Parasit Dan Penyakit Ikan Shrimp Virus

8/10/2019 Parasit Dan Penyakit Ikan Shrimp Virus

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Shrimp Viruses



Shrimp Viral Diseases

• Baculovirus penaei (BP)

• Infectious hypodermal and hepatopoietic

necrosis virus (IHHNV)

• Taura Syndrome Virus (TSV)

• White spot syndrome virus (WSSV)• Yelow Head Virus ( YHV)

• IMNV (Infectious Myonecrotic Virus)

• White Tail Disease



Baculovirus penaei (BP)

• Occurs over the natural range of all penaeid species

native to the western hemisphere

• only baculovirus known to have an impact on the production of Litopenaeus vannamei

• agent: rod-shaped DNA virus, 0.1 µM, cannot be seen

with light microscope

• pathology: infects all life stages of the shrimp, except

nauplii, horizontally transferred in water, passive

adherence to eggs and nauplii from infected spawners





Baculovirus panaei

• Clinical sign : white milky midgut high mortality in larval, postlarval and juvenile prawns,reduced growth rates in surviving juveniles and

adults,increased fouling with exoparasites

Epidemiology

• Transmission is horizontal, directly from the water column or through

cannibalism.• Eggs and newly hatched nauplii may be exposed to the virus through

faeces of infected adult spawners taken from the wild.

• Infection is restricted to the hepatopancreas and anterior midgut.

• Disease is not known to occur in wild populations infected

with Baculovirus penaei.

• Crowding, chemical stress or environmental stress may increase

pathogenicity and the prevalence of disease.

• Transmission typically occurs via the oral route, with cannibalism and

faecal-oral contamination the principal mechanisms.



Baculovirus penaei (BP)

• Diagnosis: virus induces formation of

pyramid-shaped occlusion bodies within

nuclei of hepatopancreas cells of shrimp

– wet mount of HP tissue

– histopathology

– electron microscopy

– ELIZA

– rapid methodologies??



Baculovirus penaei

• Control strategies: normally applied to

shrimp hatcheries, where most transmission

occurs

– involves stopping transmission of virus from

broodstock to offspring (REM: passive vertical)

– use broodstock SPF for BP (prevention) – use BP-free water

– drying pond bottom (not really clear connection

between benthic sediments and BP in grow-out)



1. WET MOUNT OF FECES,

Penaeus vannamei, WITH

TETRAHEDRAL OCCLUSION

BODIES

2. GRADE 3 LEVEL OF

INFECTION OF

HEPATOPANCREAS



I nfectious Hypodermal and

Hematopoietic Necrosis Virus (IHHN)

Description: parvo-like virus, 22 nM diam

• Life stages affected: L. vannamei much more

resistant than L. stylirostris, all life stages affected,

infection during embryo development or shortlyafter hatching results in runt deformity syndrome

(RDS) in L. stylirostris



Infectious Hypodermal and

Hematopoietic Necrosis Virus (IHHN)

• Major signs: if exposure occurs after PL

stage, infection limited to cuticle

deformities, vertical transmission: RDS

• transmission: rapid infection via ingestion

of tissues infected with IHHNV, possibly

through water, embryonic developmentfrom parent

• Diagnosis: gene probe, RDS size frequency



I HHNV: runt deformity

syndrome

• Applies specifically to L. vannamei culture

• harvests contain a large number of small

shrimp (reduced economic value of crop)

• caused by vertical transmission during

ovarian development or shortly thereafter

• nursery and grow-out phase affected



IHHNV/RDS

• Diagnosis: usually via population size

distribution characteristics, physical

appearance of shrimp, IHHNV status

• RDS-affected populations typically have

CV’s of 30% or greater within a downward

shift in mean size

• RDS control: use only wild PL’s, SPF

broodstock



IHHNV

IHHNV-shrimp



IHHNV-shrimp

H&E staining of antennal gland tissue w/Cowdry-

A inclusion body

Feulgen staining of IHHNV infected antennalland tissue





IHHNV

IHHNV-shrimp



IHHNV-shrimp

H&E staining of antennal gland tissue w/Cowdry-

A inclusion body

Feulgen staining of IHHNV infected antennalland tissue



IHHNVDisease agent

Infectious hypodermal and haematopoietic necrosis (IHHN), or runt-deformity

syndrome, is caused by a parvovirus.

