following some kind of virus that usually attacks the fish and shrimp
1. KHV (CyHV3) / Koi Herpes Virus
Koi herpes virus (KHV) that attack and koi carp were first discovered in Israel in 1997 (Doyle, 2003), then the United States and some European countries including the UK, Denmark, Netherlands. In Asia, attacked KHV carp and koi in 2002 in Indonesia, beginning in 2003 in Taiwan and Japan last in late 2003 (Haenen, 2003).
In Indonesia, Koi Herpes Virus attack goldfish and koi in Blitar first time in March 2002, continued to spread to the West Java in April 2002, Central Java and Bali. In February 2003, the disease spread to the island of Sumatra. (Sunarto et al, 2002).
ATTACK: Gold fish, Koi
SYMPTOMS:
Fish's movements were not controlled, gasping for air / oxygen deficiency, decreased appetite, skin blister, on the tip of lamella rusted gills then decay, mass mortality occurred within 1-5 days. SPREAD: The virus is transmitted horizontally from one fish to another fish (not through descent). Interestingly, this virus only attacks the carp (Cyprinus carpio) and does not harm other fish. The virus can live freely in fresh water for approximately 20 hours, even in the mud pond this virus can survive more than 24 hours.
Therefore once the virus is easily transmitted from live or dead fish infected by KHV. Likewise, the former fish pond inveksi KHV would be very dangerous and easily transmit to other pools, either through waste water ponds, mud base the rest of the pond, and the water in the pool itself.
Responds:
Grading, quarantine, destroy, no cure
2 WSSV (White Spot Syndrome Virus)
White dot syndrome (White Spot) first appeared in the Fujian Province of China in 1992 was soon after reported in Taiwan and Japan and has since become a disaster in all regions of shrimp farming in Asia and America. It is the most destructive disease of shrimp culture with social and economic impact of more than 15 years. WSSV attacks the organ systems of crustaceans that causes white patches on the external surface of the shrimp to cause harm in the form of high mortality (mortality) reaches 100%. The shrimp were affected in the short time that shrimp can experience very high mortality. WSSV is a virus that is caused by a virus SEMBV and belonged to the genetic material DNA viruses (Dioxyribonucleic Acid) rod-shaped (bacilliform). The beginning of the spread of this disease is usually preceded by a mass of dead phytoplankton, pond water suddenly changed color and consistency of pond water had risen (Yanto, 2006).
ATTACK: Crustaceans
SYMPTOMS:
WSSV infected shrimp will experience a change in behavior that is decreasing the activity of swimming, the lack of balance in swimming, and unfocused. Besides shrimp swim more often clustered at the edge of the pond and swim to the surface. In the acute phase there are white spots on the carapace with a diameter of 0.5-3.0 mm, but the color becomes red shrimp broodstock (Mahardika et al., 2004 in Yanto, 2006), and white patches first appeared on the cephalothorak segments to 5 and to 6 of the last abdominal and then spread throughout the body cuticle (Wang et al., 1997a in Yanto, 2006).
SPREAD:
The virus is easily spread both vertically and horizontally, meaning that the virus can be transmitted through mother to child as well as direct contact with sick shrimp, water and equipment used.
Transmission can also through animals (carrier) such as: crab, crab, rebon, jambret, and other wild shrimp entering the pond system during water change. The virus is easily spread to other shrimp through the process of eating each other (cannibalism). Shrimp are going to be eaten by shrimp healthy, so healthy shrimp will be infected. WSSV can also be transmitted from one pond to another pond through the bird. Shrimp are swimming on the surface and then eaten by birds, and the rest falls into another pond.
Responds: Grading, quarantine, destroy, harvest early, there is no cure
3 TSV (Taura Syndrome Virus)
TSV is a virus that attacks or infects vannamei shrimp (Litopenaeus vannamei) which has been introduced in Indonesia. TSV attack generally occurs at the age of 14-40 days after stocking in ponds, with a mortality rate can reach 95%. Initially, TSV disease known as juvenile shrimp diseases size from 0.05 to 5 g / tail on shrimp vanname (Widayanti, 2005). when the disease occurs in the first 30 days, meaning the source of infection or genetic parent (vertical), if more than 60 days means the infection comes from the environment (horizontal). Adults can be infected shrimp vaname TSV, but the mortality rate is relatively low. TSV infection there are two (2) phases, namely acute and chronic phase. In the acute phase of this shrimp will experience mass death. Shrimp survival of TSV disease, will experience chronic phase.
