Shewanella putrefaciens, a saprophytic gram-negative rod, is infrequently recovered from clinical specimens. Although a number of clinical syndromes have been attributed to S. putrefaciens, the pathogenic role of this agent remains largely undefined. We report 16 cases of S. putrefaciens infection that occurred at the Veterans General Hospital-Kaohsiung in Taiwan between 1990 and 1995. S. putrefaciens infection was associated with a wide clinical spectrum including bacteremia/septicemia, skin and soft-tissue infection, biliary tract infection, peritonitis, and empyema. Five of our patients had skin and soft-tissue manifestations, including fulminant periorbitofacial cellulitis, dacryocystitis, perineal abscess, finger abscess, and postcholecystectomy wound infection. These clinical features deviated from the chronic ulcers or infected burns of the lower extremities that have been described in previous reports. Seven (44%) of our 16 patients had bacteremia/septicemia, and all seven had underlying hepatobiliary diseases. S. putrefaciens was isolated in mixed cultures of specimens from 14 patients; Escherichia coli was the most common coisolate. Hepatobiliary diseases and malignancy were the major predisposing factors for S. putrefaciens infection of the biliary tract and S. putrefaciens bacteremia/septicemia.

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Categories of bacteremia acquisition was associated with different distribution of pathogens, antimicrobial resistance, and clinical outcome. Traditional classification might overestimate the problem of drug resistance in community-acquired infections. The concept of health care-associated infection should be introduced to avoid overemphasis of drug-resistant problem in true community-acquired infection.

Background: Angiostrongylus cantonensis, the rat lungworm, is the major cause of eosinophilic meningitis worldwide. Rats serve as the definitive host of the nematode, but humans can be infected incidentally, leading to eosinophilic meningitis. A previous BALB/c animal study has demonstrated increased apoptotic proteins and decreased anti-apoptotic proteins in mice infected with A. cantonensis. Steroids may be an effective treatment option for eosinophilic meningitis caused by A. cantonensis, but the involved mechanism is unclear. This study hypothesized that the beneficial effects of steroids on eosinophilic meningitis are mediated by decreased apoptosis. Methods: In a BALB/c animal model, mice were orally infected with 50 A. cantonensis L3 via an oro-gastric tube and were sacrificed every week for 3 consecutive weeks after infection or until the end of the study. Dexamethasone was injected intra-peritoneally from the 7 th day post-infection until the end of the 21-day study. Evans blue method was used to measure changes in the blood brain barrier, while western blotting, immuno-histochemistry, and TUNEL assay were used to analyze brain homogenates expression of apoptotic and anti-apoptotic proteins. Results: There were increased amounts of Evans blue, apoptotic proteins (caspase-3, -8, and -9 and cytochrome C), and decreased anti-apoptotic proteins (bcl-2) after 2-3 weeks of infection. Dexamethasone administration significantly decreased Evans blue extravasations and apoptotic protein expressions. Conclusions: Apoptosis of mice brain homogenates can be repressed by dexamethasone treatment.