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Author: Dr. Panos Varvarigos
Freelance Veterinarian - Fish Pathologist, Athens, Greece.

AquaHealthTM
Laboratory.

 

DISEASE

NODAVIROSIS
(
Viral Nervous Necrosis -VNN)
(Viral Encephalopathy and Retinopathy -VER)

Pathogen (name, taxonomy, description):

Piscine Neuropathy beta Nodavirus most often belonging to the RGNNV genogroup (serotype C). Other genogroups comprise BFNNV, SJNNV, TPNNV.

The initials of each genogroup relate to the fish species that the virus has been isolated from (RG: Red spotted Grouper, BF: Barfin Flounder, SJ: Striped Jack, TP: Tiger Puffer).

Several antigenic types (strains) may exist within each genogroup, but this hypothesis has not been adequately researched.

Economic Implications:

Severe

Frequency of occurrence:

Frequent

Farmed fish species affected:

Sea bass (Dicentrarchus labrax), Shi drum (Umbrina cirrosa).

Sea bream (Sparus auratus) is considered to assume an asymptomatic carrier status.

Age/size of fish mostly susceptible:

Sea bass is susceptible at all ages/year classes. The younger the fish the worse the losses are. Juvenile fish are often devastated in the hatcheries.

Seasonal occurrence:

In grow-out facilities, nodavirosis outbreaks are most frequently recorded from late summer until the end of autumn, when seawater temperature has risen above 24°C and often up to 28°C and stays elevated for several weeks. In hatcheries where warm borehole water is used (>18°C), VNN is a threat, especially where fertilised ova are introduced for hatching from elsewhere. Nodavirosis outbreaks are temperature dependent, although the infection may not be.

Regional pertinence:

Sites in regions with warmer waters are more prone to suffer. Nevertheless, the probability of occurrence during the summer and autumn months is high at any site and often it is linked to the introduction of latently infected fry.

Predisposing factors:

Cage sites that accept their sea bass fry from many suppliers and/or without reassurances as regards the fish health status. High stocking densities, fouling of cage nets (stress), prolonged periods of warm waters (long summers). If more than two years have lapsed after the last incident on the farm, the likelihood of occurrence increases.

Main lesions and symptoms:
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VNN presents itself in the hatcheries as a hyper-acute or acute condition. Bass larvae (even since day 10 to 25 post hatching) or juveniles go off feed and are found dead and moribund in great numbers close to the tank surface due to the gross distension of their swim bladders. There is congestion of the brain, which may be visible macroscopically. The abnormal swimming behaviour of the infected fish is dramatic. Opisthotonos (muscular cramps resulting in the bending/arching of the body) ataxic violent bursts of swimming followed by sluggish movements and muscular trembling or "hanging" head down comprise the scene in an infected tank.

Acute or sub-acute VNN in sea bass fry and young caged fish show similar clinical symptoms, although these may be somewhat less dramatic. The dead and dying fish are mostly on the surface due to their hyper-inflated swim bladder. Violent swimming bursts (darting), spiralling, looping, circling, opisthotonos and facial, eye (exophthalmia, white cornea) and mandibular necrotic lesions are evident due to collisions with the nets. Many fish are blinded and dark-coloured and are usually sluggish. The symptoms intensify when the infected population is disturbed.

In larger caged bass (>150g) VNN may show less dramatic symptoms and chronic mortality. Such fish are usually sluggish and dark with hyper-inflated swim bladders and may or may not have head lesions. The peritoneal hymens and the internal organs appear normal and the alimentary tract is empty without signs of inflammation.

Diagnosis (field, laboratory):

Season, clinical symptoms, fast rate of spreading, necropsy findings, brain and retina histology (characteristic vacuolisation in the brain and retina), or immunohistochemistry, PCR testing, isolation of the virus on suitable live cell cultures (e.g. SSN-1 cell line) showing a characteristic cyto-pathic effect (cpe). Nevertheless, in practice, a conclusive diagnosis may be reached by clinical examination and necropsy alone.

Rapid diagnostic kits, which might greatly help the diagnosticians, are available commercially for the RGNNV genogroup, but employ monoclonal antibodies, hence their result is conclusive only when positive.

Consequences
(mortality, growth reduction, extra labour):

Hatcheries may lose entire batches of bream juveniles and fall short of their production plans. Extra cost for brood-stock health checks and replacement may be added to the damage. Evidently, the entire production season is at stake.

On cage farms, the extent of losses depends on the age of the infected fish. However, the virosis may spread to all growing batches of bass, irrespective of age, within a few days of the first outbreak, very often after the unfortunate introduction of a batch of infected/carrier fry.

The death toll reaches 70% to 100% of larvae and juveniles. Young fry at the nursery may suffer anything from 30% up to 70% mortality, but it is wise to eliminate them anyway. 40% up to 60% of caged fry >2g may be lost in aggregate, whereas larger fish between 50g and 150g usually suffer 30% up to 40% mortality. In the rather chronic cases of fish larger than 150g and in lower water temperature (about 22°C) the cumulative loss may not exceed 15% or 20%.

Extra costs comprise labour for the daily removal, transport and the sanitary disposition of the dead fish. There is also a very serious adverse psychological effect on the fish farmers who not only are unable to treat their fish, but also watch the demoralising clinical symptoms of the disease.

Prevention:

There are no vaccines against VNN yet. Cage farmers should not accept sea bass fry from hatcheries unknown to them and ask for veterinary certification and proof that the health of brood-fish as well as their offspring is monitored regularly.

Treatment:

None. Administration of vitamin supplements (vitamin B complex and ascorbic acid) does not seem to help.

Management advice:

Monitor the health status of the brood-fish in the hatchery, since vertical transmission of the virus via the gametes has been proven. Apply sanitation of the hatchery water with UV light or ozone. Daily disinfections are a must. In case VNN is diagnosed, it would be wise to stamp out the larvae or juveniles in the given tank(s) and carry out thorough disinfections. If not, it is certain that it will spread to most other tanks and destroy the on-going production. Trace the origin of fertilised ova. If from own brood-stock, either destroy the fish in the responsible tank or carry out extensive PCR testing of all brood-fish in order to weed out the responsible carriers.

On infected cage farms avoid stresses, such as handling, remove daily and dispose off mortalities away from the farm in a proper sanitary way, approved by the local authorities. Never reject dead or moribund fish in the sea. Alarm the neighbouring fish farmers and the suppliers of sea bass fry.

Environmental issues:

The significance of the fish farms as amplifiers for the disease in the sea is unknown. However, it is evident that the near-by farms usually contract the disease within a few days and that many wild fish species around the cages suffer during a farm outbreak (sluggish fish around the cages), mainly groupers (Epinephelus spp.), mullets (Mugil spp.), garfish (Belone belone) and scad (Trachurus mediterraneus). On the other hand, it has been found and reported that wild fish, especially groupers, carry the virus. Hence, there may be an amphidromous effect between the farms and the environment as regards VNN.

Regulations:

No regulations are in place. The virus is wide-spread in nature, harboured by several wild fish.

 

       


Author: Dr. Panos Varvarigos
Freelance Veterinarian - Fish Pathologist, Athens, Greece.

AquaHealthTM
Laboratory.

Reproduction of this website (or parts of it) is illegal and strictly forbidden.
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Disclaimer:

Every effort has been made to ensure that the information is accurate until the date of last editing. It is based upon the accumulated personal experience of applied veterinary work. The author cannot take responsibility for incorrect interpretation or any resulting consequences. The contents may be used as an educational guide and are definitely not meant to become a stand-alone diagnostic tool or operations manual.

 

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