Fish & Invertebrate Virology Flashcards
1
Q
Describe the general principles of fish virology.
What are the largest families of viruses that fish get?
What are the eight OIE reportable viruses that fish get?
How are most fish viruses transmitted?
What are the documented stressors?
How do these fish typically present?
A
Viral Diseases (C3)
- Most viruses from 3 families: Herpesviridae, Rhabdoviridae, and Iridoviridae
- Reportable to OIE (done through USDA)
- Koi herpes virus
- viral hemorrhagic septicemia
- infectious hematopoietic necrosis
- spring viremia of carp
- epizootic hematopoietic necrosis
- red seabream iridovirus
- infectious salmon anemia
- salmonid alphavirus
- Identifying a virus in tissue insufficient to diagnose a pathogen
- Transmission:
- Horizontal transmission seen in all, but vertical important in some (IPNV)
- Aquatic invertebrates and piscivorous birds can transmit
- Survivors of clinical disease may become lifelong carriers (IPNV – infectious pancreatic necrosis virus and CCV – channel catfish virus)
- Global movement of humans increases risk of spread (viral hemorrhagic septicemia through ballast water)
- Risk factors:
- Younger fish more likely to show clinical signs
- Exposure and stressors are most significant
- Clinical signs are nonspecific in most cases and systemic infections may present with reduced appetite, lethargy, erratic swimming, erythema, ulcers, congestion, dyspnea, tachypnea, or coelomic distention.
- Systemic infections often present with organomegaly and necrosis. Inclusion bodies may be seen.
- Management – typically relies on reducing or resolving stressors or reducing exposure, but in rare cases (notifiable disease) management relies on depopulation and disinfection
- For reportable disease, management by regulatory agency (USDA) must be followed
- Prevention
- Good biosecurity, reduce or resolve stressors (especially after transport or at permissive water temperatures), reduce severity of disease (vaccination – infectious salmon anemia)
- No known zoonotic potential for fish viruses
Noga Chapter 12. Problems 77 through 88 (Viruses)
KEY POINTS
OIE Reportable Fish Viruses
- Koi herpesvirus disease
- Spring viremia of carp
- Infectious hematopoietic necrosis
- Infectious salmon anemia
- Viral hemorrhagic septicemia
- Epizootic hematopoietic necrosis
- Red sea bream iridoviral disease
General:
- Pathogenicity often temperature dependent and host specific - variable morbidity/mortality
- No commercially available/effective treatments
- Diagnosis with clinical signs, necropsy/histopathology and virus identification from a trusted laboratory or method
- Quarantine and disinfection/good biosecurity best prevention
- Depopulation or culling of positive individuals/groups frequently recommended for reportable diseases as survivors can become chronic carriers
2
Q
Describe the most common viruses that affect the following fish taxa.
What are six important viruses that affect salmonids?
What are two important viruses that affect ictalurids?
What are five important viruses that affect cyprinids?
A
List of major viral diseases associated with some families
Salmonidae
- Infectious pancreatic necrosis virus (IPN - Birnavirus)
- Infectious hematopoietic necrosis (IHN - Rhabdovirus)
- Viral hemorrhagic septicemia (VHS - Novirhabdovirus)
- Infectious salmon anemia (ISA - orthomyxovirus Isavirus)- marine only
- Salmon Pancreas Disease Virus (SPDV)/Salmonid alphavirus SAV 1,3,4,5,6 (and sudden death syndrome) - Atlantic salmon in seawater
- Sleeping disease virus (SDV); SAV 2 - Rainbow trout in freshwater
Ictaluridae
- Channel catfish virus disease (CCVD - Herpesvirus) - IcHV-1
- IcHV-2 - similar disease in black bullhead catfish
Cyprinidae
- Spring viremia of carp (SVC - Rhabdovirus carpio)
- Koi herpesvirus (KHV - CyHV-3)
- Cyprinid herpesvirus disease (CHVD - CyHV-1)/Carp Pox
- Goldfish hematopoietic necrosis (CyHV-2)/herpesviral hematopoietic necrosis virus (HVHNV)
- Carp edema virus (CEV, Poxvirus)/Koi Sleepy Disease (KSD)
Wider range of clinically affected species: VHS, Iridoviruses, Nodaviruses
3
Q
What are some of the inclusion bodies that fish get?
