پديد آورندگان :
ZORRIEHZAHRA M.J. نويسنده , NAKAI T. نويسنده , Sharifpour I. نويسنده , KAW GOMEZ D. نويسنده , SHAU CHI C. نويسنده , SOLTANI M. نويسنده , MOHD DAUD H.HJ نويسنده , SHARIF ROHANI M. نويسنده , SAIDI A.A. نويسنده
چكيده لاتين :
Abstract: An acute mortality caused by an uncertain agent occurred in wild golden
grey mullet (Lim auratus) population in the Iranian side of the Caspian Sea in
February, 2004. Clinical signs of the moribund fish were erratic behavior such as
spiral swimming, belly-up at rest and over inflation of swim bladder. Histological
examination of brain of dead fish revealed hyperaemia, degeneration and necrosis in
external granular layers as well as focal extensi on in intestine. Severe leucopenia wasalso observed. No putative causal factors were suggested by bacter iological,
parasitological or environmental examinations. In virological examina-tions,
however brains of affected golden grey mullet were positive in the reverse
transcriptase-polyrnerase chain reaction test for piscine nodavirus (Nodaviridae,
Betanodavirusי[; the causative agent of Encephalopathy and retinopathy (VER),
otherwise known as viral nervous necrosis (VNN) in a variety of cultured marine
fishes worldwide. Nucleotide sequence of the PCR amplicons is closely related with
the coat protein gene of piscine nodaviruses, particularly redspotted grouper nervous
necrosis virus (RGNNV). Although, it was not succeeded to isolate the virus,
experimental infection with the brain homogenates of the affected fish in sevenband
grouper (Epinephelus septemfasciatus), which is highly susceptible to RGNNV,
produced neuro- logical abnormality followed by mortality. These results suggest
that the mortality observed in golden grey mullet in the Caspian Sea might have been
associated with piscine nodavirus infection .