lecture 9a shrimp bacterial diseases
TRANSCRIPT
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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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