Long-term affected flat oyster (Ostrea edulis) haemocytes show differential gene expression profiles from naïve oysters in response to Bonamia ostreae.

European flat oyster (Ostrea edulis) production has suffered a severe decline due to bonamiosis. The responsible parasite enters in oyster haemocytes, causing an acute inflammatory response frequently leading to death. We used an immune-enriched oligo-microarray to understand the haemocyte response to Bonamia ostreae by comparing expression profiles between naïve (NS) and long-term affected (AS) populations along a time series (1 d, 30 d, 90 d). AS showed a much higher response just after challenge, which might be indicative of selection for resistance. No regulated genes were detected at 30 d in both populations while a notable reactivation was observed at 90 d, suggesting parasite latency during infection. Genes related to extracellular matrix and protease inhibitors, up-regulated in AS, and those related to histones, down-regulated in NS, might play an important role along the infection. Twenty-four candidate genes related to resistance should be further validated for selection programs aimed to control bonamiosis.

Mucosal CD3ε+ cell proliferation and gut epithelial apoptosis: implications in rainbow trout gastroenteritis (RTGE).

Rainbow trout gastroenteritis (RTGE) is an emerging disease that has acquired new relevance in European rainbow trout, Oncorhynchus mykiss (Walbaum), culture, because of the economic losses it causes. Disease aetiology and pathogenesis remain unclear. The lesions appear restricted to the gastrointestinal tract where extensive mucosal detachment associated with high numbers of segmented filamentous bacteria (SFB) can be detected. In this study, an RTGE outbreak in north-western Spain was investigated, and findings observed in diseased trout were compared with control fish. PAS stain and immunohistochemical assays with anti-CD3ε and anti-active caspase-3 antibodies were performed. The results showed that CD3ε+ inflammatory infiltrates were present in the intestine of diseased trout both in the lamina propria-submucosa and within the epithelium. Moreover, an increased number of caspase-3+ cells in the intestinal mucosa and also strong anti-caspase-3 immunoreactivity in desquamated cells in the gut lumen were observed. Changes in the number of goblet cells were also found, resulting in an increase or depletion of mucous cells depending on the severity of the intestinal lesions. These findings suggest that T cells and apoptosis play an important role in the development and pathogenesis of RTGE.

Outbreak of extended-spectrum beta-lactamase producing Serratia marcescens in an intensive care unit.

Serratia marcescens has recently been identified as an important etiological agent in nosocomial infections, and is considered to be an opportunistic pathogen agent in immunosuppressed patients undergoing long periods of intensive care. Research carried out in 1991 and 1992 showed that it was of epidemiological relevance in only 1-2% of clinical isolates at the Ospedale di Circolo, Varese, Italy. However, between 7 February and 11 October 1993, the incidence of cases attributable to S. marcescens had increased to 5%; 157 strains of Serratia marcescens were isolated from clinical specimens of 43 patients admitted to an intensive care unit; these strains, characterized by epidemic spread, showed the same pattern of multiresistance to antibiotics including monobactams and oxyimino-cephalosporins. During the same period 23 isolates were also recovered from 18 patients admitted to wards other than the intensive care unit; these strains, characterized by a wide range of antibiotic susceptibility, were also sensitive to beta-lactam antibiotics with the exception of first generation cephalosporins. The production of extended-spectrum beta-lactamases (ES beta Ls) and their genetic determinism were studied. All the epidemic strains of S. marcescens resistant to ceftazidime, cefotaxime, ceftriaxone and aztreonam produced three different beta-lactamases with pI 5.4, 5.5 and 8.4 respectively. In contrast, non-epidemic strains produced only a beta-lactamase with pI 8.4. The beta-lactamase with pI 5.5 was plasmid-mediated, hydrolizing ceftazidime and aztreonam, showing it to be an ES beta L; while the beta-lactamase with pI 5.4, although plasmid-mediated, did not hydrolize monobactams or oxyimino-cephalosporins.(ABSTRACT TRUNCATED AT 250 WORDS)

Extended-spectrum beta-lactamases from Klebsiella pneumoniae strains isolated at an Italian hospital.

Eighteen strains of Klebsiella pneumoniae recently isolated from hospitalized patients were resistant or moderately resistant to oxyimino-cephalosporins (ceftazidime and/or cefotaxime), aztreonam, cefoxitin and all but one were susceptible to imipenem. Analysis of enzymes produced by these clinical isolates revealed a wide pattern of extended-spectrum beta-lactamases. All isolates produced one or more beta-lactamases that were characterized preliminarily by their isoelectric point. Strains isolated early were from patients in the Intensive Care Unit and produced an ES beta-lactamase with an apparent pI of 7.6, whereas the later isolates were from surgical and medical wards of the same hospital and produced ES beta-lactamases with apparent pI of 8.2 and 8.4, respectively. This suggests the emergence of SHV-5 and MIR-1 beta-lactamases in our hospital. Agarose gel electrophoresis of plasmid DNA revealed the presence of a similar plasmid of approximate size 60 Kb in all isolates.