DAO 68:115-130 (2006)  -  doi:10.3354/dao068115

The 1988 and 2002 phocine distemper virus epidemics in European harbour seals

Tero Härkönen1,*, Rune Dietz2, Peter Reijnders3, Jonas Teilmann2, Karin Harding4, Ailsa Hall5, Sophie Brasseur3, Ursula Siebert6, Simon J. Goodman7, Paul D. Jepson7, Thomas Dau Rasmussen2, Paul Thompson8

1Swedish Museum of Natural History, Box 50007, 10405 Stockholm, Sweden
2National Environmental Research Institute, Box 358, 4000 Roskilde, Denmark
3Alterra-Marine & Coastal Zone Research, PO Box 167, 1790 AD Den Burg, The Netherlands
4Department of Marine Ecology, Göteborg University, Box 461, 40530 Göteborg, Sweden
5Sea Mammal Research Unit, Gatty Marine Laboratory, University of St. Andrews, St. Andrews, Fife KY16 8LB, UK
6Research and Technology Center Westcoast, University of Kiel, Hafentörn, 25761 Büsum, Germany
7Institute of Zoology, Zoological Society of London, Regent’s Park, London NW1 4RY, UK
8University of Aberdeen, School of Biological Sciences, Lighthouse Field Station, George Street, Cromarty IV11 8YJ, UK

ABSTRACT: We present new and revised data for the phocine distemper virus (PDV) epidemics that resulted in the deaths of more than 23000 harbour seals Phoca vitulina in 1988 and 30000 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.


KEY WORDS: Epizootic · Harbour seal · Mass mortality · Phocine distemper virus


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