A
Notable Cells/Inclusions
- CCVD (Channel Catfish Virus Disease): Intranuclear Cowdry type A inclusion bodies
- IPN (Infectious Pancreatic Necrosis): McKnight cells
- IHN (Infectious Hematopoietic Necrosis):
- pleomorphic intracytoplasmic and intranuclear inclusions (pancreas)
- Degeneration and necrosis of the granular cells of the stratum compactum and stratum granulosum are pathognomonic
- necrobiotic bodies (necrotic erythrocytes) in kidney smears - may be present to a lesser extent with IPN and VHS
- ISA (Infectious Salmon Anemia): Blood smear with degenerate and vacuolated erythrocytes, erythroblast irregular nucleus
- SVC (Spring Viremia of Carp): Purkinje cells in brain cortex may have eosinophilic inclusions
- EHN (Epizootoic Hematopoietic Necrosis): Basophilic spherical intracytoplasmic inclusions in hepatocytes
- RSIV (Red sea bream iridovirus): inclusion body - bearing cells (IBCs) in the spleen, hematopoietic tissue, gills, GIT
- Nodaviruses: intracytoplasmic, ∼1-5 μm inclusions in brain cells
- KHV (Koi Herpes virus): branchial epithelial hyperplasia with intranuclear inclusions in affected cells
4
Q
Describe the effects of cyprinid herpesivrus 1.
What species are affected?
What are the typical clinical signs? How does that change with fry?
What lesions are typically seen on histopathology?
What differentials should be considered for the clincial signs?
A
-
Cyprinid Herpesviruses (CGFM)
- Cyprinid herpesvirus-1 (CyHV-1) causes skin plaques (carp pox) in common carp (Cyprinus carpio), subspecies such as koi, and goldfish (Carassius auratus)
- Primarily a cosmetic but can cause mortalities in young fish and affect the value of koi.
- Often > 1 yr old
- Clinical signs - Usually a few in a group are affected – translucent white plaques on head, body and fins (“melted candle wax”). Lesions regress over times, particularly in summer. Usually does not scar, but this may occur. Possible to see systemic signs in young fish (inappetence, erratic swimming, erythema, mortalities)
- Histopath – epithelial hyperplasia
- Differentials for white/tan plaques – carp pox, lymphocystivirus, epitheliocystis, neoplasia
- Cyprinid herpesvirus-1 (CyHV-1) causes skin plaques (carp pox) in common carp (Cyprinus carpio), subspecies such as koi, and goldfish (Carassius auratus)
- Cyprinid herpesvirus 1 (CyHV1; carp pox)
- Carp and koi
- Usually self-limiting, primarily a cosmetic problem.
- Adult fish
- Soft, friable, translucent pink, papillomatous or plaque like areas of epidermal hyperplasia.
- Mortality in fish fry with exophthalmos and hemorrhage.
5
Q
Describe the effects of Cyprinid Herpesvirus 2.
What species are affected?
What is another name for this virus?
What are the typical clinical signs?
What signs will you see on necropsy?
What is the target tissue?
What are the inclusion bodies?
How can this virus be controlled?
A
- Cyprinid herpesvirus-2 (CyHV-2) causes necrosis of hematopoietic tissues with high mortalities in goldfish and other Carassius spp (Crucian and Prussian carps).
- Also known as herpesviral hematopoeitc necrosis virus (HVHNV)
- Often < 1 yr old
- Clinical signs – several goldfish (especially young) affected – often see lethargy, inappetence, tachypnea, dyspnea, and gill pallor. May see gill necrosis, erythema/ulcerative dermatitis, exophthalmos or enophthalmos, coelomic distention, or peracute, acute or chronic mortalities (mortality can reach 100%)
- Histopath - visceral pallor, renomegaly, splenomegaly. White nodules, necrosis or congestion in cranial kidney and spleen, with or w/o gill necrosis and hyperplasia
- Cyprinid herpesvirus 2 (CyHV2; goldfish herpesvirus, herpesviral hematopoietic necrosis virus)
- Juvenile goldfish
- Can cause high mortality.
