has a Distinct Subcellular Location in Invasive and Motile Stages of the Malaria Parasite and an Unusual Light Chain

Myosin B (MyoB) is one of the two short class XIV myosins encoded in the Plasmodium genome. Class XIV myosins are characterized by a catalytic "head," a modified "neck," and the absence of a "tail" region. Myosin A (MyoA), the other class XIV myosin in Plasmodium, has been established as a component of the glideosome complex important in motility and cell invasion, but MyoB is not well characterized. We analyzed the properties of MyoB using three parasite species as follows: Plasmodium falciparum, Plasmodium berghei, and Plasmodium knowlesi. MyoB is expressed in all invasive stages (merozoites, ookinetes, and sporozoites) of the life cycle, and the protein is found in a discrete apical location in these polarized cells. In P. falciparum, MyoB is synthesized very late in schizogony/merogony, and its location in merozoites is distinct from, and anterior to, that of a range of known proteins present in the rhoptries, rhoptry neck or micronemes. Unlike MyoA, MyoB is not associated with glideosome complex proteins, including the MyoA light chain, myosin A tail domain-interacting protein (MTIP). A unique MyoB light chain (MLC-B) was identified that contains a calmodulin-like domain at the C terminus and an extended N-terminal region. MLC-B localizes to the same extreme apical pole in the cell as MyoB, and the two proteins form a complex. We propose that MLC-B is a MyoB-specific light chain, and for the short class XIV myosins that lack a tail region, the atypical myosin light chains may fulfill that role.

Fault development and interaction in distributed strike-slip shear zones: an experimental approach

Analogue model experiments using both brittle and viscous materials were performed to investigate the development and interaction of strike-slip faults in zones of distributed shear deformation. At low strain, bulk dextral shear deformation of an initial rectangular model is dominantly accommodated by left-stepping, en echelon strike-slip faults (Riedel shears, R) that form in response to the regional (bulk) stress field. Push-up zones form in the area of interaction between adjacent left-stepping Riedel shears. In cross sections, faults bounding push-up zones have an arcuate shape or merge at depth. Adjacent left-stepping R shears merge by sideways propagation or link by short synthetic shears that strike subparallel to the bulk shear direction. Coalescence of en echelon R shears results in major, through-going faults zones (master faults). Several parallel master faults develop due to the distributed nature of deformation. Spacing between master faults is related to the thickness of the brittle layers overlying the basal viscous layer. Master faults control to a large extent the subsequent fault pattern. With increasing strain, relatively short antithetic and synthetic faults develop mostly between old, but still active master faults. The orientation and evolution of the new faults indicate local modifications of the stress field. In experiments lacking lateral borders, closely spaced parallel antithetic faults (cross faults) define blocks that undergo clockwise rotation about a vertical axis with continuing deformation. Fault development and fault interaction at different stages of shear strain in our models show similarities with natural examples that have undergone distributed shear.