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Penaeus monodon mortality syndrome (PMMS) Early mortality syndrome (EMS) Acute hepatopancreatic necrosis disease (AHPND) Dr Matt Landos Director, Future.

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Presentation on theme: "Penaeus monodon mortality syndrome (PMMS) Early mortality syndrome (EMS) Acute hepatopancreatic necrosis disease (AHPND) Dr Matt Landos Director, Future."— Presentation transcript:

1 Penaeus monodon mortality syndrome (PMMS) Early mortality syndrome (EMS) Acute hepatopancreatic necrosis disease (AHPND) Dr Matt Landos Director, Future Fisheries Veterinary Service Pty Ltd Kelly Condon James Cook University

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3 Potted International history AHPND
Emerged from China in ~ of new disease Vague reports of spread through Thailand, Vietnam, Americas Huge farm losses up to day 30 initially (now out to day 110) FAO convened workshop 2013 on EMS Pathology caused by PirAB toxin production from a Vibrio in stomach OIE definition initially confined to Vibrio parahaemolyticus, soon to be broadened to include other Vibrio’s and plasmid Now reported in Vibrio harveyi also in Asia and Australia In Asia PirAB toxin associated with a plasmid (ie independent of bacterial DNA) In Australia, PirAB not associated with a plasmid, it is part of chromosome

4 Clinical signs of AHPND
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

5 PMMS Outbreaks

6 PMMS screening 2016 13 farms from Northern NSW to Far north Qld
980 samples All P monodon sampled for PCR and tissue stored for histology Targeted prawns with signs of poor health 10 prawns per pond Pond numbers varied relative to farm size and study assumptions Add hepatopancreas to broth to improve test sensitivity JCU Results: 100% PCR test negative for PirA toxin DNA

7 Assumptions If prevalence of PirA DNA was >4% at individual prawn level & >25% of ponds affected then our test design was highly likely to find it.

8 Disease incursion vs domestic evolution?
Epidemiology does not suggest exotic incursion Bacteria can acquire new DNA into chromosome through mobile genetic elements like integrons or transposons Numerous factors can drive such DNA acquisition eg Heavy metal exposure Antibiotic exposure Urgent need to determine risk factors associated with outbreaks Increased event based sampling warranted Disinfection response protocol justified


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