- Target is hematopoietic tissue of head kidney, necrosis can lead to profound anemia, infarcts in gills.
- Large, amphophilic, Cowdry Type A, intranuclear inclusions numerus.
- Elevating water temp can be key to prevent and control CyHV 1 and 2.
6
Q
Describe the effects of cyprinid herpesvirus 3.
What are some other names for this virus?
What species are affected? What species can be asymptomatic carriers?
What age group is most susceptible?
What are the typical clinical signs?
How high can mortality rates be?
How is this diagnosed?
How is this disease controlled?
Is this a reportable disease?
What are the lesions seen on necropsy?
A
-
Cyprinid herpesvirus-3 (CyHV-3)
- also known as koi herpes virus (KHV), causes necrosis of gills and hematopoietic tissues with high mortalities in common carp, ghost carp and koi.
- Goldfish and grass carp (Ctenopharyngodon idella) can be asymptomatic carriers.
- All ages susceptible, particularly young fish < 1 year old
- Clinical signs – several carp or koi often affected with common signs including tachypnea/dyspnea, gill necrosis (multifocal white to brown discoloration), lethargy, erratic swimming, head-down swimming, or other neurologic signs. Inappetence/reduced appetite, enophthalmos, and profound erythema/congestion/ulceration of skin and fins may be seen.
- Acute mortality 1-3 wk post infection (70-100% mortality)
- Histopath – Gill necrosis and hyperplasia with visceral pallor, edema and widespread petechiae, ecchymoses and congestion, with or without skin necrosis. Renomegaly and splenomegaly in young fish
- Reportable
- Differentials for erythema, skin ulcers, and gill changes in koi or carp include KHV, spring viremia of carp, carp edema virus, viral hemorrhagic septicemia, motile aeromonad septicemia, and Flavobacterium columnare.
Koi herpesvirus disease (KHVD) - cyprinid herpesvirus 3 (CyHV-3) - Noga
- AKA Carp Nephritis and Gill Necrosis Virus (CNGV)
- Warm freshwater
- Epidemiology
- Major losses in koi and mass mortality in common carp
- Asia, North America, Europe
- Highly contagious - short lived in water (4 hours) but stable in sediment or filters
- Outbreaks most susceptible at 18-28 C (especially 23-28 C) - typically spring or summer; moving fish from cool to warmer water can rapidly induce mortality
- No disease <13 C or >30 C
- Recovered fish develop high antibody titers and often are latent carriers
- Acute morbidity/mortality (up to 100%)
- Physical examination: Pale, swollen, mottled gills (most common); abnormal coloration, skin lesions, enophthalmos, dyspnea, erratic swimming, anorexia
- Histopathology
- Massive branchial epithelial hyperplasia with degeneration and necrosis - intranuclear inclusions
- Liver, spleen, GIT parenchymal necrosis
- Diagnosis
- Definitive: virus identification with PCR of gill, kidney and spleen
- R/O carp pox (CHVD), which causes mortality in cyprinids <2 mo but only skin lesions in older fish
- Variety of testing rapid antibody or antigen, genetic testing
- Disinfect and quarantine
- Quarantine: hold fish at permissive temperature (23-28 C) for at least 4 weeks (after acclimation period)
- Include some fish known to be free of KHV to act as sentinel fish in case there are asymptomatic carriers that may shed it
- Depopulation recommended with diagnosis
- Temperature manipulation can control disease, but result in chronic carriers
- Held for at least 2 months at 13 C, should not develop disease when moved to warmer water
- Some natural resistance and recovery if exposed to virus for 3-5 days at 23 C then moved to 30 C
- Avoid mixing koi with other cyprinids
- Live attenuated vaccine KV3, Kovax used in some countries - keep in mind if screening them for antibodies
- Quarantine: hold fish at permissive temperature (23-28 C) for at least 4 weeks (after acclimation period)
- Cyprinid herpesvirus 3 (CyHV3; koi herpesvirus) - ZP
- Koi and carp industries
- Gills are primary target.
