Silver Sea Bream Sparus Sarba Research Articles

Rapid changes in renal morphometrics in silver sea bream Sparus sarba on exposure to different salinities

The kidney histology of silver sea bream Sparus sarba adapted to different salinities was studied. Renal glomeruli in silver sea bream were grouped into clusters and two distinct types of glomeruli could be discerned. Expanded glomeruli were highly vascular, probably related to an active filtering role, while collapsed glomeruli had a shrunken appearance, probably related to an abated filtering role. Collecting tubules were lined by tall columnar cells and were more prominent and muscular in hypo‐osmotic media. Chronic adaptation across a broad spectrum of salinities (0, 6, 12, 33 and 50) caused significant modifications in renal morphology. In hypo‐osmotic media, a significant increase in glomerular number, size and percentage expanded glomeruli were found, which could facilitate water excretion. Collecting tubules exhibited an increase in thickness, diameter and muscularity that tended to favour a faster glomerular filtrate flow upon hypo‐osmotic adaptation. Abrupt hypo‐osmotic exposure induced rapid changes in the morphology of renal tubules. There was an increase in diameter and thickness of collecting tubules, suggesting increased glomerular filtrate flow was stimulated by hypo‐osmotic exposure. The data suggested that the rapid change in kidney morphology is one of the osmoregulatory strategies of silver sea bream that may contribute to its ability to withstand abrupt hypo‐osmotic challenge. A fast‐acting mechanism that could be triggered within several hours could reorganize silver sea bream kidney so that the renal machinery is highly responsive to changes in environmental salinities.

Modulated heat shock protein expression during pathogenic Vibrio alginolyticus stress of sea bream

The effects of infective Vibrio alginolyticus and its extracellular product (ECP) on host fish function are not well understood. In this study a partial biochemical characterization of the ECP from an infective strain of V. alginolyticus isolated from diseased silver sea bream Sparus sarba was achieved and the effects of live V. alginolyticus and ECP on hepatic heat shock protein (hsp) expression was compared. The ECP fraction was found to contain several hydrolytic enzymes including both haemolytic and proteolytic activities. Intramuscular administration of ECP to sea bream resulted in vibriosis with similar pathological signs as those observed with live V. alginolyticus administration. Using quantitative immunoassays we assessed the levels of the major hsp families, hsp90, hsp70 and hsp60, in hepatic tissue of diseased sea bream between 12 and 48 h post-infection. Throughout the infective period, live V. alginolyticus did not alter hsp90 whereas ECP significantly reduced hepatic hsp90 during the late stages of acute infection. The levels of hsp70 were found to be rapidly and drastically increased with both live V. alginolyticus and ECP. The transcript levels of both gene members of the hsp70 family (hsc70 and hsp70) were significantly increased with both live V. alginolyticus and ECP. The levels of hsp60 remained unchanged with both live V. alginolyticus and ECP. The data presented in this study is the first report describing an effect of both live V. alginolytus and ECP on hsp expression in diseased fish.

Invasion Route and Pathogenic Mechanisms of Vibrio alginolyticus to Silver Sea Bream Sparus sarba

AbstractPotential routes of invasion and associated pathogenic mechanisms of a pathogenic strain of Vibrio alginolyticus (Vib‐01) to silver sea bream Sparus sarba were evaluated. Inoculation of V. alginolyticus into juvenile silver sea bream via the intramuscular, intraperitoneal, injury–immersion, and simple immersion routes resulted in 14‐d LD50 values (concentrations lethal to half the group studied) of 4.85 × 104 colony‐forming units [cfu]/fish, 5.01 × 105 cfu/fish, 3.16 × 106 cfu/mL and more than 2.5 × 108 cfu/mL, respectively. These findings suggest that the integrity of the fish integument is important for protecting fish against vibriosis, such that invasion through integumental breaches would be the main invasive mode of this bacterium to silver sea bream. Phagocytic activities of splenic and pronephric macrophages were significantly increased at the early stages of infection but declined significantly as infection progressed (after 24 or 36 h). The spleen and head kidney of fish inoculated with Vib‐01 bacteria exhibited high bacterial counts accompanied by a decline in the phagocytic potential of the macrophages taken from both organs. Sea bream infected with V. alginolyticus exhibited significant decreases in red blood cell count, hematocrit, hemoglobin, serum glucose, and protein. Total leukocyte count increased at the early stages of infection but declined as infection became advanced. The destruction of critical components of both the circulatory and immune systems by V. alginolyticus could be the main cause of mortality in vibriosis. Extracellular products (ECPs) of the present V. alginolyticus isolate were toxic not only to silver sea bream but also to cultured fibroblast cells derived from sea bream fin tissue. The 14‐day LD50 of ECPs to sea bream was 0.92 μg per gram of fish weight. Our data suggest an involvement of the ECPs, especially their hydrolytic and hemolytic components, in the invasive and proliferative processes of the bacteria in silver sea bream.

