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The mechanisms underlying exercise-induced neuroprotective effects after traumatic brain injury (TBI) remained elusive, and there is a lack of effective treatments for TBI. In this study, we investigated the effects of an integrative approach of exercise and Yisaipu (TNFR-IgG fusion protein, TNF inhibitor) in a mouse TBI model. Male C57BL/6J mice were randomly assigned to a sedentary group or a group that followed a voluntary exercise regimen. The effects of 6-week prophylactic preconditioning exercise (PE) alone or in combination with post-TBI Yisaipu treatment on moderate TBI associated deficits were examined. The results showed that combined treatments of PE and post-TBI Yisaipu were superior to single treatments on reducing sensorimotor and gait dysfunctions in mice. These functional improvements were accompanied by reduced systemic inflammation largely via decreased serum TNF-α, boosted autophagic flux, and mitigated lesion volume after TBI. Given these neuroprotective effects, composite approaches such as a combination of exercise and TNF inhibitor may be a promising strategy for facilitating functional recovery from TBI and are worth further investigation.

To determine the distribution and antimicrobial drug resistance in bacterial pathogens causing nosocomial infections, surveillance data on nosocomial infections documented from 1981 to 1999 at National Taiwan University Hospital were analyzed. During this period, 35,580 bacterial pathogens causing nosocomial infections were identified. Candida species increased considerably, ranking first by 1999 in the incidence of pathogens causing all nosocomial infections, followed by Staphylococcus aureus and Pseudomonas aeruginosa. Candida species also increased in importance as bloodstream infection isolates, from 1.0% in 1981-1986 to 16.2% in 1999. The most frequent isolates from urinary tract infections were Candida species (23.6%), followed by Escherichia coli (18.6%) and P. aeruginosa (11.0%). P. aeruginosa remained the most frequent isolates for respiratory tract and surgical site infections in the past 13 years. A remarkable increase in incidence was found in methicillin-resistant S. aureus (from 4.3% in 1981-1986 to 58.9% in 1993-1998), cefotaxime-resistant E. coli (from 0% in 1981-1986 to 6.1% in 1993-1998), and cefotaxime-resistant Klebsiella pneumoniae (from 4.0% in 1981-1986 to 25.8% in 1993-1998). Etiologic shifts in nosocomial infections and an upsurge of antimicrobial resistance among these pathogens, particularly those isolated from intensive care units, are impressive and alarming.

To understand quinupristin-dalfopristin resistance among clinical isolates of gram-positive bacteria in Taiwan, where this agent is not yet available for clinical use, we evaluated 1,287 nonduplicate isolates recovered from January 1996 to December 1999 for in vitro susceptibility to quinupristin-dalfopristin and other newer antimicrobial agents. All methicillin-susceptible Staphylococcus aureus (MSSA) isolates were susceptible to quinupristin-dalfopristin. High rates of nonsusceptibility to quinupristin-dalfopristin (MICs, ≥2 μg/ml) were demonstrated for the following organisms: methicillin-resistant S. aureus (MRSA) (31%), coagulase-negative staphylococci (CoNS) (16%), Streptococcus pneumoniae (8%), viridans group streptococci (51%), vancomycin-susceptible enterococci (85%), vancomycin-resistant Enterococcus faecalis (100%), vancomycin-resistant Enterococcus faecium (66%), Leuconostoc spp. (100%), Lactobacillus spp. (50%), and Pediococcus spp. (87%). All isolates of MSSA, MRSA, S. pneumoniae , and viridans group streptococci were susceptible to vancomycin and teicoplanin. The rates of nonsusceptibility to vancomycin and teicoplanin were 5 and 7%, respectively, for CoNS, ranging from 12 and 18% for S. simulans to 0 and 0% for S. cohnii and S. auricularis . Moxifloxacin and trovafloxacin had good activities against these isolates except for ciprofloxacin-resistant vancomycin-resistant enterococci and methicillin-resistant staphylococci. In Taiwan, virginiamycin has been used in animal husbandry for more than 20 years, which may contribute to the high rates of quinupristin-dalfopristin resistance.

Objectives:To describe the epidemiology of vancomycin-resistant enterococci (VRE) in a university hospital in Taipei, Taiwan.Design:Retrospective review over a 27-month period, from March 1996 to May 1998.Setting:A tertiary-care teaching hospital in Taiwan.Participants:Patients with VRE isolated from any body site.Methods:Patients were identified through hospital microbiology and infection control records. Patient charts were reviewed for clinical and epidemiology data, including age, gender, previous hospital admissions, underlying diseases, types of infection, and recent antibiotic use. VRE isolates were characterized by their typical biochemical reactions, cellular fatty acid profiles, and the presence ofvangenes. Antibiotypes using the E-test and randomly amplified polymorphic DNA (RAPD) patterns of these isolates were used to determine the clonality.Results:Twenty-five isolates of VRE recovered from 12 patients were identified. One patient with a perianal abscess had 12 isolates of VRE (4Enterococcus faecalis, 7Enterococcus faecium, and 1Enterococcus casseliflavus) recovered from perianal lesions. Among 3 patients who were hospitalized in the same room, 1 had a community-acquired cellulitis over the left leg caused byE faecalis, and the other 2 patients both had anal colonization with 2 isolates ofE faecalis. The other 8 patients had 1E faecalisisolate each from various clinical specimens. All isolates possessed vanA resistance phenotype andvanAgenes. Different antibiotypes and RAPD patterns of the isolates from different patients excluded the possibility of nosocomial spread at the hospital.Conclusions:Multiple species of VRE (E faecalis, E faecium, andE casseliflavus) and multiple clones ofE faeciumcould colonize or infect hospitalized patients. In addition, clones of VRE can persist long-term in patients' lower gastrointestinal tracts. These results extend our knowledge of the coexistence and the persistence of multiple species and multiple clones of VRE in hospitalized patients.

