Assessing the pathogenesis and host susceptibility to dolphin morbillivirus in cetaceans

Michael Moore, Woods Hole Oceanographic Institution

Abstract

Over the last 25 years, marine morbilliviruses have caused high mortality in cetaceans and

pinnipeds worldwide resulting in the death of tens of thousands of marine mammals. The

severity of infection has resulted in population level consequences in susceptible species. In 1988

and in 2002 phocine distemper virus (PDV) killed over half the population of harbor seals in

Europe. Relatively conserved strains of PDV that exhibit little genetic variability appear to

induce few differences in host adaptation, pathogenesis and epidemiology, while the more

divergent group of cetacean morbillivirus (CeMV) exhibits a broader range of host adaptation,

pathogenesis and epidemiology patterns making it increasingly difficult to predict and manage

outbreaks in cetaceans. Dolphin Morbillivirus (DMV) is currently implicated in an Unusual

Mortality Event (UME) involving over 1,500 bottlenose dolphin deaths in the U.S. Northeast and

Southeast Atlantic. Despite several large-scale epizootic events due to various strains of DMV,

susceptibility, pathogenesis and epidemiology are still not fully understood. To predict the

effects of the virus and to develop effective individual or population wide models and

interventions, including the possibility of vaccination programs for small endangered

populations, an understanding of susceptibility, transmission and reservoir dynamics of the

viruses are necessary. The results from this research will be applicable to management by

improving the allocation of resources used to address marine mammal health during UME events

and aid in risk assessments for species recovery plans. The objectives of this study are to

undertake a multidisciplinary approach to determine mechanisms of host susceptibility and

pathogenesis of DMV by examining tissues to determine distribution of infection, identifying

host reservoir species and understanding host susceptibility.