Transcript Lecture 5: Bacterial Diseases of Fish and Shrimp

Shrimp Bacterial Diseases
Shrimp Bacterial Diseases
Covered
• Vibriosis
• necrotizing hepatopancreatitis
• epicommensal fouling disease
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 PL’s in ponds
• all shrimp reared under stressful conditions are
susecptible
Shrimp Vibriosis
• Clinical Signs: high mortalities, in PL’s, 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
Shrimp Vibriosis: commonly
affected organs
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Cuticle
hepatopancreas (midgut gland)
lymphoid organ
antennal gland
heart and hemolymph
striated muscle
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)
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
Shrimp Vibriosis
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 (>10 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 (rodshaped rickettsial-like and flagellated helix
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 l:w ratios, pallid HP
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
Necrotizing Hepatopancreatitis
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)
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
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
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