155 research outputs found

    Zieke koi gevaar voor wilde karpers

    Get PDF
    Ontstoken, slijmerige kieuwen, ingevallen ogen en huidwondjes. Het zijn enkele van de ziekteverschijnselen van het koi herpesvirus (KHV). Sierkoi en gewone karpers kunnen er binnen een week aan sterven. “Er zijn veel ziektegevallen in achtertuinvijvers, bij sierkoi. In wilde karper hebben we het nog niet aangetoond, maar dat is een kwestie van tijd”, zegt Olga Haenen van het Vis- en chelpdierziektenlaboratorium van het Centraal Veterinair Instituu

    Epizoötisch Ulceratief Syndroom, EUS, in de Zambezi Rivier

    Get PDF
    Epizootic Ulcerative Syndrome (EUS) is een schimmelziekte (een oömyceet) van vis, bekend als Aphanomyces invadans of A. piscicida. het is een aangifteplichtige ziekte voor de OIE en de EU, en is nog exotisch voor de Europese Unie. Meer dan 50 vissoorten zijn gevoelig voor deze ziekte. Vooralsnog is de ziekte onschadelijk voor de men

    Visziekten in Nederland, een terugblik: 20 jaar diagnoses bij het visziektenlaboratorium

    Get PDF
    Enkele in Nederland veel voorkomende ziekten bij vissen van de afgelopen twintig jaar. Eel Virus European, Eel Virus European X, Herpesvirus van Paling, Infectieuze Hematopoietische Necrose, Infectieuze Pancreatische Necrose, Koi Herpes Virus, Snoekvirus, Spring Viremia of Carp, Virale Hemorrhagische Septicaemie en Vissen-TBC zijn daar enkele voorbeelden va

    Meercellige parasieten: metazoën (10)

    Get PDF
    Meercellige visparasieten: parasitaire vissoorten: cyclostomata (kaakloze, rondmuilige vissen): rivierprik en zeepri

    Zomerziekten in de visvijver

    Get PDF
    Met het stijgen van de watertemperatuur in het voorjaar komt ook het metabolisme van de vis op gang. Veel vissoorten paaien bovendien in het voorjaar of de vroege zomer, dus ook hormonaal verandert er van alles. Dit hoort bij een natuurlijke gang van zaken maar geeft ook stress aan de vis. Stress is een basis voor ziekte. Welke ziekten kunnen we zoal aantreffen in de buitenvijver met het stijgen van temperatuur naar zomerse waarden

    Visvirussen

    Get PDF
    In dit eerste deel een algemene inleiding over visvirusse

    Anguillicola crassus (Nematoda, Dracunculoidea) infections of European eel (Anguila anguilla) in the Netherlands : epidemiology, pathogenensis and pathobiology

