Shrimp Bacterial Diseases

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Shrimp Bacterial 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 big
  problem 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 in
  tanks
• 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
• gross signs 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 of probiotics, vaccination
  (Serafin), antibiotics
• Grow-out Control improve stocking handling to
  reduce stress, have feed in pond in 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 Mortality
  Syndrome, for obvious reasons
• this is a disease of the midgut gland, not, as
  with a vibriosis, the blood
• bacterium prefers high salinities (gt10 ppt)
• Agent believed to be a new genus of the
  Protobacteria (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 tubule epithelial cells,
  atrophy of HP, pallid HP color DIG-labeled DNA
  probe using in situ or dot blot hybridization,
  TEM of HP cells showing granulatomous lesions
• Clnical signs reduced feed intake, empty gut,
  anorexia, poor lw 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, mainly
  concentrated in the Z2 substage of larval penaeid
  shrimp
• syndrome a group of signs that occur together
  and characterize a particular abnormality
• first characterized in a paper by Lorenzo Juarez
  of 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 signs reported throughout
  the Americas, not noticed prior to 1993

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Zoea II Syndrome

• Species affected P. vannamei and P.
  stylirostris, although primarily the former
• Clinical signs nauplii appear normal and
  healthy, metamorphose to Z1 and 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
• death due to starvation in Z1-2 molt

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Zoea II Syndrome

• Mortality stops at Z3, survivors continue normal
  larval development
• Internal pathology atrophy of digestive gland,
  inflammation of gut walls
• Possible etiologies water toxicity, bacterial
  pathogen, viral pathogen (no response to
  antibiotics)
• 1997 agent determined to be intracellular
  bacteria (found by TEM in HP)
• as of yet, no known treatment