Host range

Crustaceans known to be susceptible to IHHN:

blue shrimp* ( Penaeus stylirostris)

giant black tiger prawn* ( Penaeus monodon)

grooved tiger prawn* ( Penaeus semisulcatus)Kuruma prawn* ( Penaeus japonicus)

Pacific white shrimp* ( Penaeus vannamei)

southern white shrimp* ( Penaeus schmitti)

western white shrimp* ( Penaeus occidentalis)

yellow-leg shrimp* ( Penaeus californiensis)Chinese white shrimp ( Penaeus chinensis)

Gulf banana prawn ( Penaeus merguiensis)

Indian banana prawn ( Penaeus indicus)

northern brown shrimp ( Penaeus aztecus)

northern pink shrimp ( Penaeus duorarum)

northern white shrimp ( Penaeus setiferus)



IHHNV

IHHN virus has been officially reported from Australia, Burma (Myanmar),

Indonesia, Iran, Malaysia, Thailand and Vietnam.Epidemiology

Gross signs of disease in an infected animal (ie stunted or deformed rostrum) appear

at about 35 days of postlarval development (PL-35). Earlier larval stages do not

present gross signs but may still be carriers.

The typical gross signs referred to as runt-deformity syndrome may be observed in

juveniles and subadults.

Infected adults seldom show mortalities or signs of the disease.

IHHN virus-resistant prawns and early life stages carry the virus with them,

transferring it to more susceptible species and life stages.

This is a chronic condition that suppresses the prawns' defence system, allowing

infection by other, more serious disease agents.

IHHN virus in infected shrimp tissues remains infectious after five years of storage

at – 20°C and after 10 years at – 80°C.

Transmission is horizontal via water and ingestion, and can also be vertical, from

parent to progeny.



IHHNV

Infectious hypodermal

and haematopoietic

necrosis in juvenile blueshrimp (Penaeus

stylirostrus ). Note white to

buff lesions under shell

(arrows)

Source: DV Lightner





TSV (Taura Syndrom Virus)

Clinical signs of disease in an infected animal

pale red body surface and appendages

tail fan and pleopods particularly red

shell soft and gut emptydeath usually at moulting

multiple irregularly shaped and randomly

distributed melanised cuticular lesions

Disease agentTaura syndrome is caused by Taura syndrome

virus (TSV), a small picorna-like RNA virus

that has been classified in the new family

Dicistroviridae.



Taura Syndrom Virus

Crustaceans known to be susceptible to Taura

syndrome:

blue shrimp* ( Penaeus stylirostrus)Pacific white shrimp* ( Penaeus vannamei)

Chinese white shrimp ( Penaeus chinensis)

giant black tiger prawn ( Penaeus monodon)

Kuruma prawn ( Penaeus japonicus)northern brown shrimp ( Penaeus aztecus)

northern pink shrimp ( Penaeus duorarum)

northern white shrimp ( Penaeus setiferus)

southern white shrimp ( Penaeus schmitti)



Taura Syndrom Virus

Taura syndrome virus has been officially reported from Burma

(Myanmar), China, Indonesia, Thailand and Vietnam.

Epidemiology

Taura syndrome is a disease of the nursery phase of the Pacificwhite shrimp. It usually occurs within 14 – 40 days of stocking

postlarvae into grow-out ponds or tanks, with mortality of 40 –

90%.

TSV can persist outside a host and retain infectivity at

experimental temperatures between 0°C and 121°C.

Transmission is horizontal through ingestion. Although vertical

transmission is suspected, it has not been demonstrated.

Migratory birds, aquatic insects and humans are likely

mechanical vectors of the disease.



Taura Syndrom Virus

.

Resistance of the giant black tiger prawn

and the Kuruma prawn to TSV is unclear,

but they appear to be more resistant thanthe Pacific white shrimp.

Individuals surviving the chronic phase of

Taura syndrome are thought to be carriers

of the virus.Differential diagnosis



TAURA SYNDROME VIRUS

1. Moribund, juvenile pond-reaed P. vannamei in the peracute phase of TSV: soft

shells, lethargic, distinct red tail fan 2. Focal necrosis of tail 3-4. Texas juvenile

pond-reared P. vannamei in the chronic or recovery phase of TSV (with multiple

melanized foci demonstrating epithelium necrosis)



TSV Diagnosis

• General: rapid mortality of juvenile P. vannamei, softexoskeletons, expanded chromataphores, mortality

associated with molting and severe cuticle black spot

lesions

• Histopath: “buckshot” cytoplasmic inclusions

w/pynotic nuclear debris in necrotic areas of the

epidermis

• Bioassay: subject juvenile SPF indicator shrimp

• PCR : polymerase chain reaction on hemolymph,

amplification of TSV genome in nucleic acid

• Gene probe: cDNA probe used in dot blot or in-situ

hybridization assays



TSV Control Strategies

• Apart from exclusion, no effective

strategies have been developed

• very few areas unaffected by this virus

• use of captured wild postlarvae vs. SPF

hatchery-reared

• manipulation of stocking density (2x)

