A review of the 1988 and 2002 phocine distemper virus epidemics in European harbour seals

We present new and revised data for the phocine distemper virus (PDV) epidemics that resulted in the deaths of more than 23 000 harbour seals Phoca vitulina in 1988 and 30 000 in 2002. On both occasions the epidemics started at the Danish island of Anholt in central Kattegat, and subsequently spread...

Full description

Bibliographic Details
Main Authors: Hall, Ailsa Jane, Dietz, R, Reijnders, P J H, Teilmann, J, Harding, K, Hall, A J, Brasseur, S M J M, Siebert, U, Goodman, S J, Jepson, P D, Dau Rasmussen, T, Thompson, P M
Format: Article in Journal/Newspaper
Language:English
Published: 2006
Subjects:
epizootic
harbour seal
mass mortality
phocine distemper virus
MORBILLIVIRUS INFECTION
HALICHOERUS-GRYPUS
MARINE MAMMALS
GREY SEALS
ORGANOCHLORINE CONTAMINANTS
POPULATION-DYNAMICS
IMMUNE-RESPONSES
WESTERN ATLANTIC
FLAME RETARDANTS
Phoca vitulina
Online Access:https://research-portal.st-andrews.ac.uk/en/researchoutput/a-review-of-the-1988-and-2002-phocine-distemper-virus-epidemics-in-european-harbour-seals(ea9cb932-d1ee-48d3-80e4-45172d950fee).html
http://www.int-res.com/abstracts/dao/v68/n2/
Description
Summary:We present new and revised data for the phocine distemper virus (PDV) epidemics that resulted in the deaths of more than 23 000 harbour seals Phoca vitulina in 1988 and 30 000 in 2002. On both occasions the epidemics started at the Danish island of Anholt in central Kattegat, and subsequently spread to adjacent colonies in a stepwise fashion. However, this pattern was not maintained throughout the epidemics and new centres of infection appeared far from infected populations on some occasions: in 1988 early positive cases were observed in the Irish Sea, and in 2002 the epidemic appeared in the Dutch Wadden Sea, 6 wk after the initiation of the outbreak at Anholt Island. Since the harbour seal is a rather sedentary species, such 'jumps' in the spread among colonies suggest that another vector species could have been involved. We discussed the role of sympatric species as disease vectors, and suggested that grey seal populations could act as reservoirs for PDV if infection rates in sympatric species are lower than in harbour seals. Alternatively, grey seals could act as subclinical infected carriers of the virus between Arctic and North Sea seal populations. Mixed colonies of grey and harbour seal colonies are found at all locations where the jumps occurred, It seems likely that grey seals, which show long-distance movements, contributed to the spread among regions. The harbour seal populations along the Norwegian coast and in the Baltic escaped both epidemics, which could be due either to genetic differences among harbour seal populations or to immunity. Catastrophic events such as repeated epidemics should be accounted for in future models and management strategies of wildlife populations.

Similar Items