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 PLs in ponds all shrimp reared under stressful conditions are susecptible

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

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