Outbreaks of koi sleepy disease (KSD) caused by carp edema virus (CEV) may seriously affect populations of farmed common carp, one of the most important fish species for global food production. The present study shows further evidence for the involvement of CEV in outbreaks of KSD among carp and koi populations: in a series of infection experiments, CEV from two different genogroups could be transmitted to several strains of naïve common carp via cohabitation with fish infected with CEV. In recipient fish, clinical signs of KSD were induced. The virus load and viral gene expression results confirm gills as the target organ for CEV replication. Gill explants also allowed for a limited virus replication in vitro. The in vivo infection experiments revealed differences in the virulence of the two CEV genogroups which were associated with infections in koi or in common carp, with higher virulence towards the same fish variety as the donor fish. When the susceptibility of different carp strains to a CEV infection and the development of KSD were experimentally investigated, Amur wild carp showed to be relatively more resistant to the infection and did not develop clinical signs for KSD. However, the resistance could not be related to a higher magnitude of type I IFN responses of affected tissues. Despite not having a mechanistic explanation for the resistance of Amur wild carp to KSD, we recommend using this carp strain in breeding programs to limit potential losses caused by CEV in aquaculture.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-017-0416-7) contains supplementary material, which is available to authorized users.
ABSTRACT:The first outbreaks of a disease connected with high mortality of common carp and koi carp caused by koi herpesvirus (KHV) were reported in 1998 in Israel and in the United States. Since then, several cases have been confirmed all over the world. At present, this viral disease is considered to be one of the most risky factors affecting populations of common carp and koi carp. Affected fish become disoriented and swim erratically with high breathing frequency, swollen gills and partially local skin lesions. The virus was isolated from the tissues of fish showing signs of the disease and subsequently cultured on koi fin (KF-1) cells. Electron microscopic examinations revealed morphological signs identical with viruses of the family Herpesviridae. Analysis of virion polypeptides and gene DNA showed the differences between KHV and the well-known herpesvirus of cyprinids, Herpesvirus cyprini (CHV), and Channel catfish virus (CCV). Water temperature is a factor influencing the onset and severity of disease. Fish seem most susceptible at water temperatures of 18-28°C, no morbidities occur at 13°C and 30°C. At present, diagnosis of KHV is mainly based on detection of viral DNA by PCR method.
The aim of the study was to investigate acute toxicity of clove oil for rainbow trout and, using values of haematological and biochemical profiles of blood and histological tissue examinations, to assess the effects of the fish exposure to that anaesthetic. Acute toxicity values of clove oil for rainbow trout found were 10 min LC50 81.1 mg·l -1 ; 10 min LC0.1 63.9 mg·l -1 ; 10 min LC99.9 100.1 mg·l -1 ; 96 h LC50 14.1 mg·l -1 ; 96 h LC0.1 12.5 mg·l -1 , and 96 h LC99.9 16.2 mg·l -1 .Clove oil anaesthesia had no effect on the heamatological profile of blood. A significant increase in the concentration of glucose (GLU) and ammonia (NH 3 ), and a significant decrease in the aspartate aminotransferase (AST) activity following a 10 min anaesthesia were found. A significantly decreased AST activity was also found 24 h after anaesthesia. Clove oil anaesthesia had no effect on other biochemical indices.Histological examination of the fish following anaesthesia revealed sporadic ectasia in gill lamellae 24 h after anaesthesia in 20% of fish. No histopathological changes were demonstrated in other tissues (liver, spleen, cranial and caudal kidneys).Results of the examinations suggest that the use of clove oil at a concentration of 30 mg·l -1 does not cause irreversible damage in rainbow trout.
ABSTRACT:The aim of the study was to investigate acute toxicity of clove oil for common carp and, using values of haematological and biochemical profiles of blood and histological tissue examinations, to assess the effects of the fish exposure to that anaesthetic. Acute toxicity values of clove oil for carp were found 10 minLC50 74.3 mg/l; 10minLC0.1 51.6 mg/l; 10minLC99.9 110.1 mg/l; 96hLC50 18.10 mg/l; 96hLC0.1 15.45 mg/l; and 96hLC99.9 19.80 mg/l. The fish were divided into four groups for haematological and biochemical examinations of blood and histological examinations of tissues. The groups were Control I (before the anaesthetic administration), Experiment I (immediately after 10 min anaesthesia at the concentration of 30 mg/l), Experiment II (24 hrs after 10 min anaesthesia) and Control II (controls examined in parallel with Experiment II). A total of 40 carp were examined. Clove oil anaesthesia had not effect on the haematological profile. The 10-min exposure to clove oil at a concentration of 30 mg/l caused a significant (P < 0.01) increase in the concentration of glucose (GLU) and inorganic phosphate (PHOS) immediately after anaesthesia. Clove oil anaesthesia had not effect on other biochemical indices. Histological examination showed capillary ectasia of gill filaments immediately after clove oil anaesthesia. Twenty-four hours after anaesthesia, no ectasia was observed. No histopathological changes were demonstrated in other tissues following anaesthesia. Results of the examinations suggest that the use of clove oil at a concentration of 30 mg/l does not cause irreversible damage in carp.
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