This virus was first discovered in P. vannamei and P. stylirostris in the America, starting in Hawaii. However, it was probably not an indigenous virus, but was thought to have been introduced along with live P.monodon from Asia. IHHNV has probably existed for some time in Asia without detection due to its insignificant effects on P. monodon, the major cultured species in Asia, meaning that nobody was looking for it. Recent studies have revealed geographic variations in IHHNV isolates, which suggested that the Philippines were the source of the original infection in Hawaii, and subsequently in most shrimp farming areas of Latin America.




IHHNV is a small single-stranded DNA-containing parvovirus, which is only known to infect only Penaeid shrimp. “Natural” infections are known to have occurred with P. stylirostris, P. vannamei, P. occidentalis and P. schmitti, while P.californiensis, P. setiferus, P. aztecus and P. duorarum were proven susceptible experimentally in Latin America. Penaeus monodon, P. semisulcatus, P. japonicas and P. chinensis and others are known to be susceptible in Asia. Catastrophic epidemics and multi- million dollar losses in shrimp culture have been attributed to IHHNV and it has had significant negative consequences for cultured P. vannamei in the America. Some indication of its impact may be gauged from work done in intensive culture systems in Hawaii, which improved yields by 162 percent through the stocking of shrimp bred specifically to be IHHNV resistant.


IHHNV was also largely responsible for the temporary cessation of Mexican commercial shrimp fishing for several years once it escaped from farms into the wild shrimp populations. IHHNV is now commonly found in cultured and wild Penaeid on the Pacific coast of Latin America from Mexico to Peru, but not yet from the eastern coast of Latin America. It has also caused problems for the Hawaiian broodstock and farm- based culture industries. IHHNV has also been reported from both cultured and wild Penaeid from throughout the Indo-Pacific region. IHHNV is fatal to P. stylirostris (unlike P. vannamei), which, although highly resistant to TSV are extremely sensitive to IHHNV , especially in the juvenile stages. However, IHHNV has not been associated with mass mortalities of P. stylirostris in recent years, probably due to the selection of IHHNV-resistant strains (i.e. the so-called “supershrimp” P. stylirostris. This emphasises the potential benefits offered from the domestication and genetic selection of cultured shrimp.


Penaeus vannamei are fairly resistant to this disease with certain modifications in management practices. In P. vannamei, IHHNV can cause runt deformity syndrome (RDS), which typically results in cuticular deformities (partic ularly bent rostrums), slow growth, poor feed conversion and a greater spread of sizes on harvest, all combining to substantially reduce profitability. These effects are typically more pronounced where the shrimp are infected at an early age, so strict hatchery biosecurity including checking of broodstock by PCR, or the use of SPF broodstock, washing and disinfecting of eggs and nauplii is essential in combating this disease. Even if IHHNV subsequently infects the shrimp in the grow-out ponds, it has little effect on P. vannamei if the PL stocked can be maintained virus free.




Some strains of IHHNV, however, have recently been found to be infectious for P. vannamei, including a putative strain collected from Madagascan P. monodon and a putative attenuated strain in an American laboratory. In addition, recent laboratory studies with P. stylirostris has shown that juveniles that are highly infected with IHHNV (by feeding them with IHHNV-infected tissue) were able to show 28-91 percent survival three weeks after subsequent infection with WSSV (by feeding them with WSSV infected tissue), whilst control animals suffered 100 percent mortality within five days. Surviving shrimp were found to be heavily infected by IHHNV, but had at most only light infection with WSSV which was not enough to kill all of them. Similar trials showed that neither IHHNV pre-infected P. vannamei nor IHHNV-resistant P. stylirostris (SPR “Supershrimp”) were able to tolerate subsequent WSSV infections. Nonetheless, these results raise the question whether exposing shrimp to putative strains of IHHNV may prevent them from getting infected by an infectious strain of IHHNV or possibly WSSV.


IHHNV typically causes no problems for P. monodon since they have developed a tolerance to it over a long period of time, but they may suffer from runt deformity syndrome (RDS). Penaeus merguiensis and P. indicus meanwhile appear refractory to the disease. They are, however, life-long carriers of the disease and so could easily pass it onto P. vannamei, which typically suffer from slow growth (RDS) when exposed to IHHNV. This presents a potential problem if the two species are cultured in close proximity at any phase of their life cycle. This should be a cause for great concern for P. vannamei farms that are currently being established throughout Asia.


As with most important shrimp viruses, transmission of IHHNV is known to be rapid and efficient by cannibalism of weak or moribund shrimp, although waterborne transfer due to cohabitation is less efficient. Vertical transmission from broodstock to larvae is common and has been shown to originate from the ovaries of infected females (whilst sperm from infected males was generally virus-free). Although the embryos of heavily infected females may abort, this is not always true and selection of IHHNV-free broodstock (by nested PCR) and disinfection of eggs and nauplii would help ensure production of virusfree PL.




As with TSV, IHHNV may be transmitted through vectors such as insects, which have been shown to act as carriers for the disease. However, their mode of action is thought to be mechanical rather than real, as insect extracts do not react to in situ hybridisation tests for IHHNV. The probability that IHHNV in frozen shrimp can cause problems is suggested from OIE data that IHHNV remains infectious for more than 5 years of storage at minus 20oC. Gross signs of disease are not specific to IHHNV, but may include: reduced feeding, elevated morbidity and mortality rates, fouling by epicommensals, bluish coloration, whilst larvae PL and broodstock rarely show symptoms.


Diagnosis and detection methods include DNA probes for dot blot and in hybridisation and PCR techniques as well as histological analysis of H&E-stained sections looking for intracellular, Cowdrey type A inclusion bodies in ectodermal and mesodermal tissues. One of the big problems with IHHNV is its eradication in facilities once they have been infected. The virus has been shown to be highly resistant to all the common methods of disinfection including chlorine, lime, formalin and others in both ponds and hatcheries. Complete eradication of all stocks, complete disinfection of the culture facility and avoidance of restocking with IHHNV-positive animals.


White Spot Syndrome Virus (WSSV) will continue in Part 3