Acute Hepatopancreatic Necrosis Disease Aetiology Epidemiology Diagnosis Prevention

Acute Hepatopancreatic Necrosis Disease

Aetiology Epidemiology Diagnosis Prevention and Control References

Acute hepatopancreatic necrosis disease (AHPND) emerged as a new disease of shrimp in 2010. The disease is sometimes referred to as early mortality syndrome, which is a broader term used to describe a range of shrimp health problems that lead to early mortality. The information presented in this technical fact sheet reflects the epidemiological observations and research information available to date (December 2013),together with additional data on Vibrio parahaemolyticus. 

AETIOLOGY

Classification of the causative agent

AHPND has a bacterial aetiology. A bacterial isolate identified as a member of the Vibrio harveyi clade, most closely related to Vibrio parahaemolyticus, has been found to cause AHPND experimentally. Further studies to characterise the causative agent, including genetic characterisation, are continuing.

Resistance to physical and chemical action

Data are from transmission experiments for AHPND and strains of V. parahaemolyticus occurring in seafood:

Temperature: 

Freezing – Attempts to transmit AHPND using infected frozen shrimp have been unsuccessful. Strains of V. parahaemolyticus in seafood are known to be sensitive to freezing (–18 to –24°C) and reductions in culturable cells to non-detectable levels have been reported after freezing for several weeks. Time of total inactivation depends on the initial number of bacteria and temperature. 

Refrigeration – Strains of V. parahaemolyticus in seafood are known to be sensitive to refrigeration (4°C) and reductions in culturable cells have been reported, but not to nondetectable levels during the storage life of seafood products at this temperature.

Heating – Strains of V. parahaemolyticus in seafood are known to be sensitive to heating and reductions in culturable cells to non-detectable levels have been reported at 55°C for 5 minutes and 80°C for 1 minute. 

Chemicals/ Disinfectants: 

Susceptible to common disinfectants. No culturable cells after exposure to pH 5 for 15 minutes

Survival: 

Survival to 9 and 18 days in filtered estuarine water and filtered seawater respectively. Densities of V. parahaemolyticus in seawater are known to be temperature dependant

EPIDEMIOLOGY

Hosts

AHPND has been reported from farmed populations of the following shrimp species:

• Penaeus vannamei
• Penaeus monodon
• Penaeus chinensis

Transmission

AHPND has been transmitted experimentally by immersion and reverse gavage. Based on these experiments, transmission by oral routes and cohabitation should be expected.

Occurrence

AHPND has been officially reported in China (People’s Rep. of) and Vietnam (2010), Malaysia (2011) and Thailand (2012) and Mexico (2013). AHPND is not listed by the OIE. However the disease does meet the definition of an emerging disease in the OIE Aquatic Animal Health Code (Aquatic Code). Member countries should consider their obligation to report any occurrence of the disease in accordance with Chapter 1.1 of the Aquatic Code

Food safety

Consumption of raw or undercooked seafood contaminated with V. parahaemolyticus can lead to development of acute gastroenteritis in humans. Results of preliminary investigations of AHPND did not detect the human pathogenic strains producing thermostable direct haemolysin (TDH) and TDH-related haemolysin (TRH), in the V. parahaemolyticus causing AHPND. There has been no report of human-related disease (e.g. gastroenteritis) linked to the consumption of affected shrimp from any of the affected countries since the emergence of AHPND (FAO, 2013).

DIAGNOSIS

A disease card for AHPND is available from the Network of Aquaculture Centres in Asia Pacific (NACA: see references).

Clinical diagnosis 

Typical signs of AHPND begin within 10–30 days after stocking of post larvae into a newly prepared pond.

• The following signs may be observed:
• Hepatopancreas (HP) often pale to white due to pigment loss in the connective tissue capsule
• Significant atrophy (shrinkage) of HP
• Often soft shells and guts with discontinuous contents or no content
• Black spots or streaks sometimes visible within the HP
• HP does not squash easily between thumb and finger
• Onset of clinical signs and mortality starting as early as 10 days post-stocking
• Moribund shrimp sink to the bottom

Histopathology

• Acute progressive degeneration of the HP accompanied initially by a decrease of R-, B- and Fcells followed last by a marked reduction of mitotic activity in E-cells
• Progress of lesion development is proximal to distal with dysfunction of R-, B-, F-, and lastly Ecells, with affected HP tubule mucosal cells presenting prominent karyomegaly (enlarged nuclei), and rounding and sloughing into the HP tubule lumens
• The sloughed HP cells provide a substrate for intense bacterial growth, resulting in massive secondary bacterial infection and complete destruction of HP at the terminal phase of the disease
• Accompanying the initial sloughing of HP tubule epithelial cells and the development of a secondary bacterial infection is intense intertubular haemocytic aggregation and haemocyte encapsulation of necrotic HP tubules and melanisation of the more proximal portions of HP tubules in some shrimp

Laboratory diagnosis

Samples

For culture of bacteria:

Live shrimp

For histopathology:

Whole juvenile shrimp fixed in Davidsons fixative

For molecular tests:

Whole juvenile shrimp fixed in 100% ethanol or frozen

Procedures

Identification of the agent

• Bacterial culture
• Biochemical methods
• PCR and sequencing

Histopathology

Demonstration of characteristic histopathology

PREVENTION AND CONTROL