Fish disease - virus

Infection Pancreatic Necrosis (IPN)
Spring Viraemia of Carp (SVC)
Lymphocystis
Epizootic Haematopoeitic Necrosis (EHN)
Infectious Haematopoietic Necrosis (IHN)
Viral Encephalopathy and Retinopathy ( VER)


Infectious Pancreatic Necrosis

Aetiology: Birnavirus
Characteristics: replicates in cytoplasm
Epizootiology: as it applies to salmonid disease
Reservoir: Carrier fish which secrete virus in the faeces or sexual products
Transmission: eggs, water, direct contacts, piscivors can transport virus
Occurance: any age
Geographic distribution: Japan, Korea, North America, Europe, Taiwan and Chile
Grass carp: Gross signs & pathology: Massive mortalities in grass carp fingerlings, with lower levels of mortality in yearlings, exophthalmia and haemorrhagic areas at the base of the operculum, haemorrhages in the musculature , mouth , intestine , liver and kidney
(Trout): Gross Signs & Patho : whirling about long axis, weak respiration, darkening, exophthalmia , abdominal distention , pancreatic necrosis, multiple petechiae in omental fat, pale liver & spleen, empty gut & white mucus in the intestine
Histopath: characteristic changes in pancreatic acinar cells; necrosis, pyknotic nuclei with a clear halo around them and the surrounding adipose cells wall still be normal
Dx: isolation & presence of typical CPE in cell culture , use RTG-2 cell lines , CPE- stringly lysis; typical histopathology; confirmed with VNT
Ctl: reduce stress, eradication from farm (certified broodstock), disinfect eggs, rear fry in spring water, disinfect tanks and ponds, quarantine

Spring Viraemia Of Carp

Aetoilogy : Rhabdovirus carpio and Aeromonas hydrophila
Characteristics: replicates in cytoplasm
Epizootiology: species affected-cyprinids
Reservoir: carrier fish, latent infections as the virus is only detected in outbreak Transmission: via water, highly infectious
Occurrence: any age affected
Classically seen in the spring as the temperatures rise to greater than 15-20C
Geographic distribution : Europe
Gross signs : darkening, exophthalmia, abdominal distension, lethargy
Then- lie on sides, distended anus, faeces castes trail in water , petechial haemorrhages on gills, skins and fins
Pathology : fibrinous peritonitis, petechial haemorrhages over internal organs , catarhal enteritis, asites
Histopathology: focal haemorrhages, necrosis of haematopoietic elements in kidney & spleen, submucosal odema of intestine & stomach
Confirmed by isolation of virus
Use FHM, BB or RTG cell lines
Serum neutralization test
Note that history , gross signs and histopathology are all non specific
Prevention and Control:
Prophylatic use of antibiotics
Quarantine country
Treatment: experimentally –injected antibiotics reduce mortalities

Lymphocystis

Cottonwool disease
Aetiology: Lymphocyctis virus
Replication on fibroblast
Epizootiology : Species effected- many species , marine most commonly infected , but also freshwater & ornamental fish
Reservoir: infected fish
Transmission: direct contact
Occurance: lesions seen in 5-30% of some wild fish populations
Geographic distribution: worldwide
Gross signs: the virus infection does not usually result in death , economics losses occur due to consumer rejection of the affected fish, raised growths that appear to consist of small many white nodules on the skins and fins, occasionally single white nodules are seen in the internal organs, over time these lesions grow, necrotise and become secondarily infected by bacteria.
Pathology: lesions consists of massively enlarged fibroblasts (2mm).
Histopathology: dark blue inclusions in cytoplasm, 3 months after infection see a host response , a hyaline capsule around the enlarged fibroblast
Diagnosis: gross signs and histopathology
Isolation can be difficult unless primary cell lines from infected species are used
Prevention & Control: not a major problem but common
If present at a cage site, remove infected fish and disinfect nets etc.
Treatment: At early stage of infection by surgically removing the raised growths and disinfecting the resulting wound with acriflavine.


Epizootic Haematopoeitic Necrosis ( EHN)

Aetiology: Iridovirus
Host range: Redfin perch ( Perca fluviatis), Rainbow trout ( Oncorhynchus mykiss)
Mosquito fish ( Gambussia affins), Silver perch ( Bidyanus bidyanus)
Geograhics distribution: restricted to mainland Australia
Clinical Signs: No specific clinical signs
Mortalities are characterized by necrosis of liver ( with or without white spots), spleen , haemtopoeitic tissue of kidney and other tissue
Distruption of blood function, leads to osmotic imbalance, haemorrhagic lesions, buildup of body fluids in body cavity
Assoc. water quality, temperature
Diagnosis: Isolation of EHNV, ESV and ECV in cell culture
Confirmation: neutralization test, indirect fluorescent antibody test, enzyme-linked immunosorbent assay ( ELISA), polymerase chain reaction (PCR) & sequencing



Infectious Haematopoietic Necrosis

Aetiology: Rhabdovirus
Host range: rainbow or steelhead trout & Pacific Salmon
Geographical Distribution: North America, Europe & Asia
Transmission: vertical & horizontal
Clinical Signs: dark discolouration of body, distended abdomen, haemorrhage at the base of fins, operculum and around eyes “ pop-eye”, weaked swimming ability, white discharge from anus
Pathology: IHNV multiplies in endothelial cells of blood capillaries, spleen, kidney cells, which results in osmotic imbalance as well as systemic haemorrhagic lesions pale internal organs and or pin point bleeding in the musculature and fatty tissues
Kidneys, spleen, brain and digestive tract are the sites where virus is most abundant during advanced infection
Diagnosis: gross observations, histopathology, virology, ELISA, TEM

Viral Encephalopathy and Retinopathy( VER)

Also known as Striped Jack Nervous Necrosis Virus ( SJNNV), Viral Nervous Necrosis ( VNN), Fish Encephalitis Virus ( FEV)
Aetiology: nodavirus
Host Range: cultured marine fish ( seabass, turbot, halibut, Japanese parrotfish, red- spotted grouper, striped jack, Japanese flounder, brown spotted grouper )
Geographic Distribution: Asia, Mediterranean, Pacific
Clinical Signs: VER affects nervous system
Abnormal swimming behaviour, swimming bladder hyperinflation, reduced feeding, changes in colouration & mortality
Diagnosis: gross observations, histopathology ( vacuolization in brain or retinal tissues)


Fish Disease- Fungus

Integumentary Mycoses

Gills or skin following some kind of damage to the epithelium
Agent: Saprolegnia sp.
Culture: sabourauds agar
Epizootiology: Species affected-all freshwater sp & occasionally brackishwater/marine fish
Reservoir: normal inhabitant of water and oil
Transmission: motile zoospores in water
Occurance: any age
Important problem in hatcheries and aquarium
Never a primary infection, always follows damage to the gills/ skin or a physiological change
Geographic distribution: worldwide
Gross signs: circular, superficial, grayish white, cotton wool like growths on the fish these collapse when the fish is removed from water
If bacteria also present, lesions have haemorrhagic appearance
If gills affected, see signs of respiratory insufficiency
Pathology: death due to osmotic shock, hyphae invade stratum spongiosum & spread laterally over the dermis, epidermis shows oedema, spongiosis & necrosis
Diagnosis: gross signs, fungi isolated & cultured
Prevention and control : As Saprolegnia is an ubiquitous and secondary invader, control of primary factors reduce the incidence of fungus infections
Treatment: Malachite green, Methylene blue, Salt