shrimp bacterial diseases

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 (rod-

shaped 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