Light and electron microscopic studies were carried out on the gills of grouper (Epinephelus malabaricus) fed diets supplemented with or without crystalline ascorbic acid for 12 weeks. Fish fed the diet without ascorbic acid supplementation showed various clinical signs such as haemorrhages of fins, deformed opercula and caudal fin erosion. Histological observations of the gills of scorbutic fish showed hyperplasia of epithelial cells of primary and secondary lamellae, fusion of secondary lamellae, gill cartilage distortion and detachment of the epithelium from the basal membrane of the secondary lamellae. By electron microscopy, degeneration of chloride cells, mucous cells and epithelium cells as well as hyperplasia and edema of epithelium cells were observed.
Cross neutralization tests with serotype-specific rabbit antisera were completed for three recent Canadian isolates of aquatic birnavirus (i.e. infectious pancreatic necrosis virus, IPNV). The three virus isolates, which were serologically related to each other, significantly crossreacted (>10% relatedness) with two of the five serotypes which have been previously reported in Canada (i.e. with aquatic birnavirus provisional serotypes A7 and A8). It is suggested that the aquatic birnavirus provisional serotypes A7 and A8 are highly similar and may be geographically widespread in Canada.
Pasteurella piscicida strains resistant to florfenicol (FF), (Minimal inhibitory concentration 6.25 μg/ml) were isolated for the first time from diseased cultured yellowtail (Seriola quinqueradiata) in 1992. A transferable R plasmid encoded with resistance to FF was identified in FF resistant strains co-cultured with Escherichia coli RC85 (nal). The R plasmid also had resistance to chloramphenicol (CP), kanamycin (KM), sulfamonomethoxine (SA), and tetracycline (TC). The frequency of R plasmid transfer ranged from 10-4 to 10-6 per input donor cell for 2 h of co-cultivation with E. coli at 37°C. The R plasmid was highly homologous in DNA profiles with the R plasmids, encoding resistance to CP, KM, SA, and TC, that were detected in 1989 and 1991. The R plasmid detected in 1992 is thought to be a FF resistant determinant inserted into the R plasmid encoding resistance to CP, KM, SA, and TC.
Effects of thermal conditions on CHV infection were investigated both in vitro and in vivo. CHV multiplied in FHM cells at incubation temperatures from 10°C to 25°C, but not at 30°C, optimal temperature being 15-20deg;C. Experimental infection of CHV was done on carp fry under controlled water temperatures of 15, 20 and 25°C. The mortality of carp fry due to CHV infection was markedly high at 15°C and decreased with the increase in water temperature. A papilloma was formed after 11 weeks at all temperatures tested. A regression of the papilloma was observed by shifting water temperature from 7.5°C to 20, 25 and 30°C but no regression of papilloma was observed by the shift of water temperature from 7.5°C to 15°C.
Investigations on some biological aspects of the two species of sanguinicolid trematodes, viz. Paradeontacylix grandispinus and P. kampachi, infecting the vascular system of cultured amberjack, Seriola dumerili were conducted. In a survey of 50 naturally infected fish, P. grandispinus was the dominant of the two species. P. grandispinus mostly infected the afferent branchial arteries, while nearly half of P. kampachi infected the sinus venosus and heart. Eggs were first found in the gill filaments in November, about four 'months after introduction of amberjack seedlings to culture site. Egg numbers tended to increase until March (average egg number per gill filament : 452), and decreased toward July. Cercarial invasion to amberjack, determined by transferring fish from an endemic area to an infection-free site at different times of year, started sometime in September, suggesting that the two species of blood flukes matured about two months after invasion to fish.
Monoclonal antibody (Mab) P3C3 raised against V. vulnificus reacted with nine of thirteen V. vulnificus strains. In comparison, Mab P3F10 reacted with only three V. vulnificus strains. No cross-reactions were observed among fourteen non-V. vulnificus strains. P3C3 and P3F10 isotypes were characterized as IgG1k. When examined via an indirect fluorescent antibody procedure, epitopes that were recognized by the P3C3 and P3F10 Mabs were found to be on the cell surface. Results of an additivity test suggest that these two epitopes are at different positions on the cell surface. The number of P3F10 epitopes on the TG617 strain was larger than the number of P3C3 epitopes. In addition, the former. was probably physically more accessible than the latter. The resultant additive index suggested that the binding of Mab P3F10 to its corresponding epitopes interferes in three dimensions with the binding of Mab P3C3 to its epitopes; however, the reverse is not true. Epitope P3C3 was shown to be a protein with a molecular weight of 40 kDa, but epitope P3F10 was shown to be a glycopeptide with a molecular weight ranging from 10 to 21 kDa.