Abstract

Grey seal (Halichoerus grypus) and harbor seal (Phoca vitulina) mortalities in New England during 2006, which constituted a 2006 Unusual Mortality Event, were confirmed to be the result of a North American isolate of phocine distemper virus (PDV USA 2006), representing the first cases of clinical disease and death associated with an isolated strain of PDV in North American seals.¹ European strains of PDV were responsible for the mass mortality of harbor seals in Europe in 1988 and again in 2002.⁵ In contrast to the European mortality events, grey seals in the U.S. were notably affected.^1,6 Evidence from natural pinniped population exposures to PDV 2006 and PDV strains in 1988 and 2002 suggests that a difference exists in seal species susceptibility to infection.³ In order to experimentally determine if differences in species susceptibility exist in New England seals, peripheral blood mononuclear cells (PBMCs) were isolated and in vitro infection by PDV USA 2006 was carried out until 11 days post infection. RNA was isolated and virus quantified by multiplex real time RT-PCR in lymphocytes, monocytes and supernatant fractions.^2,4,7 Tissues from dead stranded seals during the 2006 Unusual Mortality Event (UME) were also obtained to quantify virus loads in tissues from known PDV positive, PDV negative and PDV unknown animals. Tissues from 22 seals of three species: harbor seal, harp seal (Phoca groenlandica), and grey seal, revealed that virus was detectable from tissues from harp seals with the highest frequency (4 of 6 animals), and harbor seal tissues carried the highest quantity of PDV. The highest quantity of PDV in harbor seal was present in liver, spinal cord and spleen, while the highest quantity for harp seal was found in spinal cord and lung. Grey seals only tested positive in one lung sample. In PBMC infection experiments, 5 individuals of each species were compared. Differences were apparent in cell fraction compartments throughout the 11-day time course and infection quantity differed between species. These results suggest that there are differences in the quantity of virus present in tissues of different seal species during the time course of infection. Differences in the course of infection of lymphocytes and monocytes together with the frequency, distribution and intensity of infection in different tissues may affect the outcome of PDV infection in different species of seals.

Acknowledgements

Many thanks to the U.S. Northeast Region Stranding Networks and funding support from the NOAA Prescott Program

* Presenting author
+ Student presenter

Literature Cited

1.  Earle PJA, Melia MM, Doherty NV, Nielsen O, Cosby SL. Phocine Distemper Virus in Seals, East Coast, United States, 2006. Emerging Infectious Diseases 2011;17(2):216–220.

2.  Grant RJ, Banyard AC, Barrett T, Saliki JT, Romero CH. Real-time RT-PCR assays for the rapid and differential detection of dolphin and porpoise morbilliviruses. Journal of Virological Methods 2009;156:1–2.

3.  Hall AJ, Jepson PD, Goodman SJ, Haerkoenen T. Phocine distemper virus in the North and European Seas - Data and models, nature and nurture. Biological Conservation. Vol. 131, no. 2, pp. 221–229. Aug 2006. 2006.

4.  Hammond JA, Hall AJ. Identification and real-time PCR quantification of Phocine distemper virus from two colonies of Scottish grey seals in 2002. Journal of General Virology 2005;86(9):2563–2567.

5.  Härkönen T, Rune D, Peter R, Jonas T, Karin H, Ailsa H, Sophie B, Ursula S, Simon JG, Paul DJ and others. The 1988 and 2002 phocine distemper virus epidemics in European harbour seals. Volume 68. 2006. p 115–130.

6.  Harwood J. Lessons from the Seal Epidemic. New Scientist. Vol. 1989;121:38–38.

7.  Visser IKG, Van Bressem MF, De Swart RL, Van de Bildt MWG, Vos HW, Van der Heijden RWJ, Saliki JT, Oervell C, Barrett T, Osterhaus A. Characterization of morbilliviruses isolated from dolphins and porpoises in Europe. Journal of General Virology. Vol. 74, no. 4, pp. 631–641. 1993. 1993.