|
|
|
Abstracts
Session: The State of Oyster Disease
Current State of Knowledge on MSX Disease caused by Haplosporidium nelsoni, and Priorities for Future Research
Presented By:
Eugene M. Burreson, Virginia Institute of Marine Science, gene@vims.edu
Large-scale oyster mortality attributable to Haplosporidium nelsoni began in Delaware Bay in 1957 and in Chesapeake Bay in 1959. There is now good evidence from molecular studies that H. nelsoni is a natural parasite of the Pacific oyster, Crassostrea gigas, and was introduced to California and to the east coast of the United States. The exact timing or location of the introduction (or introductions) along the east coast has not been established, but the pathogen seems to have spread north and south from an initial epizootic in the middle Atlantic area.
The seasonal infection pattern of H. nelsoni is well established. New infections are acquired each year beginning in May and most infections occur in May, June and July; infection may continue through late summer in dry years. Infection intensity increases rapidly and oyster mortality usually peaks in August of the same year, within two to three months after infection. Intensity of infections acquired in late summer remains low through the winter and then increases in April and May as water temperature increases resulting in a second mortality peak in the spring.
Temperature and salinity tolerances of H. nelsoni are also well known. The parasite cannot survive at salinities of 10 ppt or below for more than 10 days. At salinities between 10 and 15 ppt the parasite can survive in oysters, but intensity usually remains low and little host mortality results. Above 15 ppt and temperatures above 20C the parasite multiplies rapidly and host mortality occurs with a few months of infection. There is some evidence from Delaware Bay that unusually cold winter temperatures result in lower prevalence and intensity of H. nelsoni the following summer.
Molecular diagnostic tools have been developed for H. nelsoni. Specific and sensitive PCR primers and DNA probes are available and have been used to provide evidence that H. nelsoni was introduced from the Pacific Ocean. Molecular diagnostic tools are currently being used in life cycle studies.
Mathematical models have been developed for population dynamics of H. nelsoni in oysters, and they accurately reflect actual data in areas not subject to high seasonal river flows. Models also suggest that an intermediate host is necessary in the life cycle to explain population dynamics of the parasite.
Oysters that demonstrate increased survival to H. nelsoni have been developed at Rutgers University and at VIMS through selective breeding. These oysters have been used successfully in New England and are being used in restoration and aquaculture efforts in Chesapeake Bay. There is also evidence that natural resistance to H. nelsoni has developed in oysters in Delaware Bay.
The four-year consecutive drought in the Mid-Atlantic from 1999 through 2002 has resulted in significant changes in the distribution of H. nelsoni in 2002. In Virginia, H. nelsoni was widely distributed and intensity was high, especially in upper tributaries. Prevalence at Horsehead Rock in the upper James River was a record high of 72%, and H. nelsoni occurred at Deep Water Shoal in the upper James River for the first time in history. In Maryland, 38 of 43 (88%) samples during 2002 had H. nelsoni infections and reflects a distribution record. Only five samples were free of H. nelsoni. The previous record high prevalence was 74% set in 1992. In 2002 H. nelsoni was found in the Chester River, Maryland for the first time in history.
However, the most significant range extension of H. nelsoni during 2002 was the epizootic oyster mortality in the Bras d'Or lake system in the Cape Breton area of Nova Scotia, Canada. H. nelsoni was not previously reported from Canada. Bras d'Or is a shallow, more or less isolated embayment that experiences warmer temperatures than surrounding locations, and 2002 was an unusually warm year, facilitating the establishment of H. nelsoni. It will be interesting to follow H. nelsoni abundance in this system when temperatures return to normal. H. nelsoni is also present in Prince Edward Island, Canada, probably as a result of oyster transplantation from the Cape Breton area.
Although much has been learned about H. nelsoni biology over the last 40 years, critical gaps in our knowledge still exist. Most important is that the life cycle remains unsolved. Most scientists believe that an intermediate host is involved in the life cycle, but none has been identified to date. Life cycle studies have been hindered by a scarcity of spores, which are undoubtedly the infective stage to another host. Lack of knowledge on the life cycle has hindered interpretation of distributional changes, such as the recent range expansion into Canada, and has also rendered impossible controlled laboratory experiments to investigate pathological mechanisms and control measures. Controlled experiments have also been hindered by lack of a ready supply of the organism. Many advances in our knowledge of Perkinsus marinus were made possible because of successful continuous culture of the organism. Few attempts have been made to culture H. nelsoni, and none has been successful.
Future research efforts should concentrate on life cycle studies and obtaining continuous cultures of the organism. Both of these research avenues are relatively high risk, and expensive, but our understanding of H. nelsoni population dynamics and pathology cannot advance significantly until both are achieved. In addition, selective breeding, or other approaches, to increase tolerance of oysters to H. nelsoni should be continued.
![[Maryland Sea Grant]](../mdsg_logo.gif){kind=logo}
![[NOAA]](../noaa_logo.gif){kind=logo}
![[Virginia Sea Grant]](../vasg_logo.gif){kind=logo}