The Etiological Agent of Juvenile Oyster Disease (JOD)

JOD has caused mass mortalities of cultured Crassostrea virginica in north-eastern US since the late 1980’s in juvenile animals. This normally occurs in water temperatures of over 20°C. It is normally worst on oysters less than 25mm in shell height and can cause losses of more than 90% of annual production. The oysters typically develop the disease at grow-out site where mortalities occur within 1-2 weeks after the first signs of JOD. The first sign of JOD is a sudden termination in growth, flaking away of the new periostracal growth in the upper or flat valve then occurs. This causes uneven valve margins. Lesions can also develop, causing tissue disruption accompanied by hemocyte infiltration into the affected area. Affected oysters begin secreting successive layers of conchiolin onto the surface of the inner valves. Bacteria may be observed between successive layers of conchiolin and can also be present with ciliates in and around lesions. Rosevirus crassostreae has been consistently isolated from JOD-affected population. Lab exposure of seed oysters to RC has also shown JOD-like mortalities, without accompanying disease signs. The aim of this study was to satisfy remainder of Koch’s postulates by reproducing JOD-like conchiolin deposition via experimental challenge with RC.

Bacteriological analysis was conducted on different groups of oysters in different locations; some had a single inoculation of a rifampicin resistant (Rif^r) strain of R. crassostreae. Another group of oysters received one injection, two injections, five injections or by proximity only to injected oysters. The mortality rate in oysters receiving no injections was 41% but they were instead exposed to R. crassostreae via proximity to challenged oysters. A significantly higher incidence of conchiolin deposition was observed in the group which received injections.

A field experiment was carried out, where oysters were selected for bacteriological analysis and scored for various health indicators. R. crassostreae isolates from infected oysters went through PCR and RFLP analysis. Results showed that mortality among challenged oysters was 50% over 18 weeks; however this was not significant in comparison to the control. Anomalous deposits of conchiolin were observed in 20% of the oysters that died in the challenge group. Bacteriological sampling resulted in the isolation of R. crassostreae from 43% of challenged oysters. Some samples were also used for histopathology. Histological alterations observed were typical of those described in other JOD outbreaks. Early outbreaks consisted of multiple layers of conchiolin, often associated with diapedesis and sloughing of hemocytes, on the epithelial surface.

Two of Koch’s postulates have already been fulfilled by R. crassostreae, this paper aimed to discern the etiology of JOD. Overall, it has been shown that R. crassostreae has the ability to induce JOD-like conchiolin in laboratory-held C. virginica. The bacterium was also found to be a capable coloniser of healthy juvenile C. virginica and the initial colonisation was coincident with the formation of microscopic lesions on the mantle surface. These gross disease signs and mortality was typical of JOD. These findings, made the authors conclude that R. crassostreae is the etiological agent of JOD. It is also recognised that juvenile oysters may suffer diseases and mortality that is not caused by R. crassostreae. The authors then propose that JOD should be renamed to Roseovarius Oyster Disease (ROD). This provides a more descriptive accuracy and eliminated possible confusion with other diseases of juvenile oysters.

Overall, I think that this paper is significant; because of this study the name change to Roseovarius Oyster Disease was accepted!

Roseovarius crassostreae, the etiological agent of Juvenile Oyster Disease (now to be known as Roseovarius Oyster Disease) in Crassostrea virginica

Maloy et al., (2007)

http://www.sciencedirect.com/science/article/pii/S0044848607002955