Amyotrophia of Abalone
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Category
Category 3 (Host Not in Canada)
Common, generally accepted names of the organism or disease agent
Amyotrophia, Epizootic fatal wasting disease.
Scientific name or taxonomic affiliation
Etiological agent is unknown. However, virus-like particles were observed in the cytoplasm of cells near the nerve trunk of diseased Haliotis discus discus examined with an electron microscope (Otsu and Sasaki 1997). Virus-like particles of similar size and retrovirus-like morphology were also isolated from diseased H. discus discus in primary cultures of abalone haemocytes but the isolates from the primary culture of abalone haemocytes did not reproduce the disease (Nakatsugawa et al. 1999). The OIE ad hoc Group (2008) indicated that Nakatsugawa et al. (1999) suggestion of a retroviral nature of amyotrophia was not well supported by the published scientific data, nor has it been corroborated by further studies. Glioma and tumor-like lesions have also been associated with virus-like particles in the nervous tissues of cultured juvenile Haliotis (=Nordotis) discus in Japan (Nagatsugawa et al. 1988, Harada et al. 1993).
Note that the virus reported by Otsu and Sasaki (1997) and Nakatsugawa et al. (1999) were considered to be herpes-like viral pathogens by Chen et al. (2012). However, the relationship between this abalone viruses reported from Japan and abalone viral ganglioneuritis (AVG) and the various reports of viral infections of abalone in China is not known. Nevertheless, the OIE ad hoc Group (2008) suggested that this virus and cracked-shell disease from northern China) may constitute a subacute to chronic syndrome within the abalone viral mortality complex.
Geographic distribution
Various culture facilities throughout western Japan. A similar looking disease (i.e., shrinking of the meat within the shell) was reported in farmed Haliotis discus hannai from Shandong and Liaoning provinces of China (Guo et al. 1999).
Host species
First observed in cultured juvenile Haliotis discus discus in the early 1980s (Muroga 2001). Initially Haliotis discus hannai was thought to be resistant to the disease. However, when the major species for seed production was changed to H. discus hannai, this species was also found to be vulnerable to amyotrophia (Nakatsugawa et al. 1999). Haliotis madaka was also susceptible to infection (Momoyama et al. 1999).
Impact on the host
Abalone with amyotrophia develop muscle atrophy in the mantle and foot which impedes feeding and adhesion to the substrate, followed by impaired shell growth and mortality. Epizootic mass mortalities attributable to this disease have been observed in juvenile abalone during seed production and subsequent nursery stages at several facilities in Japan. Disease usually occurs among juvenile abalone reared at 18 to 20°C. The progress of the disease was suppressed when the ambient water temperature rose to 23°C or higher (Nakatsugawa 1990). Specifically, histopathology changes characteristic of amyotrophia in the nerve trunk and peripheral nerve of the foot muscle were observed in exposed (to water containing homogenized tissue from diseased abalone filtered to 450 nm) juvenile Haliotis discus discus after 40 days at 18°C. When the exposed abalone were reared at 12°C only slight histopathology was observed even after 60 days (the end of the test). At 24°C, although the abnormal cell masses were formed earlier than the other 2 water temperature groups, they appeared to be resolved after 40 days post-exposure (Momoyama 2000). Amyotrophia could be experimentally transmitted horizontally between abalone with a filtrate (0.22 µm membrane filter) from diseased H. discus discus or by exposing healthy abalone to the water drained from an aquarium containing diseased abalone (Nakatsugawa 1990; Nakatsugawa et al. 1999, 2000). Nakatsugawa (1995) determined that in sterile sea water, the infectivity of the virus was lost in 5 days at 25°C or 20 days at 18°C but was maintained for 20 days at 10°C.
Two families selected for resistance to amyotrophia had survival ratios between 87 and 93% in comparison to 2 unselected families and hybrids of the 2 families with survival ranging for 0 to 37% after the occurrence of a mass mortality event in the abalone farm (Hara et al. 2004). Also, survival performance of offspring of the selected families was significantly greater in mixed rearing tanks indicating that resistance to the disease is a heritable trait (Hara et al. 2004). The existence of various degrees of tolerance to amyotrophia was detected in wild populations of H. discus discus (Hara et al. 2004).
Diagnostic techniques
Gross observations
Muscle atrophy in the mantle and foot which impedes feeding and adhesion to the substrate, followed by impaired shell growth and mortality. The gross signs of disease in Haliotis diversicolor depicted by Di et al. (2016) may have been caused by amyotrophia and not withering syndrome (WS) as claimed because detection and/or identification of the etiological agent of WS was not indicated in the publication.
Histology
Moribund and dead abalone have many tumours (abnormal cell masses) and muscle atrophy near the nerve trunk of the pedal ganglia (pleuro-pedal neuro-trunk) and their transverse commissures. The nuclei of tumour cells were contracted and the centres of some tumours were necrotic (Nakatsugawa 1990, Nakatsugawa et al. 1999, Hara et al. 2004). Momoyama et al. (1999) also reported abnormal cell masses in the mantle, gills, mid-gut and renal glands, and the digestive tract including associated connective tissue. No pathogens were detected during histopathology examinations (Momoyama et al. 1999).
