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Affetcs of Yellow Head Virus (YHV)

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Yellow Head Virus (YHV)

 

Yellow Head Virus was the first major viral disease problem to affect Asian shrimp farms when it was diagnosed as causing extensive losses for shrimp farming. YHV and its close relatives GAV and LOVV are single stand RNA viruses, similar to TSV.

 

 

b2ap3_thumbnail_YHV.jpg

 

 

The first records of this virus were from P. monodon ponds in Eastern Thailand, it had moved to Southern Thailand and was causing substantial mortality. YHV is prevalent wherever P. monodon are cultured, including Thailand, Taiwan Province of China, Indonesia, Malaysia, Mainland China, the Philippines and Viet Nam. It may also have been responsible for the first major crashes in Taiwan. Losses due to YHV continued, although the severity and frequency of outbreaks declined sharply when WSSV became the prime cause of mortality in cultured P. monodon. Although research has shown that YHV is still present in culture ponds, the shrimp now rarely show gross symptoms and are latently infected. There thus appears to be a currently unknown mechanism for rapid tolerance or resistance to RNA-type viruses (such as YHV in Asia, and TSV in Latin America) in Penaeid shrimp. It is known that YHV occurs in wild shrimp, but there is no data on the extent or effects of YHV on populations of wild shrimp in Asia and its impacts are thus currently unknown.

 

The primary mechanism of spread of YHV in pond culture appears to be from water and mechanical means or from infected crustacean carriers. Some infected carriers appear to have latent infections (i.e. P.merguiensis, Metapenaeus ensis, Palaemon styliferus and Acetes spp.), while others may die from it (i.e. Euphausia superba). Other crustaceans, such as Macrobrachium rosenbergii and many crab species and Artemia appear unsusceptible. Since, like most viruses, the viability of the free virus in seawater is not more than a couple of hours, the most serious threat to farmers is latent or asymptomatic carriers, from which the virus can be spread either by ingestion or cohabitation. In addition, infected broodstock can pass on the virus to larvae in the maturation/hatchery facilities if thorough disinfection protocols are not strictly adhered.

 

b2ap3_thumbnail_Yellow-head.jpg

 

Although a distinct possibility, YHV has not yet been reported from Latin America apart from some probably spurious results from Texas. However, from work in Hawaii, YHV is known to cause high mortality in P. vannamei, P. stylirostris, P. setiferus, P. aztecus and P. duorarum when it is injected as viral extracts. Despite this, there are still no reports of “natural” infections in shrimp farms of P. vannamei and P.stylirostris with YHV in Asia. There is a strong possibility, however, that YHV may cause problems for the new culture industries for P. vannamei and P. stylirostris in Asia. This will probably be true at least until these species can gain some degree of tolerance or resistance to the virus as P. monodon appears to have done. In the meantime, the large number of latent infected hosts (including P.monodon) will serve as a potential reservoir of infection and should not be permitted to come into contact with cultures of P. vannamei or P. stylirostris.

 

YHV principally affects pond reared P. monodon in juvenile stages from 5-15 g. Shrimp typically feed voraciously for two to three days and then stop feeding abruptly and are seen swimming near the pond banks. YHV infections can cause swollen and light yellow coloured hepatopancreas in infected shrimp, and a general pale appearance, before dying within a few hours. Total mortality of the crop is then typically seen within three days. Experimentally infected shrimp develop the same signs as those naturally infected, indications of the disease are noted after two days and 100 percent mortality results after three to nine days. Yellow head virus can be detected by RT-PCR or with a new probe for dot-blot and in situ hybridisation tests. It can also be diagnosed histologically in moribund shrimp by the presence of intensely basophilic inclusions, most easily in H&E stained sectioned stomach or gill tissue, or simply by rapid fixation and staining of gill tissue and microscopic examination. Exact protocols for all of these techniques are given in the OIE website and by Flegel et al

 

Eradication methods in ponds are much the same as for other viruses and involve a package including: pond preparation by disinfection and elimination of carriers, storage and/or disinfection of water for exchange with chlorine (30ppm active ingredient), filtering water inlet to ponds with fine screens, avoidance of fresh feeds, maintenance of stable environmental conditions, disinfection of YHV infected ponds before discharge, and monitoring (by PCR) and production of virus free broodstock and PL for pond stocking. Various immunostimulants, nutrient supplements and probiotics have been tried, but there remains a paucity of conclusive evidence of the benefits of such treatments.