    Get PDF
    In the 1980s an eel parasitic nematode, Anguillicola crassus (Nematoda, Dracunculoidea), which infects the swimbladder of European eels ( Anguilla anguilla ) and other freshwater fish species, was introduced into The Netherlands. This thesis describes the epidemiology, pathogenesis, and pathobiology of the parasitic infection.Originating from Southeast Asia, the parasite caused severe swimbladder lesions in European eels soon after its introduction: dilation of blood vessels, inflammation and rupture of the swimbladder in both wild and farmed eels, often resulting in severe fibrosis of the swimbladder ( chapter 2 ). High prevalences of infection were recorded (80 to 100% in 1987 in Dutch inland waters). Elvers became infected directly after entering the freshwater. Furthermore, the parasite was able to reach adulthood in the swimbladder lumen of these small eels. Infected farmed eels were particularly susceptible to secondary bacterial infections, which caused additional mortalities.When fish from Dutch lakes were subsequently investigated for A. crassus ( chapter 3 ), it was found that freshwater smelt ( Osmerus eperlanus ), ruffe ( Gymnocephalus cernuus ), perch ( Perca fluviatilis ), zander ( Stizostedion lucioperca ), and three-spined stickleback ( Gasterosteus aculeatus ) contained third stage (L3) larvae of A. crassus in their swimbladders. Roach ( Rutilus rutilus ) and bream ( Abramis brama ), however, did not contain the nematode. Pro-adult A. crassus were also found in ruffe, perch, and three- spined stickleback, but adult specimens were missing. It was suggested, that some of the fish species containing L3 larvae are preyed upon by eels and may act as paratenic hosts for the transmission of the parasite to eels.To test whether L3 larvae of A. crassus could be transmitted from infected smelt and ruffe to uninfected eels, eels were force-fed with infected smelt or ruffe swimbladders ( chapter 4 ). The L3 larvae migrated actively to the eel swimbladders, where they developed into adult A. crassus . It was concluded that eels can indeed become infected by eating infected prey fish.In experimentally induced infections using oral inoculation of L3 larvae, the pathogenesis of A. crassus infection was studied ( chapter 5 ). L3 larvae migrated directly through the intestinal wall and body cavity of the eels to the swimbladder within only 17 h. Fourth-stage A. crassus larvae were detected 3 months after infection, and pre-adults within 4 months after infection. The L3 larvae occasionally showed aberrant migration paths. The lesions of the swimbladders were less severe than those of naturally infected eels. A. crassus developed much faster in the European eels than in the Japanese eel, Anguilla japonica , as reported in the literature.The pathobiology of A. crassus in The Netherlands was investigated from 1986 to 1992 in freshwater eels and smelts ( chapter 6 ). Throughout the 6-year sampling period, young eels (up to 17 cm) showed severe lesions due to the parasite. Larger eels (23-34 cm) showed the highest prevalence of infection (96% from 1987 to 1988) and the highest intensity of infection, defined as the number of parasites per Infected fish (about 16 per fish from 1988 to 1989). After 1989 the prevalence and the severity of the swimbladder lesions decreased. Although larger eels (23-34 cm) from the Waddenzee (salt water) showed high prevalences of infection (85-90%) from 1987 to 1990, the intensities of infection decreased (7.7 to 4.8 per eel) from 1987 onwards, and the percentage of fibrotic swimbladders decreased from 1988 (maximum 24.5%). Smelts showed a sharp decrease in prevalence (88% to 48%) of the parasite shortly after 1988. Thereafter the prevalence stayed rather constant, at about 40% of the smelt population. No pathological changes were observed in the smelt.By improving our method for producing infective L3 larvae of A. crassus , we were able to isolate distinct L3 larvae from copepods (intermediate host) and to count exactly the infective L3 larvae for inoculating eels ( chapter 7 ). This method was used in subsequent experiments.To investigate why the A. crassus infection in naturally infected eels began to decrease, we conducted a dose-effect experiment in which some eels were primed and others not ( chapter 8 ). At day 0 uninfected eels were orally infected with various doses up to 40 L3 larvae of A. crassus per fish. At day 56 eels were either killed and examined, or were reinfected with 20 larvae each. At day 112 all remaining eels were killed and examined. The numbers of A. crassus recovered from the eels ranged between 14-20% at day 56 and 9-26% at day 112. These percentages were positively related to the total infection dose. There was no difference in percentages between primary and secondary infection. The swimbladder lesions were also positively related to the total dose, but were again not related to reinfection.An enzyme linked immuno sorbent assay (ELISA) was developed to test blood samples for antibodies against adult cuticula antigen of A. crassus ( chapter 8 ). None of the sera from the experimental eels showed a titer in the ELISA, whereas sera from naturally infected eels showed high titers. However, when these sera were tested in Western blots, no protein band indicating specific antibodies against A. crassus cuticula antigen was detected. It was concluded that under our experimental conditions, the eels do not develop an antibody response or resistance against the parasite. Future research should focus on examining the possible roles of specific and nonspecific immune responses in the decrease in the A. crassus infection in naturally infected eels

    Nieuw boek: Vis-, schaal- en schelpdierenziekten, van belang voor de Nederlandse aquacultuur.

    Get PDF
    Sinds decennia verschijnen er artikelen in “de Ziekenboeg” van het blad Aquacultuur over ziekten van vissen, schaal- en schelpdieren. Parasieten, bacteriën, virussen en schimmels kwamen aan bod. Nu is in opdracht en op kosten van het Ministerie van EL&I, Directie AKV door het CVI een boek over vis-, schaal- en schelpdierziekten geschreven, deels gebaseerd op de artikelen uit het blad Aquacultuur. Het boek, getiteld “Vis-, schaal- en schelpdierziekten, van belang voor de Nederlandse Aquacultuur” is geschreven door Olga Haenen, Marc Engelsma en Steven van Beurden van het CVI van WUR, met bijdragen van dierenarts Peter Werkman

    Aangifteplichtige schelpdierziekten, deel 2: Bonamia ostreae en Marteilia refringens

    Get PDF
    Bespreking van Bonamia ostreae en Marteilia refringens : aangifteplichtige schelpdierziekte
    • …
    corecore