Electron microscopy
Virus-like particles (about 100 nm in diameter) were observed in the cytoplasm of cells near the nerve trunk of diseased H. discus discus (Otsu and Sasaki 1997). Momoyama et al. (1999) observed smaller virus-like particles (50-60 nm in diameter) in secondary lysosomes in the cytoplasm of abnormal cells from lesions. They indicated that these particles were not likely to be the etiological agent because the size of the amyotrophia-causing pathogen was estimated to be between 100-220 nm by filtration experiments (Momoyama et al. 1999, Momoyama 2000).
Culture
Virus-like particles about 100 nm in diameter and retrovirus-like morphology were isolated from diseased H. discus discus in primary cultures of abalone haemocytes but these isolates did not reproduce the disease in challenged susceptible abalone (Nakatsugawa et al. 1999).
Methods of control
No known methods of prevention or control. To avoid the risk of introducing this pathogen to other culture facilities or natural stocks, only animals certified to be free of infection should be considered for transplantation from areas where the disease occurs. In addition, imported animals must be held in quarantine and assayed for cryptic or subclinical infections prior to release into the new environment.
According to Nakatsugawa (1990) and Momoyama (2000), the progress of the disease can be suppressed in an aquaculture facility by increasing the ambient water temperature to 23°C or higher. Hara et al. (2004) suggested that using selective breeding techniques with H. discus discus showing resistance to the disease would likely help mitigate the problem of mass mortality caused by amyotrophia. Muroga (2001) indicated that various measures to impede vertical and horizontal transmission of the disease were conducted and the occurrence of the disease was remarkably reduced.
References
Bower, S.M. 2000. Infectious diseases of abalone (Haliotis spp.) and risks associated with transplantation. In: Campbell, A. (Editor), Workshop on Rebuilding Abalone Stocks in British Columbia. Canadian Special Publication of Fisheries and Aquatic Sciences 130: 111-122.
Chen, M.H., S.T. Kuo, T. Renault, C.S. Friedman and P.H. Chang. 2012. Development of a polymerase chain reaction for the detection of abalone herpesvirus infection based on the DNA polymerase gene. Journal of Virological Methods 185: 1-6.
Di, G., X. Kong, G. Zhu, S. Liu, C. Zhang and C. Ke. 2016. Pathology and physiology of Haliotis diversicolor with withering syndrome. Aquaculture 453: 1-9.
Guo, X., S.E. Ford and F. Zhang. 1999. Molluscan aquaculture in China. Journal of Shellfish Research 18: 19-31.
Hara, M., M. Sekino, A. Kumagai and T. Yoshinaga. 2004. The identification of genetic resistance to amyotrophia in Japanese abalone, Haliotis discus discus. Journal of Shellfish Research 23: 1157-1161.
Harada, T., N. Okazaki, Y. Otoishi, Y. Hayakawa and S.S. Kubota. 1993. Tumors in nervous tissues of abalones, Nordotis discus. Journal of Invertebrate Pathology 62: 257-261.
Momoyama, K. 2000. Experiments for characterizing the causative agent of amyotrophia in juvenile abalones Haliotis spp. Fish Pathology 35: 179-184. (In Japanese with English abstract).
Momoyama, K., T. Nakatsugawa and N. Yurano. 1999. Mass mortalities of juvenile abalones, Haliotis spp., caused by amyotrophia. Fish Pathology 34: 7-14. (In Japanese with English abstract).
Muroga, K. 2001. Viral and bacterial diseases of marine fish and shellfish in Japanese hatcheries. Aquaculture 202: 23-44.
Nakatsugawa, T. 1990. Infectious nature of a disease in cultured juvenile abalone with muscular atrophy. Fish Pathology 25: 201-211. (In Japanese with English abstract).
Nakatsugawa, T. 1995. Duration of infectivity of the causative agent for abalone "amyotrophia" in sea water. Fish Pathology 30: 283-284.
Nakatsugawa, T., K. Hatai and S.S. Kubota. 1988. Histopathological findings on cultured juvenile abalone, Nordotis discus, with muscular atrophy. Fish Pathology (Tokyo) 23: 203-204. (In Japanese)
Nakatsugawa, T., T. Nagai, K. Hiya, T. Nishizawa and K. Muroga. 1999. A virus isolated from juvenile Japanese black abalone Nordotis discus discus affected with amyotrophia. Diseases of Aquatic Organisms 36: 159-161.
Nakatsugawa, T., M. Okabe and K. Muroga. 2000. Horizontal transmission of amyotrophia in Japanese black abalone. Fish Pathology 35: 11-14. (In Japanese with English abstract).
OIE ad hoc Group. 2008. Report of the Meeting of the OIE ad hoc Group on the OIE List of Aquatic Animal Diseases - Mollusc Team - for the OIE Aquatic Animal Health Code. Paris, 25-27 January 2008., pp. 135-162. Available in the Report of the Meeting of the OIE Aquatic Animal Health Standards Commission. Paris, 3–7 March 2008.
Otsu, R. and K. Sasaki. 1997. Virus-like particles detected from juvenile abalones (Nordotis discus discus) reared with an epizootic fatal wasting disease. Journal of Invertebrate Pathology 70: 167-168.
Citation information
Bower, S.M. (2022): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Amyotrophia of Abalone.
Date last revised: May 2022
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