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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 • • • • • • 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