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USGS2014

Viability and infectivity of Ichthyophonus sp. in post-mortem Pacific herring, Clupea pallasii

Ichthyophonus -infected Pacific herring, Clupea pallasii , were allowed to decompose in ambient seawater then serially sampled for 29 days to evaluate parasite viability and infectivity for Pacific staghorn sculpin, Leptocottus armatus . Ichthyophonus sp. was viable in decomposing herring tissues for at least 29 days post-mortem and could be transmitted via ingestion to sculpin for up to 5 days. The parasite underwent morphologic changes during the first 48 hr following death of the host that were similar to those previously reported, but as host tissue decomposition progressed, several previously un-described forms of the parasite were observed. The significance of long-term survival and continued morphologic transformation in the post-mortem host is unknown, but it could represent a saprozoic phase of the parasite life cycle that has survival value for Ichthyophonus sp.

Journal of Parasitology↗

USGS1999

Controlled field and laboratory studies on VHS and Ichtyophonus in Pacific herring: Section II in Investigations of disease factors affecting declines of Pacific herring populations in Prince William Sound

From 1995 through 1998 the controlled disease studies covered a wide range of topics including virus survival in seawater, development of natural immunity, effects of oil exposure on immunity, effect of synthetic immunosuppressants, epizootiology of VHSV in net pens, antibody production and the natural history of VHS in Pacific herring. Both VHSV and I. hoferi were was observed in fish that reached two-years-old while in captivity. Prior to 2 years old, fish that shown to be. serious pathogens of juvenile hening. A natural age-related resistance to VHS virus plaque assay and resistance to reinfection with the known minimum lethal dose of virus. survived an initial infection by VHSV developed an acquired immunity detectable by in vitro Three years of consecutive monthly sampling of wild 0-year herring in Puget Sound revealed a VHSV carrier rate below 1%, but that this level of virus shedding was adequate to initiate an epizootic under confined conditions, and probably resulted in infection of free-ranging fish also. Over 50% of the virus was recoverable from seawater after 2 hours, was still detectable after six hours, and survived up to 100 h when ovarian fluid was present in the water. Studies in PWS demonstrated that closed pounds play a role in transmission of VHSV to impounded fish steadily increased with confinement time and viral tissue titers were at very high susceptible fish, resulting in the rapid spread of virus within the pens. Prevalence of VHSV from levels in fish being released after 8 days in captivity. Viable virus was also recovered from the water inside and outside the net pens at levels adequate to initiate an epizootic in susceptible fish. of herring and that vitro culture was the most sensitive method for detecting it. Studies on Ichthyophonus hoferi demonstrated that the organism is a potential serious pathogen No evidence for increased susceptibility, mortality or loss of disease resistance was observed in wild or laboratory-reared herring exposed to oil or synthetic corticosteroids, either prior to or following exposure to VHSV.

Report↗

USGS1976

Transmission of avian pox from starlings to Rothchild's mynahs

Several wild species of birds, including starlings ( Sturnus vulgaris ), house sparrows ( Passer domesticus ) and pigeons ( Columba livia ) gained access to an aviary housing Rothchild's mynahs ( Leucospar rothchildii ) and over 100 additional birds representing a variety of species. Six of approximately 15 mynahs became infected with avian pox and all of them died. None of the other birds in the aviary developed lesions. Pox virus was isolated from mynah facial lesions on chicken chorioallantoic membrane and in duck embryo fibroblast cell culture. It did not produce lesions in white Leghorn chickens, but did produce lesions in 4 of 11 wild starlings captured outside the aviary. Results indicated the agent was an indigenous starling pox capable of infecting and producing disease in mynah birds. Destruction of the captive starlings and isolation of the remaining mynahs immediately stopped the mortality.

Journal of Wildlife Diseases↗