Hepatopancreatic Parvo-like Virus (HPV) Disease
Parvovirus (22-24 nm)
Postlarvae, juveniles and adults of P. monodon, P. merguiensis, P. vannamei, P.esculentus, P. semisulcatus, P. penicillatus, P. indicus, P. chinensis.
Affected shrimps develop loss of appetite and retarded growth. Benthic dia-toms, protozoans such as Zoothamnium sp., and filamentous bacteria may cause fouling on the exoskeleton of infected shrimps. Occasionally, white opaque areas on the tail/abdominal muscles are observed.
EFFECT ON HOST:
Postlarvae (PL-1–PL-19) from three hatcheries in Iloilo showed prevalence rates of 7.8 to 26.4%. Mortalities among P. merguiensismay reach as high 50% within 4-8 weeks of disease onset. The virus cause hypertrophy of the hepatopancreatic nucleus with lateral displacement and compression of the nucleolus and chromatin margination with development of a prominent baso-philic occlusion body. This leads to cell death and shrinkage of the hepatopan-creas. Damage of this organ can result in abnormal metabolism and eventually death.
Signs of disease and histological demonstration of single prominent basophilic (H&E stain) intranuclear occlusion body in the hypertrophied nucleus of the hepatopancreatic cell (Fig. 2-11) are diagnostic. Electron microscopy, DNA Probe, PCR, infection bioassay are confirmatory tests.
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