Prevalence of morbillivirus antibodies in Scottish harbour seals.

SINCE May 2002, a new outbreak of phocine distemper virus (PDV) in harbour seals (Phoca vitulina) has been spreading through the North Sea (Harding and others 2002, Jensen and others 2002). By late September 2002, over 17,200 dead harbour seals had been reported dead in European waters (Reineking 2002), approaching the 18,000 deaths resulting from the PDV outbreak in 1988 (Heide-Jørgensen and others 1992b). In the UK, the first cases of PDV were reported in midAugust, and over 1800 seals had been found on the English coast by late September 2002. However, most of the UK’s 36,000 plus harbour seals are found around the Scottish coast, where PDV was only confirmed to be present in mid-September. Serological studies following the 1988 outbreak of PDV indicated that a high proportion of surviving seals came into contact with the virus (Heide-Jørgensen and others 1992b). The spread and impact of the current outbreak depends critically on levels of resistance in these different North Sea populations, but few serological data exist to help evaluate this threat. This short communication describes a study undertaken to determine how the prevalence of morbillivirus antibodies has changed in the Scottish populations since 1988, and to assess the current vulnerability of these animals to the spread of PDV. Blood was collected from free-living harbour seals in the Moray Firth between 1988 and 1996, and in the Tay estuary between 1998 and 2000. Over 300 seals were captured at haulout sites throughout the year, but predominantly in the spring and autumn (Thompson and others 1992). As harbour seal pups are born in June and early July, data were pooled into year classes based on the period June 1 to May 30. Measurements of pelage hairs (Corpe and others 1998) confirmed that 108 of the captured seals were aged between two and 14 months. These seals ranged in size from 83 to 113 cm and 13·6 to 37 kg, and it was assumed that all seals longer than 115 cm or weighing more than 40 kg were more than one year of age. Samples from pups (less than 100 cm long or less than 25 kg in weight) captured before September were excluded to avoid any possibility of detecting maternally derived antibodies (Cornwell and others 1992). Blood samples were taken using heparinised or plain vacutainers, and the plasma or serum was frozen and stored at –20°, before being sent overnight on ice to Glasgow University Veterinary School. Virus neutralisation tests were carried out in microtitration plates as described by Cornwell and others (1992). Titres were expressed as the reciprocal of the serum dilution that reduced the proportion of wells infected from 100 per cent to 50 per cent. Antibody titres from seals captured before the 1988 epizootic were all up to 32 (Thompson and others 1992). Based upon these data, and inspection of frequency distributions of titres from this study, it was assumed that all samples with titres of 68 or more were seropositive. The sensitivity of the present results to this assumption was investigated by using logistic regression to determine how the prevalence changed under different threshold titres. Of the 300 plus seals which were captured and sampled, 81 were confirmed to be in their first year and born after 1990. None of these seals was seropositive, even using a threshold titre of 32. Since the 1988 epidemic, there had been a significant decline in the prevalence of antibodies among seals over one year of age (Fig 1). These data suggest that between 2·7 per cent and 8·6 per cent of the current population were exposed to PDV during 1988. Mean log10 titres of seropositive seals also showed a significant decline over this period (r2=0·59, P<0·05) (Table 1). These data represent the most extensive serological survey of healthy, free-living seals in any of the areas affected by the