- Severe, segmental, necrotizing and proliferative bronchitis, high mortality for all ages.
7
Q
How are the cyprinid herpesviruses transmitted?
What are some of the risk factors for disease transmission?
How are these diseases diagnosed?
What husbandry changes can be made to reduce mortalities?
How can outbreaks be prevented?
A
- Etiology – Alloherpesvirus
- Enveloped DNA viruses
- Transmission
- Horizontal and likely vertical
- Direct contact or water (especially if skin/mucus damaged
- Mechanical vectors – aquatic invertebrates and piscivorous birds
- Latency common and stress can lead to overt disease and shedding
- Risk factor – permissive water temperatures (59-82F), general stress/overcrowding/water quality, and introduction of new fish
- Diagnosis:
- PCR is gold standard for diagnosis
- Carp pox – skin sawb
- KDV – gill swab, spleen or kidney
- ELISA and SN on blood available for KNV to detect prior exposure but may not reliably detect asymptomatic carriers
- Intranucuear inclusion bodies ay be seen with all 3 viruses.
- PCR is gold standard for diagnosis
- Husbandry
- Carp pox – slowly increase water temperature to > 77F
- HVHNV and KHV - isolate, increase dissolved oxygen, decrease water temperature by 5F or to < 59F
- Increase salinity to reduce osmotic stress
- Depopulation and disinfection may be considered – carriers make it challenging to ensure new animals are negative
- Prevention
- Avoid keeping goldfish, koi, or other carp in the same system
- Purchase KHV seronegative
- Quarantine at permissive temp (72F) for prolonged qt (60-90d)
- Do not exposure to KHV outside of permissive temps – may produce latent infection
8
Q
Describe the effects of the ictalurid herpesviruses.
What is IcHV-1? What species does it affect?
What is IcHV-2? What species does it affect?
How are these viruses transmitted?
What are the known risk factors?
What are the typical clinical signs?
How is this disease diagnosed?
How is it managed?
How high is the mortality rate?
What lesions are seen on necropsy?
A
-
Ictalurid Herpesviruses
- IcHV-1 is also known as channel catfish virus (CCV)
- Causes hemorrhagic septicemia in fry or fingerling channel catfish (Ictalurus punctatus) in aquaculture during warm weather.
- Found in aquaculture in US. Only channel catfish, blue catfish and their hybrids
- Disease is rare if > 6 mo old.
- IcHV-2 causes similar disease in black bullhead catfish (Ameiurus melas).
- Not found in North America and its introduction is considered a high risk to catfish aquaculture.
- Etiology – Alloherpesviridae, DNA viruses
- Transmission – horizontal and vertical
- Viruses do not survive long in the environment
- Fish that resolve clinical signs likely lifelong carriers
- Risk factors
- Permissive water temperature is high for IcHV-1 (77-82F); IcHV-2 shows wider temperature tolerances
- Clinical signs
- Multiple conspecifics usually affected – inappetence or reduced feeding typically first sign. May swim near surface or show abnormal swimming with head up position or erratic spirals, coelomic distention (effusion or organomegaly), gill petechiae/pallor, exophthalmos, erythema/petechial hemorrhage (base of fins and along ventrum)
- Morbidity and mortality typically low but can reach 100% in populations under other stressors.
- Common differentials for systemic inflammation in channel catfish include CCV, Edwardsiella ictaluri, motile aeromonad septicemia, and Yersinia ruckeri.
- Diagnosis
- Signalment, time of year, signs. Confirm with virus isolation. Best sample is kidney tissue
- Histo – multifocal necrosis, intranuclear inclusions, visceral pallor, coelomic effusion, organomegaly, petechial hemorrhages, especially in kidneys
- Management
- Isolate fish, reduce water temperature by 10F or < 66F to reduce mortality.
