Baculoviral midgut gland necrosis virus (BMNV) has been found in cultured and wild kuruma shrimps, Penaeus japonicus , in Japan (12, 13, 15) and Korea (11). Type C baculovirus, which is considered to be identical to BMNV, has been reported from Penaeus monodon in the Philippines (10), Australia and Indonesia. BMN epizootics have been reported in Japan since 1971 (15) where it is considered to be one of the major problems in hatcheries. As with Baculovirus penaei (BP) and Penaeus monodon-type baculovirus (MBV), the main target organ for BMNV is the hepatopancreas, and the virus may initiate mass mortality in the infected larvae. However, unlike BP and MBV, it does not produce an intranuclear occlusion body in the infected hepatopancreatocyte.
The BMNV-infected moribund shrimp larvae show a nuclear hypertrophy and remarkable cellular necrosis or collapse of the midgut gland (hepatopancreas).
Experiments with artificial infection revealed that BMN caused high mortality in healthy P. japonicus larvae (7, 8, 14). BMN has been experimentally transmitted to P. monodon, P. chinensis and P. semisulcatus (9).
Two diagnostic techniques, wet-mount and histopathology of the hepatopancreas, have been used for the demonstration of BMNV infection in P. japonicus (1). Under the electron microscope, enveloped virions measuring approximately 310 nm x 72 nm were observed (15). No occlusion bodies have been found in the infected nuclei of hepatopancreatocytes.
Results of infectivity trials and field surveys showed that BMN may initiate mass mortality in the healthy larvae. It was also noted that, as for BP and MBV, viruses released with faeces from spawners (or broadstock) into the environmental water of intensive culture systems of P. japonicus play an important role in disease spread (3).
As the oral route has been strongly suggested to be the main infection pathway for BMNV infection, complete or partial eradication of viral infection may be accomplished by thorough washing of fertile eggs or nauplii using clean sea water (8).