• use of alternative species ( L. stylirostris)

• selective breeding for resistance to TSV



TAURA SYNDROME VIRUS

1. Moribund, juvenile pond-reaed P. vannamei in the peracute phase of TSV: soft

shells, lethargic, distinct red tail fan 2. Focal necrosis of tail 3-4. Texas juvenile

pond-reared P. vannamei in the chronic or recovery phase of TSV (with multiple

melanized foci demonstrating epithelium necrosis)



IMNV (Infection Myonecrosis Virus)

Disease signs at the farm level

large numbers of sick animals and significant mortalities in juvenile and

subadult pond-reared stocks of Penaeus vannamei

Clinical signs of disease in an infected animalacute form of disease produces gross signs and elevated mortalities, but

disease progresses to a chronic phase with persistent low-level mortalities

focal to extensive white necrotic areas in the striated muscle, especially of

the distal abdominal segments and tail fan (which might become necrotic

and reddened in some individuals)

Disease agent

The causative agent is infectious myonecrosis virus, an RNA virus.



Host range

Crustaceans known to be

susceptible to infectiousmyonecrosis:

white shrimp* ( Penaeus

vannamei)

tiger prawn ( Penaeus monodon) blue shrimp ( Penaeus stylirostris)

* naturally susceptible (other

species have been shown to be

experimentally susceptible)

IMNV



Infectious myonecrosis has been officially reported from Indonesia.

Epidemiology

Infectious myonecrosis is a new viral disease identified recently in

northeast Brazil in cultured P. vannamei. However, shrimps withsimilar gross signs have been also reported from other countries

where P. vannamei are cultured.

Affected life stages include juveniles and subadults. Significant

mortalities occur in juvenile and subadult pond-reared populations.

Extremes in salinity and temperature seem to be associated with

disease outbreaks.Horizontal transmission has been demonstrated, but there is no

information on vertical transmission.

IMNV



IMNV

Gross signs of infectious myonecrosis in naturally infected farmed

Pacific white shrimp (P. vannamei ), exhibiting various degrees of

skeletal muscle necrosis, visible as an opaque, whitish discolouration

of the abdomen

Source: DV Lightne



White Spot Syndrome Virus

(WSSV)

• At least three viruses in the white spot

syndrome (WSS) complex have been named

in the literature, all appear very similar

• geographical range: reported from China,

Thailand, Indonesia, Taiwan, Malaysia,

even Texas

• first documented case of WSS in western

hemisphere was recognized in 1995

• found in pond-reared L. setiferus in south

Texas




• Host range: Natural infections have been

observed in the following species:

monodon, japonicus, orientalis, indicus,merguensis, setiferus

• vannamei, stylirostris and all Gulf species

infected experimentally



WSSV

• Crustaceans known to be susceptible white spot syndrome virus:

black tiger prawn* ( Penaeus monodon)Chinese white shrimp* ( Penaeus chinensis)

Gulf banana prawn* ( Penaeus merguiensis)

Indian banana prawn* ( Penaeus indicus)

Kuruma prawn* ( Penaeus japonicus)

Pacific white shrimp* ( Penaeus vannamei)red claw freshwater crayfish* (Cherax quadricarinatus)

blue shrimp ( Penaeus stylirostris)

green tiger prawn ( Penaeus semisulcatus)

• White spot syndrome virus also occurs naturally in many other

decapods, including:mud crabs* (Scylla serrata, Charybdis feriatus, Portunus pelagicus, P.

sanguinolentus)

sand shrimp* ( Metapenaeus spp) and other arthropods

• * naturally susceptible (other species have been shown to be

experimentally susceptible)




• Clinical signs: rapid reduction in food consumption,

lethargy, loose cuticle with white spots (0.5-2 mm) on

inside surface of carapace

• also manifested as red coloration (disease also known

as “red disease”, chromatophore aggregation, not

unique

• 100% mortality within 3-10 days of onset of clinical

signs• Presumptive diagnosis: clinical signs, history

• Confirmatory diagnosis: histological demonstration

in cuticular, antennal gland, lymphoid gland

epithelium

WSSV



WSSV

• White spot disease has been officially reported from Bangladesh,

Burma (Myanmar), Cambodia, China, Hong Kong, India, Indonesia,

Iran, Japan, Malaysia, the Philippines, the Republic of Korea,

Singapore, Thailand and Vietnam.

