bacterial diseases of shrimp

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BACTERIAL DISEASES OF SHRIMP : 

BACTERIAL DISEASES OF SHRIMP K.SARAVANAN FPM 40

CONTENT : 

CONTENT Introduction Vibriosis Necrotizing hepatopancreatitis Mycobacteriosis Rickettsial infection Conclusion

Common name Species affected Causative agent Distribution Route of infection Effect on host Biology and epizootiology Gross signs Method of diagnosis Prevention Treatment

INTRODUCTION : 

INTRODUCTION Bacteria – natural microflora of seawater Accumulation of unutilized feed & metabolites of shrimp with organic matter supports multiplication of bacteria Bacterial infections – primarily stress related Adverse environmental conditions or mechanical injuries - important factors of bacterial infections The expansion and intensification of shrimp farming industry impose stress on shrimps and making them susceptible to disease

VIBRIOSIS : 

VIBRIOSIS Common name : Vibrio disease of shrimp, syndroma gaviota or seagull syndrome, summer syndrome, syndrome 93, luminiscent vibriosis and penaeid bacterial septicemia Species affected : All penaeid sp Causative agent : ;: G(-)ve,motile,rod shaped bacteria belonging to the genus vibrio includes Vibrio parahaemolyticus, V.alginolyticus, V.harveyi, V.penaeicida,V.anguillarum, V.splendidus,V.vulnificus and V.damsela other sp isolated responsible are Pseudomonas sp ,Flavobacterium sp and Aeromonas sp

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Geographic distribution : Ubiquitous Route of infection : Vibrio spp – chitinoclastic bacteria may enter through wounds in exoskeleton or pores. Gills - covered by thin exoskeleton. Midgut (DG+MGT) is not lined by exoskeleton Transmission - water or through ingestion of infective material

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Effect on host : Mortalities upto 100 % Biology and epizootiology : Majority are secondary infections,occuring as a result of other primary conditions. Vibriosis – multitude of infections known as blackshell disease,septic hepatopancreatic necrosis,tail rot,brown gill disease,swollen hindgut syndrome and luminous bacterial disease.

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Gross signs : Erratic and disoriented swimming and lethargy. Black to brown colouration on gills,cuticle,appendages due to melanin production. Opaqueness of abdominal muscle,anorexia. Expansion of chromatophores on the dorsal surface,periopods,pleopods and appendages giving red colouration.

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Larval and PL signs of vibriosis includes melanisation and necrosis of appendages tips. Affected shrimp shows off-feed and empty guts. The gills,lymphoid organ and DG shows degenerative changes Detachment of epithelium from the midgut trunk. Specific morphological changes to the DG includes tissue necrosis, loss of epithelium and infiltration of hemocytes. Hemolymph clots very slowly Hemocytes number drastically reduced

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Method of diagnosis : Isolation of Vibrio sp from tissue or hemolymph of moribund shrimp Media – TCBS agar, Tryptic-soy agar and Zobell’s marine agar(0.5 to 3 % Nacl is added) Yellow colonies on TCBS

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Prevention : Adequate water quality Nutritionally adequate feed Sterilization and filtration of incoming water Reduction of stress Vaccination with killed Vibrio sp Terrestrial Lactic acid bacteria as dietary probiotic

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Treatment : Formalin at 10 to 25 ppm Malachite green at 5 to 10 ppb EDTA at 10 to 50 ppm Furanace at 1 ppm Chloramphenicol at 1 to 10 ppm OTC at 1 to 10 ppm

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Present status of vibriosis : Common problem particularly in the Philippines V.harveyi – chronic mortalities upto 30 % among the Australian P.monodon larval and PL stages Highly pathogenic strain of Vibrio sp (AM 23), recently identified with Syndrome 93 from New caledonia among P.stylirostris An active research programme is underway to develop cost effective immunodiagnostic for Vibriosis using polyclonal antisera

NECROTIZING HEPATOPANCREATITIS : 

NECROTIZING HEPATOPANCREATITIS Common name : Texas Necrotizing Hepatopancreatitis (TNHP),Granulamatous hepatopancreatitis, Texas Pond Mortality Syndrome (TPMS), Peru Necrotizing Hepatopancreatitis (PNHP) Species affected : Litopenaeus vannamei, L.stylirostris, L.setiferus, Farfentepenaeus aztecus and F.californiensis

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Causative agent : Two or three types of bacteria Pleomorphic,rod shaped,rickettsia-like bacteria of 0.3 to 0.9 micron A helical form mollicute-like bacteria of 0.3 to 0.9 micron A filamentous mollicute-like bacteria Recent studies - causative agents are G(-)ve bacteria and are mostly rod and helical forms

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Distribution : Geographically limited. Western hemisphere includes Panama,Columbia, Mexico,Ecuador,Brazil,Costa Rica,Nicaragua,Peru and Venezuela Route of infection : Horizontal transmission via contaminated water and by cannibalism

