Koi Herpesvirus infection: etio-pathogenetic and health aspects of an emergent fish pathogen. Infezione da Koi Herpesviros: aspetti eziopatogenetici e sanitari di una malattia emergente.

Koi Herpesvirus (KHV) is a herpes-like virus now recognized as a worldwide cause of high morbidity (100%) and mortality in all ages of common carp, Cyprinus carpio, and Cyprinus carpio var. Koi, an expensive ornamental fish worldwide cultured, including Italy (4,7). Since 1997, outbreaks has occurred in Israel, USA, Germany, England, Italy, Netherlands and, more recently, in Indonesia and Japan, with severe economic losses for fish industries (1, 2, 3, 5, 7). Initial characterization of the virus showed that it resembles members of the family Herpesviridae, even if KHV is clearly different from two previously described herpes-like virus from fish, Herpesvirus cyprini (CHV) and the Channel catfish virus (CCV). Although the high host specificity, the virus has been found adapted to other close animal species. No information are available on human risk due to the contact with contaminated water or fish, but it has not to be undervalued, because few is known on KHV pathogenicity and pathogenesis (1). Experimental studies, carried out by intra-peritoneal injection route, bathing and cohabitation of sick and healthy carps, have demonstrated that the virus from a single plaque (propagated and purified) causes lethal disease killing 85 to 100% of the fish within 7-21 days, depending on water temperature (9). Immunohistochemistry, immunofluorescence and PCR analysis found a large amounts of the virus in the kidney and blood at very early time after infection but it appears in brain, liver and spleen only in the late stage of the disease, remaning not solve three aspects: the viral entry, whether through the gills or through the intestine, the propagation mechanism and the viral latency, that it has been hypothesised but not yet demonstrated. The latency could represent a very dangerous way of viral spread, because apparently health but infected animals could be commercialised from uninfected to infected aquaria. Then, intensive fish culture, koi shows, domestic and international trading, in the absence of specific sanitary laws, health certifications or inspections contribute to the rapid global spread of KHV also in common carp, the most widely cultivated fish for human consumption mainly in Asian and in Europe countries, including Italy (4). In 2002 the OIE and the EC considered the impact of KHV in relation to possible notification of the disease and it was recognised as an untreatable disease of great detrimental potential to the carp industry worl-wide (6). A presumptive diagnosis of koi disease includes observation of seasonally devastating when water temperature ranged from 17°-26°C. The fishes show lethargy, fatigue, disorientation, erratic swimming, gasping and they die within few hours since first signs appearing, but at lower temperatures the course of the disease is more protracted (10). Commonly reported clinical signs include swollen and necrotic gill filament, anorexia, enophthalmia, fin erosion, superficial haemorrhaging at the base of the fins, pale, irregular patches on the skin associated with excess mucus secretion and also decreased production of mucus in patches, leaving the epidermis with a sandpaper texture (7). The virus isolation in the koi fin cell line (KF-1 e CCB) and/or PCR analysis represent the current diagnostic approaches. However, these tools are unable to routinely detect virus or viral DNA in the tissues of suspected carriers of KHV. More recently it has been developed a real time quantitative PCR assay, Taq-man PCR and a sensitive PCR assay based on sequence of essential virulence gene of KHV that encodes a protein with significant homology to thymidine kinase (1, 4). As it is not known if these assays are suitable to detect latent KHV in carrier fish by non lethal testing on blood, faeces or other bioptic tisssues, more exhaustive studies of the pathogenesis are necessary to elucidate about the time of infection in vivo and the sites of the latent state to apply preventive plans and eradication of koi disease.