Bonamiosis here refers only to the diseases in oysters caused by Bonamia ostreae in the Northern Hemisphere, and by Bonamia exitiosus and Mikrocytos roughleyi in the Southern Hemisphere. If detected outside the known range of Mikrocytos roughleyi and Bonamia spp., electron microscopy or DNA-based assays, when available, must be used to identify and distinguish the detected organism from other microcell species (Bonamia ostreae, Bonamia exitiosus , Mikrocytos mackini and M. roughleyi). The presence of these pathogens in any bivalve should be regarded as potentially serious and the OIE Reference Laboratory should be consulted.
Bonamiosis is caused by the haplosporidians Bonamia ostreae, B. exitiosus and Mikrocytos roughleyi( 3-5, 8, 11, 17, 21 ) . Bonamiosis is also known as microcell disease, haemocyte disease of flat oysters (B. ostreae), haemocyte disease of dredge oysters (Bonamia exitiosus) or winter mortality (Mikrocytos roughleyi).
Bonamia ostreae occurs naturally in Ostrea edulis and O. conchaphila (= O. lurida), and can infect O. puelchana, O. angasi and Ostrea chilensis (= Tiostrea chilensis, T. lutaria) when moved into endemic zones ( 12, 13, 20 ) . Bonamia exitiosus occurs in O. angasi, O. denselammellosa and T. chilensis( 8 ) . Species of Ostrea and Tiostrea and other ostreids (Crassostrea rivularis = C. arakensis)( 6 ) should be considered to be potentially susceptible to Bonamia spp. Mikrocytos roughleyi infects the Sydney rock oyster Saccostrea glomerata (commercialis).
The geographical distribution of B. exitiosus is: New Zealand ( around South Island and lower North Island )( 9 ) and Australia ( Western Australia, Victoria and Tasmania ) . Bonamia ostreae has been reported from France, Ireland, Italy, the Netherlands, Spain, the United Kingdom ( excluding Scotland ) , and the United States of America ( California, Maine and Washington State )( 2, 10, 18, 19, 22, 23 ) , but is now thought to be absent from Denmark. Mikrocytos roughleyi occurs in New South Wales, Australia.
Bonamiosis is a lethal infection of the haemocytes of flat oysters, sometimes accompanied by yellow discoloration and extensive lesions on the gills and mantle ( 21 ) . However, most of the infected oysters appear normal. Lesions occur in the connective tissue of the gills, mantle, and digestive gland. These intrahaemocytic protistans quickly become systemic with overwhelming numbers of parasites coinciding with the death of the oysters. In highly susceptible hosts, bonamiosis is a lethal infection of the haemocytes. Some evidence suggests that the pathology caused by Bonamia spp. depends on which host species and population is infected. For example, B. exitiosus in oysters from Tasmania were highly epitheliotropic and associated with focal abscesses in some populations without evidence of systemic spread. Mikrocytos roughleyi is associated with focal abcess-type lesions in the gill, connective and gonadal tissues and alimentary tract ( 11 ) . It induces a systemic intracellular infection in the haemocytes ( but never in the connective tissue cells ) .
Bonamia spp. may occur throughout the year, but prevalence and intensity of infection tend to increase during the warm season ( 7, 12, 15 ) . There is a seasonal variation in infection by B. ostreae with the highest prevalence occurring in September in the Northern Hemisphere. In the Southern Hemisphere, B. exitiosus shows the highest prevalence from January to April with the parasite being barely detectable in September and October. The prepatent period for B. ostreae and B. exitiosus is usually 3-4 months but can be up to 5 months. In the Southern Hemisphere, the disease caused by M. roughleyi is associated with low temperatures and high salinities. It can kill up to 70% of mature Sydney rock oysters in their third winter before marketing, and has a prepatent period of 2.5 months ( 11 ) .
Bonamiosis can be transmitted experimentally by cohabitation or inoculation ( 14 ) .
Examination of stained tissue sections and tissue imprints of susceptible organs are the recommended methods for screening ( 1, 24 ) . For diagnosis, the recommended guidelines for sampling are those stated in Chapter 1.1.4 and Chapter I.2. of this Aquatic Manual . However, the disease may be not detectable by the usual methods during the first 5 months of infection.