The total number of persons infected or colonised with vancomycin-resistant enterococci mandatorily reported to the Swedish Institute for Infectious Disease Control increased dramatically during 2007 and 2008. During a period of twenty months from 1 July 2007 to 28 February 2009, a total of 760 cases were reported compared with 194 cases reported during the entire period from 2000 to 2006. This rise was mainly attributed to a wide dissemination of vancomycin resistant enterococci which started in a number of hospitals in Stockholm in the autumn of 2007 and was followed by dissemination in various healthcare facilities (hospitals and homes for the elderly) in a further two Swedish counties in 2008. The majority of the cases (97%) were acquired in Sweden and among these, healthcare-acquired E. faecium vanB dominated (n=634). The majority of these isolates had identical or closely related pulsed-field gel electrophoresis patterns indicating clonal dissemination in the affected counties. The median minimum inhibitory concentration of vancomycin was 32 mg/L (ranging from 4 to >128 mg/L) and of teichoplanin 0.12 mg/L (ranging from 0.06 to 0.25 mg/L). Particular emphasis was placed on countermeasures such as screening, contact tracing, cleaning procedures, education in accurate use of infection control practices as well as increasing awareness of hygiene among patients and visitors. With these measures the dissemination rate decreased substantially, but new infections with the E. faecium vanB strain were still detected.

It was previously found that Arcanobacterium haemolyticum, which can cause tonsillitis with exanthema, is not eradicated from the pharynx by administration of phenoxymethylpenicillin, despite minimum inhibitory concentration values of 0.015-1.0 micrograms/ml. Therefore, recent clinical isolates were studied for penicillin tolerance by using a disk diffusion screening test and a pour plate assay. Macrobroth dilution minimum inhibitory and bactericidal concentrations and antibiotic kill kinetics were determined for 4 isolates. Tolerance was present in 38 of 40 clinical isolates with the disk diffusion assay. With the pour plate assay all 40 isolates were tolerant, 34 of them highly tolerant. The presence of the tolerant phenotype was confirmed by macrobroth dilution assays. It is concluded that A. haemolyticum is often penicillin-tolerant, suggesting that phenoxymethylpenicillin administration would be ineffective in eradicating A. haemolyticum from the pharynx.

We have previously reported that a wild strain of Francisella tularensis is much less efficiently killed by human polymorphonuclear leukocytes than is an attenuated strain. In the present study, the killing of the attenuated strain was found to be strictly oxygen dependent. The wild and the attenuated strains both induced a respiratory burst in the leukocytes. The difference between the strains in susceptibility to agents produced at the burst could be explained by a difference in susceptibility to hypochlorous acid.

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Encapsulated Streptococcus pneumoniae of serotypes 2, 9N, 14, 21, and 23F and an unencapsulated variant of type 2 pneumococci were efficiently phagocytosed by both aerobically and anaerobically incubated human leukocytes. In the presence of 02, the pneumococci rapidly lost their viability, whereas during anaerobiosis, killing was considerably delayed. Type 14 pneumococci radiolabeled with [14C]choline or [14C]ethanolamine for cell wail teichoic acid, [14C]uracil for nucleic acids, or [14C]arachidonic acid for unsaturated cytoplasmic membrane lipids were used in studies of the fate of bacterial macromolecules after phagocytosis. The degradation of teichoic acid, RNA, and DNA during anaerobiosis approached that recorded in air at 60 min of incubation (45 to 70% and 55 to 75%, respectively). In contrast, the marked loss of [14C]arachidonic acid from pneumococcal membrane lipids observed in aerobic leukocytes did not occur during anaerobic incubation. Hence, lipid peroxidation could be involved in the rapid aerobic leukocyte killing of pneumococci, whereas a different leukocyte function of as yet unknown nature appears to be responsible for the killing seen in anaerobiosis. Autolysis-resistant type 14 pneumococci were obtained by substituting ethanolamine for choline in a defined culture medium. Differences between such bacteria and normal (autolytic) pneumococci in their killing and degradation by leukocytes were not detected in either the presence or the absence of 02. The aerobic and anaerobic handling of phagocytosed pneumococci by human blood leukocytes thus proceeded independently of the bacterial autolytic system.