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The transmission through water of the disease caused by the fish pathogen, Photobacterium damselae subsp. damselae, as well as the role of the skin mucus in the initial steps of the infection, have been studied. All tested strains resisted the bactericidal activity of the mucus and showed an ability to adhere to it, but only those virulent by the intraperitoneal route were infective through water. Moribund fishes showed the typical signs of the disease: haemorrhaged areas on the body surface and ulcerative lesions with mucus degradation. These results suggest that the pathogen can be transmitted to fish through water and use the skin as a portal of entry.

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Vibrio vulnificus serovar E (formerly biotype 2) is the etiologic agent that is responsible for the main infectious disease affecting farmed eels. Although the pathogen can theoretically use water as a vehicle for disease transmission, it has not been isolated from tank water during epizootics to date. In this work, the mode of transmission of the disease to healthy eels, the portals of entry of the pathogen into fish, and their putative reservoirs have been investigated by means of laboratory and field experiments. Results of the experiments of direct and indirect host-to-host transmission, patch contact challenges, and oral-anal intubations suggest that water is the prime vehicle for disease transmission and that gills are the main portals of entry into the eel body. The pathogen mixed with food can also come into the fish through the gastrointestinal tract and develop the disease. These conclusions were supported by field data obtained during a natural outbreak in which we were able to isolate this microorganism from tank water for the first time. The examination of some survivors from experimental infections by indirect immunofluorescence and scanning electron microscopy showed that V. vulnificus serovar E formed a biofilm-like structure on the eel skin surface. In vitro assays demonstrated that the ability of the pathogen to colonize both hydrophilic and hydrophobic surfaces was inhibited by glucose. The capacity to form biofilms on eel surface could constitute a strategy for surviving between epizootics or outbreaks, and coated survivors could act as reservoirs for the disease.Vibrio vulnificus serovar E (formerly biotype 2) is a primary pathogen for eels and a secondary pathogen for humans (2, 35). As a human pathogen, this serovar probably behaves like the biotype 1 of the species, causing sporadic diseases and outbreaks in immunocompromised hosts (27,36). As an eel pathogen, this serovar causes a primary septicemia, named vibriosis, that affects captured eels maintained in farms, occasionally resulting in economic losses (5,7,8,13,18). The incidence of the vibriosis in natural populations of wild eels is unknown. In farms, the disease can suddenly appear and cause high mortality rates (7,8,13,18). After antibiotic treatment, the disease usually disappears and reappears as recurrent outbreaks that are often associated with stress factors such as changes in pH and nitrite levels (R. Barrera, personal communication). The onset of a new outbreak can be delayed by lowering water salinity, which partially inhibits the pathogen's ability to survive and spread (3, 21). However, the origin of the infection, the mode of transmission, and the reservoir between outbreaks or epizootics have yet to be determined.It has been suggested that eel-virulent strains, like the avirulent ones (biotype 1), are natural inhabitants of aquatic ecosystems (3, 21). This hypothesis is mainly based on laboratory results that demonstrate the ability of eel-virulent isolates to survive in artificial seawater microcosms for years (21) a...

The objective of this study was to evaluate the usefulness of comprehensive chromosome screening (CCS) using array comparative genomic hybridization (aCGH). The study included 1420 CCS cycles for recurrent miscarriage (n = 203); repetitive implantation failure (n = 188); severe male factor (n = 116); previous trisomic pregnancy (n = 33); and advanced maternal age (n = 880). CCS was performed in cycles with fresh oocytes and embryos (n = 774); mixed cycles with fresh and vitrified oocytes (n = 320); mixed cycles with fresh and vitrified day-2 embryos (n = 235); and mixed cycles with fresh and vitrified day-3 embryos (n = 91). Day-3 embryo biopsy was performed and analyzed by aCGH followed by day-5 embryo transfer. Consistent implantation (range: 40.5–54.2%) and pregnancy rates per transfer (range: 46.0–62.9%) were obtained for all the indications and independently of the origin of the oocytes or embryos. However, a lower delivery rate per cycle was achieved in women aged over 40 years (18.1%) due to the higher percentage of aneuploid embryos (85.3%) and lower number of cycles with at least one euploid embryo available per transfer (40.3%). We concluded that aneuploidy is one of the major factors which affect embryo implantation.