Attacking: Shrimp Vanname
SYMPTOMS:
In the chronic phase, the shrimp are able to live and grow relatively normal, but the shrimp is a carrier (carrier) TSV that can be transmitted to other healthy shrimp. In infe
ction severe (acute) often result in mass death, dying shrimp dominated by shrimp that are or recently completed the process of changing the skin (molting), empty digestive tract and body reddish color. The red color can be seen firmer on the tail fan (telson) (Widayanti, 2005). Meanwhile, the shrimp that survived the acute phase, generally will be able to live and grow normally with black spots mark (melanization) irregular under the cuticle layer.
SPREAD:
This virus is spreading from parent, fry, water, carrier, feed, actors and all components of the aquaculture production of shrimp
Responds : Grading, quarantine, destroy, harvest early, there is no cure
4. VNN (Viral nervous necrosis)
Viral Nervous Necrosis (VNN), is a type of virus that attacks Nodaviridae groupers, especially in the larval stage and seed. VNN can cause mass mortality of up to 100% prevalence (Johnny et al., 2010; Suratmi and Ni Luh, 2008).
Viral Nerveus Necrosis (VNN) becomes a major problem in the production of the world's marine fisheries. Identification of the virus that causes this is VNN Nodaviridae family members obtained by investigating nucleic acids and structural proteins of the virus Pseudocaranx dentex larvae.
Family Nodaviridae there are two types, namely types Alphanodavirus and Betanodavirus, both these types of very virulent in infected fish. Betanodaviruses (family Nodarideae) is the causative agent of viral attack nerveus necrosis (VNN) in marine fish farming. Betanodaviruses is a small virus, spherical, no capsid with a genome consisting of two single bonds.
ATTACK: Different Types of grouper, snapper
5. IMNV (Myonecrosys Infectious Virus)
Myo (Infectious myonecrosis virus) which includes first-class attacking picornavirus shrimp in Brazil in 2003 in Indonesia, myo appears first in the Situbondo in 2006 After that, myo outbreaks in aquaculture Banyuwangi, Lampung, then spread to Bengkulu, Sumatra north, Borneo, Bali, and Nusa Tenggara. Currently, myo almost spread to 2/3 parts of Indonesia (Anonymous, 2009).
ATTACK: Vannamei Shrimp
SYMPTOMS:
This disease was originally found in the two-month-old shrimp. Myo also attacked the young shrimp 30 days after stocking. The shrimp were exposed to this virus has been the emergence of clinical symptoms of plaque color or white cotton on the muscle that is visible from the side or above. Is increasingly evident, which further contained a reddish color in the fifth and sixth abdominal segment, accompanied by a gradual shrimp mortality (Yanto, 2006). SPREAD: According to Yanto (2006), some suspected as a trigger for the emergence of cases of Myo including declining water quality from the optimum conditions, the high content of plankton and toxic compounds. It is also caused by plankton that are too concentrated and excess floc (blooming).
6. Iridovirus
Iridovirus is a virus that infects animals poikilotermik invertebrates and vertebrates, such as fish, insects, amphibians, and reptiles (Williams, 1996). Iridovirus is a form of double-stranded DNA virus with icosahedral symmetry, not everything is enveloped, and have a diameter of 120-300 (Tidona et al., 1998). Iridovirus virion consists of three domains, namely concentric outer capsid protein, lipid membrane containing the protein subunits in the middle, and the cores are composed of DNA-protein complexes. This virus has a 25-75 structural proteins with a molecular weight range 12000-150000 kDa. Generally iridovirus capsid protein is about 50 kDa and is a major structural component, which accounted for 45% of the total virion protein. Iridovirus genome size varies between 105-212 kbp). Iridovirus have a replication strategy that involves nuclear and cytoplasmic stage, generating complete genomes with multiple gene duplications at the tip (terminal redundancy) and between the different ends of the viral particles produced (cyclic Permutation). Capsid protein-coding genes of several vertebrate and invertebrate iridovirus has been sequenced and its coding region has a lot of similarities.
SYMPTOMS:
Iridovirus-infected fish appear weak, decreased appetite, suffered severe anemia, red patches (ptechiae) on the gills, swelling of the spleen, and kidneys. According Tidona et al. (1998), malabar grouper iridovirus infected show symptoms gills and pale body color, loss of balance so that the fish still in the net basis and will usually die within days after symptoms appear.
SPREAD:
it's spread vertically and horizontally, through the medium of water and direct contact
RESPONSE: Grading, quarantine, destroy, no cure
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