• Epidemiology

• Although many species of crustaceans are susceptible to infection,

white spot disease is mainly a disease of farmed penaeid prawns.• High mortalities have been reported in many countries.

• Experience has shown the production of prawn farms to fall to about

40% of normal for two years, and then recover to about 70% over the

long term.

• Resistance to white spot syndrome virus has not been reported for anyof the penaeid species listed above.

• Viral multiplication and disease appear to be induced by environmental

stress.



WSSV

• Vertical transmission occurs from infected broodstock, causing chronic

infection in postlarvae.

• Transmission of disease is usually via cannibalism of sick or dying

prawns, or directly through contaminated water.

• Many other crustaceans (such as crabs, krill, lobsters and possibly

copepods) and insects are potential carriers of infection while not

suffering from the disease.

• Birds can transmit the disease from pond to pond by releasing caught

prawns over neighbouring ponds.

• White spot syndrome virus can persist and retain infectivity in

seawater for 4 – 7 days.

• White spots in the cuticle are unreliable even for preliminary diagnosis

of white spot disease, as similar lesions can be produced by some

bacteria, high alkalinity and other infectious or environmental

conditions.




• Rapid test?: squash of gills, appendages or

moribund shrimp, fixed in methanol, stained with

Giemsa (bluish inclusion bodies in cells) • Gene probe (DIG DNA) currently available via

Diagxotics (don’t react to those available for other

shrimp viruses)



WHITE SPOT VIRUS (Penaeus monodon)



Clinical signs of disease in an infected animal

Abdomen (tail) is particularly milky and opaque. Discolouration starts at

the tail extremity (telson region) and gradually progresses towards the

head. Eventually, all muscles in the abdomen and cephalothorax are

affected.Affected postlarvae are more milky and opaque than unaffected

postlarvae. These clinical signs are usually followed by death, with

variable mortality rate up to 95%.

The tissues most affected in moribund postlarvae and early juveniles are

striated muscles of the abdomen and cephalothorax and the intratubular

connective tissue of the hepatopancreas.

Disease agent

The causative agent is Macrobrachium rosenbergii Nodavirus ( Mr NV)

and extra small virus (XSV). Both of these viruses have been found to be

associated with the disease, but their respective roles are not yet clear.

White Tail Disease



White tail disease has been officially reported from

Thailand and Vietnam.

Epidemiology

Very few postlarvae showing the clinical signs of

white tail disease survive. Survivors seem to grow

normally in grow-out ponds.

Outbreaks most commonly occur in larvae, postlarvae

and early juveniles. There is no evidence of adult lifestages being affected, but adults might act as carriers.

Transmission is both vertical and horizontal.

White Tail Disease



White Tail Disease



Yellow Head VIRUS

epidemiology

The tiger prawn suffers acute epidemics, with mortality

reaching 100% within 3 – 5 days from first appearance of

the gross signs.

Transmission is horizontal, direct from the water

column and through ingestion of infected material.

Tiger prawns younger than 15 days postlarvae (PL-15)

are fairly resistant to yellowhead disease compared to

those from PL-20 – 25 to subadult,Massive mortality usually affects early to late juvenile

stages in rearing ponds.



Yellow Head Virus

Penyebab : Yellow head baculovirus (RNA Virus dari

family Ronoviridae)

Terdapat warna kuning pada bagian hepatopancreas,

warna tubuh pucat, Nafsu makan turun kemudian

berhenti sama sekali, berkumpul dipermukaan,

bengkak pada bagian digestive

Diagnosis : PCR



Shrimp Virus Agents



Pencegahan Virus

1. Blm ada vaksin maupun obat kimia yang mampu mengatasi

virus

2. Jika terserang virus makan udang harus dimusnahkan

3. Managemen kesehatan :

Meliputi :Biosecuirtie

Persiapan tambak

Persiapan air dan pengisisan tambak: disinfeksi, pemupukan

filterisasiPenyediaan benih : seragam, test PCR, hindari stress, padat

tebar

Pengelolaan kualitas air: filter 1mm, penggantian air, salinitas

dijaga



Pencegahan virus

5. Monitoring dan evaluasi :Pengelolaan

dasar tambak, sampling, data base6. Pengelolaan pakan

7. Penggunaan bahan kimia dan

antibiotik harus dihindari

Documents

Parasit Dan Penyakit Ikan Shrimp Virus