From 7 to 24 March 1997, four patients developed Pseudomonas fluorescens bacteremia at the hospital; one on the oncology ward and the other three in the chemotherapy room. These patients all had underlying malignancies and had the Port-A-Cath (Smiths Industries Medical Systems, Deltec, Inc., St. Paul, Minn.) implants. Three patients had primary bacteremia, and one had Port-A-Cath-related infection. None of these patients had received a blood transfusion before the episodes of bacteremia. All patients recovered: two received antimicrobial agents with in vitro activity against the isolates, and the other two did not have any antibiotic treatment. A total of eight blood isolates were recovered from these patients during the febrile episodes that occurred several minutes after the infusion of chemotherapeutic agents via the Port-A-Cath. These isolates were initially identified as P. fluorescens or Pseudomonas putida (four), Burkholderia ( Ralstonia ) pickettii (three), and a non-glucose-fermenting gram-negative bacillus (one) by routine biochemical methods and the Vitek GNI card. These isolates were later identified as P. fluorescens on the basis of the characteristic cellular fatty acid chromatogram and the results of supplemental biochemical tests. The identification of identical antibiotypes by the E test and the random amplified polymorphic DNA patterns generated by arbitrarily primed PCR of the isolates showed that the outbreak was caused by a single clone of P. fluorescens . Surveillance cultures of the possibly contaminated infusion fluids and disinfectants, which were performed 7 days after recognition of the last infected patient, failed to isolate P. fluorescens . This report of a small outbreak caused by P. fluorescens suggests that timely, accurate identification of unusual nosocomial pathogens is crucial for early initiation of an epidemiological investigation and timely control of an outbreak.

Brain abscesses are occasionally associated with a dental source of infection. An unusual case of frontal lobe abscess in a nonimmunocompromised child infected with multidrug-resistant Capnocytophaga ochracea is described and confirms the pathogenic potential of this organism to cause human disease in the central nervous system.

We report a case of persistent bacteraemia caused by a single clone of Burkholderia cepacia with unusual characteristics. Six isolates of B. cepacia were recovered from a patient with acute myeloid leukaemia and chemotherapy-induced neutropenia within a 3-week period. All six isolates were initially incompletely identified as B. cepacia with the API 20NE system. The further use of cellular fatty acid analysis and PCR-restriction fragment length polymorphism of the 16S rDNA confirmed the identification. These isolates also displayed an identical but unusual antibiotype. The identical cellular fatty acid profiles and genomic typing generated by random amplified polymorphic DNA identified theseisolates as derivatives of a single strain.

From December 1997 to March 1998, 25 methicillin-resistant Staphylococcus aureus (MRSA) isolates exhibiting negative Staphylase (Oxoid Ltd., Basingstoke, England) reactions were identified from various clinical specimens from 13 patients in six intensive care units (ICUs) or in wards following a stay in an ICU at the National Taiwan University Hospital. The characteristics of these isolates have not been previously noted in other MRSA isolates from this hospital. Colonies of all these isolates were grown on Trypticase soy agar supplemented with 5% sheep blood and were nonhemolytic and unpigmented. Seven isolates, initially reported as Staphylococcus haemolyticus (5 isolates) and Staphylococcus epidermidis (2 isolates) by the routine identification scheme and with the Vitek GPI system (bioMerieux Vitek, Inc., Hazelwood, Mo.), were subsequently identified as S. aureus by positive tube coagulase tests, standard biochemical reactions, and characteristic cellular fatty acid chromatograms. The antibiotypes obtained by the E test, coagulase types, restriction fragment length polymorphism profiles of the staphylococcal coagulase gene, and random amplified polymorphic DNA patterns generated by arbitrarily primed PCR of the isolates disclosed that two major clones disseminated in the ICUs. Clone 1 (16 isolates) was resistant to clindamycin and was susceptible to trimethoprim-sulfamethoxazole (TMP-SMZ) and was coagulase type II. Clone 2 (eight isolates) was resistant to clindamycin and TMP-SMZ and was coagulase type IV. These two epidemic clones from ICUs are unique and underline the need for caution in identifying MRSA strains with colonial morphologies not of the typical type and with negative Staphylase reactions.

From January 1995 to September 1996, 14 isolates of Sphingomonas paucimobilis, including 11 from clinical specimens from six patients with nosocomial infection and three from environmental sources, were collected. Two of the six patients had intravascular catheter-related bacteremia and one each had bacteremic biliary tract infection, urinary tract infection, ventilator-associated pneumonia, and wound infection. The S. paucimobilis isolates were identified according to biochemical profiles established with use of the API 20NE system and Vitek GNI card and the characteristic cellular fatty acid chromatogram. Ten biotypes, 11 antibiograms (by the Etest), and 12 random amplified polymorphic DNA (RAPD) patterns (by arbitrarily primed polymerase chain reaction) were identified. The identical biotype, antibiogram, and RAPD pattern of the two isolates (one each from blood and bile) from a patient with biliary tract infection indicated the invasiveness of the organism. Two patients with intravascular catheter-related bacteremia had isolates of this organism repeatedly recovered, and these isolates had heterogeneous RAPD patterns. The present study highlights the wide distribution in hospital environments of various clones of S. paucimobilis, which may cause recurrent infections by a single strain or several episodes of infection due to two or more clones of this organism in hospitalized patients.