lecture 9a shrimp bacterial diseases

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  • 8/13/2019 Lecture 9a Shrimp Bacterial Diseases

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    Shrimp Bacter ial Diseases

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    Shrimp Bacterial Diseases

    Covered

    Vibriosis

    necrotizing hepatopancreatitis

    epicommensal fouling disease

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    Shrimp Vibriosis

    Known in Latin America as the Sea Gull

    Syndrome due to shrimp swimming at surface of

    pond (seagulls eat them)

    numerous etiological agents: V. harveyi, V.vulnificus, V. parahaemolyticus, V. alginolyticus

    Wide variety of gram negative motile rods

    most frequently found in hatcheries, but a bigproblem for young PLs in ponds

    all shrimp reared under stressful conditions are

    susecptible

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    Shrimp Vibriosis

    Clinical Signs: high mortalities, in PLs, young

    juveniles; moribund shrimp appear hypoxic and

    often come to the pond surface or edge; sea birds

    preying on shrimp; presence of luminescence intanks

    Presumptive Diagnosis: clinical signs, large

    amounts of bacteria in hemolymph, slow clotting,melanosis of shell

    Confirmatory Diagnosis: isolation/purification

    with appropriate media (TCBS), API RAPID-NFT

    strips

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    Shrimp Vibriosis: commonly

    affected organs

    Cuticle

    hepatopancreas (midgut gland)

    lymphoid organ

    antennal gland

    heart and hemolymph striated muscle

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    Shrimp Vibriosis:

    hepatopancreas

    Most farms in Central America evaluate

    shrimp on a weekly basis for vibriosis

    grosssigns: black spots on cuticle internal signs: evaluation of hepatopancreas

    using wet squash and evaluate blind tubules

    for constrictions, presence of G- rods rate HP on a scale of 0-3, 3 being worse

    medicated feed at 4g/kg oxytet,

    nitrofurizolidone, sarafloxathin (Sarafin)

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    Shrimp Vibriosis

    Hatchery Control: improve husbandry,

    especially in the areas of sanitation, feed

    quality, water source purity, use ofprobiotics, vaccination (Serafin), antibiotics

    Grow-out Control: improve stocking

    handling to reduce stress, have feed in pondin advance of stocking, use of molasses and

    nitrates as fertilizers

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    Shrimp Vibriosis

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    Necrotizing Hepatopancreatitis

    Also known as NHP or Texas Pond MortalitySyndrome, for obvious reasons

    this is a disease of the midgut gland, not, as with a

    vibriosis, the blood

    bacterium prefers high salinities (>10 ppt)

    Agent: believed to be a new genus of theProtobacteria (alpha) group

    found from Peru to Texas

    small, G-, exists in two morphological forms(rod-shaped rickettsial-like and flagellated helix

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    Necrotizing Hepatopancreatitis

    Host range: P. vannamei, P. aztecus, P.

    setiferus, P. stylirostris, P. californiensis

    Diagnostic methods: presence of massive

    numbers of G- bacteria in HP tubuleepithelial cells, atrophy of HP, pallid HP

    color; DIG-labeled DNA probe using in situ

    or dot blot hybridization, TEM of HP cellsshowing granulatomous lesions

    Clnical signs: reduced feed intake, empty

    gut, anorexia, poor l:w ratios, pallid HP

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    Necrotizing Hepatopancreatitis

    Simple diagnosis: most farmers use wet

    mounts of HP and look for reduced lipid

    droplets, melanization of tubules

    Control strategy: frequent histopathological

    examinations, use of oxytet at 4 g/kg (4,000

    ppm), avoidance of high salinity conditions

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    Necrotizing Hepatopancreatitis

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    Zoea II Syndrome

    Problem facing hatcheries throughout the western

    hemisphere

    condition results in heavy mortalities, mainlyconcentrated in the Z2substageof larval penaeid

    shrimp

    syndrome: a group of signs that occur together

    and characterize a particular abnormality

    first characterized in a paper by Lorenzo Juarezof

    Grupo Granjas Marinas (Florida)

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    Zoea II Syndrome

    Because different larval diseases can share

    common clinical signs, it is difficult to

    characterize as distinct pathological agent could be associated with water quality, nutrition

    and/or pathology

    it is felt to be a distinct syndrome, per se, because

    of its life-stage specificity, remarkable similitude

    of clinical signsreported throughout the Americas,

    not noticedprior to 1993

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    Zoea II Syndrome

    Species affected:P. vannameiandP. stylirostris,

    although primarily the former

    Clinical signs: nauplii appear normal and healthy,metamorphose to Z1and start eating normally,

    long fecal strands are exhibited

    36-48 hrs after achieving Z1, first signs appear:

    anorexia, evacuation of guts, lethargy, erratic

    swimming, loss of normal pigmentation

    deathdue to starvation in Z1-2molt

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