Symbol of the Government of Canada

WarningThis page has been archived.

Archived Content

Information identified as archived on the Web is for reference, research or recordkeeping purposes. It has not been altered or updated after the date of archiving. Web pages that are archived on the Web are not subject to the Government of Canada Web Standards. As per the Communications Policy of the Government of Canada, you can request alternate formats on the "Contact Us" page.

Archived - Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish

Necrotizing Hepatopancreatitis of Penaeid Shrimp

Category | Common Name | Scientific Name | Distribution | Host Species
Impact on Host | Diagnostic Technique | Methods of Control | References | Citation


Category

Category 3 (Host Not in Canada)

Common, generally accepted names of the organism or disease agent

Necrotizing hepatopancreatitis, NHP, Texas necrotizing hepatopancreatitis, TNHP, Texas pond mortality syndrome, TPMS, Peru necrotizing hepatopancreatitis, PNHP.

Scientific name or taxonomic affiliation

Determined to be a new genus and new species of bacterium in the alpha Proteobacteria that is apparently obligate intracellular in hepatopancreatic epithelial cells.

Geographic distribution

Peru, Ecuador, Venezuela, Brazil, Panama, Costa Rica and United States in Texas.

Host species

Only in American penaeids: Penaeus vannamei, Penaeus aztecus, Penaeus setiferus, Penaeus stylirostris and Penaeus californiensis.

Impact on the host

Anorexia with empty intestinal tract, markedly reduced growth with thin tails as indicated by poor length weight ratios and lethargy. Elevated mortality rates may approach more than 90% within 30 days of the onset of clinical signs if left untreated.

Diagnostic techniques

Gross Observations: Soft shells and flacid bodies with black or darkened gills and darkened edges of the pleopods and uropods due to expansion of chromatophores. Body surfaces tend to become heavily fouled with epicommensal organisms and bacterial shell disease is more prevalent. There is marked atrophy of the hepatopancreas accompanied by any of the following characteristics: pale whitish center rather than the normal tan to orange; pale with black streaks due to melanization of some tubules; and soft and watery (edematous), with a fluid filled center.

Wet mount: Reduced or abscent lipid droplets and a few to multiple melanized tubules in the hepatopancreas.

Histology: Atrophied hepatopancrease with moderate to extreme atrophy of the tubule mucosa and multifocal granulomatous lesions involving one or more of the tubules. Hepatopancreatic tubule epithelial cells adjacent to granulomatous foci are typically atrophied with simple columnar cells reduced to cuboidal in morphology, little or no stored lipid vacuoles in R-cells and markedly reduced or no secretory vacuoles in B-cells. Hepatopancreatic tubule epithelial cells within the granulomatous foci may be hypertrophied and contain masses of pale basophilic Gram negative, rickettsial-like organisms free in the cytoplasm. The organisms are highly pleomorphic and vary between rod-shaped forms (0.3 9.0 m) and helical forms (0.2 2.6 - 2.9 m). Infected cells may have normal or pyknotic nuclei. Vibrio-like bacteria are often present as presumed secondary infections in tubule lumens in severely affected individuals and may become systemic.
Note: the lesions produced by NHP in P. vannamei are histologically similar to those in P. monodon and P. stylirostris with red disease and septic hepatopancreatic necrosis, and in penaeids experimentally exposed to aflotoxin B1. Lesions attributable to NHP can be distinguished by special stains such as Giemsa's stain, Brown & Brenn Gram stain and Steiner's silver stain or with a DIG-labeled gene probe using in situ hybridization to demonstrate the pleomorphic intracellular NHP pathogen.

Electron Microscopy: The bacterium in the cytoplasm of hepatopancreatic tubule epithelial cells within hepatopancreatic lesions is highly pleomorphic with two distinct morphological variants as described above. The rod-shaped forms have no flagella while the helical forms have eight flagella on the basal apex and an additional flagellum (or possibly two) on the crest of the helix), Both forms of NHP occur free in the cytoplasm and not in membrane bound vacuoles as do the other rickettsia-like organisms of penaeid shrimp.

DNA Probe: A DIG-labelled probe to be used in in situ hybridization assays is available in kit form from DiagXotics Inc. (27 Cannon Rd., Wilton, CT 06897, USA).

Methods of control

Avoid high water temperatures (more than 29 - 31 C) and elevated salinities (more than 20 - 38 ppt) for periods of several weeks which have been shown to precede the development of this epizootic disease.

 

References

Frelier, P.F., R.F. Sis, T.A. Bell and D.H. Lewis. 1992. Microscope and ultrastructural studies of necrotizing hepatopancreatitis in Pacific white shrimp (Penaeus vannamei) cultured in Texas. Vet. Pathol. 29: 269-277.

Krol, R.M., W.E. Hawkins and R.M. Overstreet. 1991. Rickettsial and mollicute infections in hepatopancreatic cells of cultured Pacific white shrimp (Penaeus vannamei). Journal of Invertebrate Pathology 57: 362-370.

Lightner, D.V., R.M. Redman and J.R. Bonami. 1992. Morphological evidence for a single bacterial etiology in Texas necrotizing hepatopancreatitis in Penaeus vannamei (Crustacea: Decapoda). Diseases of Aquatic Organisms 13: 235-239.

Lightner, D.V. (ed.). 1996. A Handbook of Shrimp Pathology and Diagnostic Procedures for Disease of Cultured Penaeid Shrimp. World Aquaculture Society, Baton Rouge.

 

Citation Information

Bower, S.M. (1996): Synopsis of Infectious Diseases and Parasites of Commercially Exploited Shellfish: Necrotizing Hepatopancreatitis of Penaeid Shrimp.

Date last revised:  September 1996
Comments to Susan Bower