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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 M, 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
There are few visible signs indicating
infection with this disease other than rapid
high mortality of hatchery prawns in the
early life stages. Therefore, diagnosis is
usually based on microscopic and
histological examination.

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

Infectious 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 shortly
after 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 development
from parent
Diagnosis: gene probe, RDS size frequency

IHHNV: 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
CVs of 30% or greater within a downward
shift in mean size
RDS control: use only wild PLs, SPF
broodstock

IHHNV

IHHNV-shrimp

IHHNV-shrimp
H&E staining of antennal gland tissue w/CowdryA inclusion body

Feulgen staining of IHHNV infected antennal


gland tissue

IHHNV
Disease signs at the tank and pond level
reduced food consumption
sometimes prawns repeatedly float slowly to water
surface, roll over and then sink to bottom
increasing morbidity/mortality
Clinical signs of disease in an infected animal
reduced and irregular growth in juveniles and
subadults (runt-deformity syndrome)
white to buff mottling of shell, especially at the
junction of shell plates of the abdomen
giant black tiger prawn (Penaeus monodon) may
appear blue
deformed rostrums grow to one side

IHHNV

IHHNV-shrimp

IHHNV-shrimp
H&E staining of antennal gland tissue w/CowdryA inclusion body

Feulgen staining of IHHNV infected antennal


gland tissue

IHHNV
Disease 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 20C and after 10 years at 80C.
Transmission is horizontal via water and ingestion, and can also be vertical, from
parent to

progeny.

IHHNV
Infectious hypodermal
and haematopoietic
necrosis in juvenile blue
shrimp (Penaeus
stylirostrus). Note white to
buff lesions under shell
(arrows)
Source: DV Lightner

IHHNV

IHHN in juvenile blue


shrimp. Note classic
rostrum deformation

IHHN in juvenile blue shrimp.


Note deformed tail fan and sixth
abdominal segmentSource: 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 empty
death usually at moulting
multiple irregularly shaped and randomly
distributed melanised cuticular lesions
Disease agent
Taura 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 Pacific
white shrimp. It usually occurs within 1440 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 0C and 121C.
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 than
the 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, soft
exoskeletons, 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 animal
acute 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.

IMNV

Host range
Crustaceans known to be
susceptible to infectious
myonecrosis:
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 with
similar 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

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

White Spot Syndrome Virus


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)

White Spot Syndrome Virus


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
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 any
of 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 47 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.

White Spot Syndrome Virus


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 (dont react to those available for other
shrimp viruses)

WHITE SPOT VIRUS (Penaeus monodon)

White Tail Disease


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 (MrNV)
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 life
stages being affected, but adults might act as carriers.
Transmission is both vertical and horizontal.

White Tail Disease

Yellow Head VIRUS


epidemiology
The tiger prawn suffers acute epidemics, with mortality
reaching 100% within 35 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-2025 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
filterisasi
Penyediaan 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 base
6. Pengelolaan pakan
7. Penggunaan bahan kimia dan
antibiotik harus dihindari