 

The rapid tolerance gained by P. monodon to YHV provoked theories as to its mechanism. Whether this theory is correct or not, field data has indicated that shrimp surviving a YHV epidemic are already infected and thus are not killed by subsequent infections, suggesting that some type of “vaccination” with a dead or attenuated virus might provide some resistance. Some commercial products are already being marketed and trials have been partially successful. YHV is not causing much loss at present in Asia, but general management practices as described above (to maintain optimal environmental conditions and minimize viral loadings) are still required to help prevent infections.

 

Lymphoid Organ Vacuolization Virus (LOVV)

 

Lymphoid Organ Vacuolization Virus was first noted in P. vannamei farms in the Americas in the early 1990. In P. vannamei, LOVV has been shown to result in limited localized necrosis of lymphoid organ cells, but has never been shown to impact production. It was later discovered in Australia, along with the other TSV-like virus GAV.

 

 b2ap3_thumbnail_Fig-6-Light-micrograph-of-longitudinal-section-of-P-monodon-lymphoid-organ-with-H-E.png

 

Due to the coincidence in dates, it is possible that the main cause of the problems with P. monodon, was a result of the introduction of viral pathogens carried by P. vannamei. A RNA viral pathogen very similar to LOVV in P. vannamei has recently been discovered in Thailand in the lymphoid organ of P. monodon. This new type of LOVV might be the causative agent of this slow growth phenomenon. Evidence for this was provided by Timothy Flegel (per. com.), who found that juvenile P. monodon injected with this virus grew to only 4g after two months, whilst those injected with a placebo reached 8g in the same time. Injections of the same virus into P. vannamei caused no obvious effects, suggesting that it probably originated from this species.

 

Other viruses

 

There are a number of other viruses in the Asia-Pacific region. Penaeus monodon from Australia have been found to be hosts for a number of viruses not yet present in other Asian countries. These include two viruses closely related to YHV: GAV (only 20 percent genetically different to YHV) and MOV (only 10 percent genetically different from GAV), which are quite recently discovered viruses that are already prevalent in 100 percent of P. monodon from Queensland. MOV was only discovered in 1996, but has already been found in P. japonicus and is associated with disease episodes in P. monodon farms in Australia and elsewhere in Asia. The strong possibility for the introduction of these viruses into Asia exists due to frequent shipments of P. monodon broodstock from Australia into Thailand, Viet Nam and other Southeast Asian countries.

 

Many of the viruses infecting shrimp are hidden or cryptic and, although present in their host, may produce no gross signs of disease or notable mortality. Many of these viruses, without methods of diagnosis, are probably being harboured unknown within the wild and cultured populations of shrimp throughout the world. It may not be until shrimp species from one location are moved to another and their viral flora comes into contact with new and/or naive or intolerant hosts that disease epidemics begin. Crustaceans may be particularly problematic since they tend to have persistent, often multiple, viral infections without gross or even histological signs of disease.

 

 

Examples of this problem include the transfer of IHHNV from the tolerant P. monodon in Asia to the susceptible white shrimp P. vannamei and P. stylirostris in Latin America. Another possibility in this category is the LOVV virus thought to be causing the slow growth phenomenon in P. monodon around Asia. This virus may have been imported with live P vannamei broodstock and PL brought to Asia from the Americas in the mid 1990s. For this reason, extreme caution should be placed on the transboundary movements of live shrimp.

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