1. Shrimp Bacterial Diseases

2. Shrimp Bacterial Diseases Covered
Vibriosis
necrotizing hepatopancreatitis
epicommensal fouling disease

3. 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

4. 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

5. Shrimp Vibriosis: commonly affected organs
Cuticle
hepatopancreas (midgut gland)
lymphoid organ
antennal gland
heart and hemolymph
striated muscle

6. 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)

7. 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

8. Shrimp Vibriosis

9. 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

10. 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

11. 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

12. Necrotizing Hepatopancreatitis

13. 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)

14. 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

15. 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

16. 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