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Effect on host : Reduced feed intake,reduced growth,soft shells and black gills Lethargy and mortality.If untreated losses upto 50 to 99 % Elevated salinity(30-38 ppt) and elevated temperature(30-35 C)- factors associated with disease outbreak Biology and epizootiology : First observed in Texas shrimp farm during 1985 Principal lesion- inflammation and necrosis (TNHPS)

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Gross signs : Large cytoplasmic masses of basophilic bacteria in HP HP is necrotic,non-functional and having granulomatous lesions Empty gut and pale-white colouration of atrophied HP Secondary invasion

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Method of diagnosis : 3 methods Routine histological analysis Insitu Hybridisation(ISH) with NHP-specific gene probes PCR using NHP-specific oligonucleotide primers Prevention : Avoid high temperature and elevated salinity Treatment : OTC at 0.5 to 2 kg per 1000 kg of feed Metaphalatic therapy- effective treatment scheme

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Present status of NHP : NHPB - unculturable through invitro methods Method for continuous development of NHPB in SPF stock of L.vannamei recently developed by GCRL Dr.Donald V.Lightner and Farming Intelligene Tech Corporation developed – IQ 2000 NHPB Detection and Prevention system Adopted the Nested PCR and differentiate infected shrimps into 4 levels: severe,moderate,light and very light

MYCOBACTERIOSIS : 

MYCOBACTERIOSIS Common name : Mycobacterium infection of shrimp and shrimp tuberculosis Species affected : All penaeid species Causative agent : Gram(+)ve,rod shaped,acid fast bacteria - Mycobacterium marinum and M.fortuitum Distribution : Ubiquitous

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Route of infection : Unknown. Probably by ingestion or wound contamination Effect on host : Abnormally dark pigmentation having multifocal melanised hemocytic nodules Larger prominent melanised granulamatous lesions composed of multiple nodules

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Biology and epizootiology : Infected shrimp creates a problem to marketing Accidental infections of shrimp farm workers produce nodular skin lesions – difficult to treat Gross signs : Lesions in lymphoid organ,heart,cuticle,loose connective tissues of muscle,HP,antennal gland,ovary and gills These lesions containing cellular debris,acid fast bacterial rods surrounded by multiple concentric layers of flattened hemocytes

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Method of diagnosis : Gross observations - Histology - Palely basophilic rod shaped bacteria with hemocytic nodules Smears - Impression smears with Zeihl-Neelsen stain

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Prevention : Good husbandry practice Avoid diseased fish Use treated water Destroy the diseased stock Treatment : No known method of treatment

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Present status of Mycobacteriosis : Mycobacterium sp – not reported in cultured Penaeids of Australia,reported only in captive M.rosenbergii Wild adult P.vannamei – Panama and Ecuador Cultured juvenile P.vannamei – Mississippi Fish Mycobacteriosis as zoonosis – scientific report shows that 76 % associated with aquatic environment Prolonged use of a combination of antimicrobials thought to be effective

RICKETTSIAL INFECTION : 

RICKETTSIAL INFECTION Common name : Rickettsial infection of Penaeid shrimp Species affected : P.monodon,P.marginatus,P.merguiensis and P.stylirostris Causative agent : Rickettsia or Rickettsia like microorganisms with a size range of 0.2 to 0.7 x 0.8 to 1.6 micron Order – Rickettsiales Family – Rickettsiaceae

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Distribution : Wild caught juveniles of P.marginatus – Hawaii Cage cultured P.monodon- Singapore,Malaysia and Indonesia Route of transmission : Horizontal Effect on host : Host target cells- Hepatopancreatic epithelium in P.merguiensis and P.marginatus Impaired function of HP

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Impaired digestion and absorption In P.monodon fixed phagocytes,connective tissue cells,antennal gland and Y- organ are affected Inflammatory lesions and intravascular aggregations of hemocytes in gills Slow growth rate and eventual death Biology and epizootiology : P.marginatus – natural reservoir of Rickettsia Rickettsia of P.marginatus cause high mortality disease syndrome in juvenile P.stylirostris

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Gross signs : Hepatopancreatic infection – Heavily infected shrimp Lethargic Off -feed Atrophy and pale colouration of HP Systemic infection Congregated in shallow pond edges Brown discoloured gills Opaque abdominal muscle Mushy texture of HP

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Method of diagnosis : Histologic demonstration Large granular, rickettsia- filled cytoplasmic vacuoles Microcolonies size – 5 to 50 microns Stained basophilic Fuelgen (+) Gram (-)

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Prevention : Quarantine Sreening of potential carriers Destruction of infected stock Disinfection Treatment : None reported Tetracycline

CONCLUSION : 

CONCLUSION G(-) bacteria causes epizootics Concentration of farming activities and release of untreated effluents into water source Poor pond management avoided by improved practices Therapeutants approved by FDA is limited Replacement of antibiotics by probiotics is needed

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