The response of sea bream following abrupt hyposmotic exposure

The response of a marine teleost, silver sea bream Sparus sarba, to abrupt hyposmotic exposure was investigated over a 120‐h period following direct exposure from sea water (SW, 33‰) to a hyposmotic environment of 6‰. Aspects of serum chemistry, stored metabolites and gill morphology were used to gain further insight into the biochemical, physiological and morphological alterations that take place following low salinity exposure of a marine fish. Rapid (<1 h) reductions in serum [Cl−] occurred while serum [Na+] exhibited only transient perturbations during initial exposure. Serum total [Ca] declined 24 h after exposure and returned to pre‐exposure levels by 120 h. Despite a tendency for muscle moisture to increase during the early stages of low salinity exposure to significant change could be detected. The response of the branchial chloride cell (CC) was rapid, with apical and fractional exposure area increasing after 6 h. The number of CCs exposed at the branchial surface reduced after 6 h but subsequently increased to elevated levels. Serum cortisol levels had increased three fold 1 h after hyposmotic exposure and stabilised at pre‐exposure levels within 12–24 h. Serum triiodothyronine (T3) levels exhibited a biphasic response, significantly elevating and decreasing after 3 and 6 h respectively. Significant post‐hyposmotic exposure elevations in serum glucose and protein occurred after 1 h, peaking at 3 h and returning to lower levels after 6 h. Total free ninhydrin reactive substances were significantly elevated 3 h post‐hyposmotic exposure, a phenomenon attributable to elevated levels of ammonia, alanine, arginine, glycine, isoleucine, lysine, methionine, phenylalanine, serine, taurine, threonine and valine. Of these substances, glycine, lysine, serine and taurine remained elevated for up to 12 h or longer. Serum urea levels elevated 1 h after exposure to 6%‰ and returned to SW levels 3 h post‐exposure. The relevance of these results is discussed within the context of current knowledge on the effects of hyposomotic adaptation on marine fish.

Study of toxicity and bioaccumulation of copper in the silver sea bream Sparus sarba

The toxicity and bioaccumulation of copper were studied in fingerlings (mean body weight = 9.4±2.1 g) and subadults (mean body weight = 85.5±27.1 g) of the silver sea bream Sparus sarba. Test fish were obtained from local fish culture sites. Static tests over 96 h showed that subadults were not more tolerant to copper than the much smaller fingerlings. The 24-h, 48-h, 72-h, and 96-h LC50 for fingerlings were 2.01 mg Cu L −1, 1.28 mg Cu L −1, 1.17 mg Cu L −1, and 1.03 mg Cu L −1, respectively. The values for subadults were 2.36 mg Cu L −1, 1.52 mg Cu L −1, 1.34 mg Cu L −1, and 1.24 mg Cu L −1, respectively. Copper concentrations corresponding to 13%, 25%, and 40% of the 96-h LC50 value were used to study the effects of copper exposure on the growth rate of S. sarba in 30-d bioassays. The growth rate of fingerlings was higher than that of subadults by approximately a hundred-fold. For both fingerlings and subadults, reduced growth was observed at 0.15 mg Cu L −1 (∼40% of the 96-h LC50 value). Growth appeared to be a more sensitive endpoint for toxicity tests than mortality. Fish exposed to copper for 30 d contained more copper than control animals. The highest copper concentrations for both fingerlings and subadults were found in the intestine. The order of copper concentration was intestine > liver > gonad > gills, skin and muscle.