National Institute of Oceanography and Fisheries, NIOF, Cairo, Egypt.
Department of Fish Biology and Ecology, Central Laboratory for Aquaculture Research, Agricultural Research Center, Abbassa, Abo-Hammad, Sharqia, 44662, Egypt.
BMC Vet Res. 2024 Apr 25;20(1):156. doi: 10.1186/s12917-024-04004-z.
The present study aimed to determine the major cause of the high mortality affecting farmed gilthead seabream (Sparus aurata) and controlling this disease condition. Fifteen diseased S. aurata were sampled from a private fish farm located at Eldeba Triangle, Damietta, fish showed external skin hemorrhages, and ulceration. Bacterial isolates retrieved from the diseased fish were identified biochemically as Pseudomonas putida and then confirmed by phylogenetic analysis of the 16 S rRNA gene sequence. P. putida was also isolated from three batches of tilapia-trash feed given to S. aurata. Biofilm and hemolytic assay indicated that all P. putida isolates produced biofilm, but 61.11% can haemolyse red blood cells. Based on the antibiotic susceptibility test results, P. putida was sensitive to florfenicol with minimum inhibitory concentrations ranging between 0.25 and 1.0 µg mL, but all isolates were resistant to ampicillin and sulfamethoxazole-trimethoprim. Pathogenicity test revealed that P. putida isolate (recovered from the tilapia-trash feed) was virulent for S. aurata with LD equal to 4.67 × 10 colony forming unit (CFU) fish. After intraperitoneal (IP) challenge, fish treated with 10 mg kg of florfenicol showed 16.7% mortality, while no mortality was recorded for the fish group that received 20 mg kg. The non-treated fish group showed 46.7% mortality after bacterial challenge. HPLC analysis of serum florfenicol levels reached 1.07 and 2.52 µg mL at the 5th -day post-drug administration in the fish groups received 10 and 20 mg kg, respectively. In conclusion, P. putida was responsible for the high mortality affecting cultured S. aurata, in-feed administration of florfenicol (20 mg kg) effectively protected the challenged fish.
本研究旨在确定导致养殖真鲷（Sparus aurata）死亡率高的主要原因，并控制这种疾病状况。从位于达米埃塔 Eldeba 三角区的一家私人养鱼场采集了 15 条患病的真鲷，这些鱼表现出皮肤外部出血和溃疡。从患病鱼中分离出的细菌经生化鉴定为恶臭假单胞菌（Pseudomonas putida），然后通过 16S rRNA 基因序列的系统发育分析得到确认。恶臭假单胞菌也从投喂给真鲷的三批罗非鱼-垃圾饲料中分离出来。生物膜和溶血试验表明，所有恶臭假单胞菌分离株都能产生生物膜，但 61.11%能溶血红细胞。根据抗生素药敏试验结果，恶臭假单胞菌对氟苯尼考敏感，最小抑菌浓度范围在 0.25 和 1.0μg mL 之间，但所有分离株均对氨苄西林和磺胺甲噁唑-甲氧苄啶耐药。致病性试验表明，恶臭假单胞菌分离株（从罗非鱼-垃圾饲料中分离得到）对真鲷具有毒力，LD 等于 4.67×10 个 CFU 鱼。经腹腔（IP）接种后，接受 10mg kg 氟苯尼考治疗的鱼死亡率为 16.7%，而接受 20mg kg 氟苯尼考治疗的鱼死亡率为 0。未经治疗的鱼组在细菌攻毒后死亡率为 46.7%。在接受 10 和 20mg kg 氟苯尼考治疗的鱼组中，第 5 天血清氟苯尼考浓度分别达到 1.07 和 2.52μg mL。综上所述，恶臭假单胞菌是导致养殖真鲷死亡率高的原因，饲料中添加氟苯尼考（20mg kg）可有效保护受感染的鱼。