- Control of concurrent infections (E. ictaluri or Flavobacterium columnare)
- Prevention - Avoid handling/transport of channel catfish when water temp > 68F
- IcHV-1 is also known as channel catfish virus (CCV)
Channel Catfish Virus Disease (CCVD) - Noga
- Prevalence: channel catfish, other Ictalurids experimentally (blue catfish); warm freshwater
- History: acute to chronic morbidity/mortality
- Motralities most severe at higher temperatures (25-30 C/77-86 F)
- Exam: reddening on body and base of fins, depression, exophthalmos, swollen coelom, equilibrium deficit (head up), corkscrew spiral swimming
- Younger more robust fish die first; epidemics in <1 year (most <4 mo) and <15 cm fish
- Diagnosis: definitive diagnosis requires isolation of tissues (kidney is the best organ)
- Intranuclear Cowdry type A inclusion bodies: strong presumptive diagnosis
- Serum collected 1-2 months after exposure for antibody titers in recovering fish; false negatives common
- Treatment: disinfect, quarantine, reduce temperature to less than 15 C (59 F), treat secondary infections
- Pond disinfection: 20-50 mg/l chlorine eliminates virus
- Surviving fish often stunted and brood stock are latent carriers- euthanasia
- Vaccines experimentally effective
- Horizontal and vertical transmission
- Necropsy: yellow peritoneal fluid, punctate hemorrhage in viscera
- Histopathology: Focal necrosis at posterior kidney to diffuse necrosis, hemorrhage, edema, neurological effects (vacuolated neurons, edematous nerve fibers)
9
Q
What are some of the importnat rhabdoviruses affecting fish?
What species do they affect?
How are they transmitted?
What are the typical clinical signs?
How are they diagnosed?
A
- Rhabdoviruses
- Viral hemorrhagic septicemia viruses (VHSV) and infectious hematopoietic necrosis viruses (IHNV) - hemorrhagic septicemia in salmonids and other teleosts.
- VHSV can infect freshwater, brackish and saltwater. Rainbow trout particularly susceptible
- IHNV typically infects cold freshwater and saltwater salmonids
- Spring viremia of carp virus (SVCV) - hemorrhagic septicemia in cyprinids and is a serious disease of cultured cyprinids including koi.
- Also known as rubella, infectious dropsy, swim bladder inflammation, or Rhabdovirus carpio virus
- Typically infects cyprinids
- VHSV highest mortalities 40-54F, no signs if >72F. IHNV disease at 45-60F. SVCV disease at 52-65F, no signs if >70F
- Transmission
- Enveloped RNA viruses with horizontal transmission common
- persist for days to weeks in water or sediment but can persist for months, particularly in freshwater habitats. They survive freezing.
- Fish that resolve signs are resistant to disease, but some become carriers.
- Invasive gobies in Great Lakes are carriers
- Signs
- Similar nonspecific signs of systemic inflammation with multiple fish affected.
- Lethargy, loss of equilibrium, sporadic hyperexcitability, circuling, decreased appetite, petechia, congestion, cloacal/anal prolapse. Exophthalmos, gill pallor/edema, pale or mucoid fecal casts.
- Mortality can reach 100% in youn, naïve, or and stressed fish.
- Diagnosis
- Viral isolation and molecular tests required for definitive identification
- Necropsy shows hemorrhagic septicemia with hematopoietic necrosis
- Widespread hemorrhage and serosanginous ascites, viscerla pallor, with multifocal necrosis, degeneration and vasculitis on histology
- Petechiae and hemorrhages in the swim bladder in cyprinids nearly pathognomonic for SVCV
- IHNV commonly associated with pancreatic necrosis and inclusions
- ELISA or PNT can identify seropositive fish
- Recommended to sample spleen, cranial kidney, heart and brain for virus isolation and FA, ELISA or PCR
- VHSV, IHNV and SVCV reportable to OIE
- Consider surveying female broodstock through ELISA or VI on ovaries and disinfection of eggs using iodophors
- Viral hemorrhagic septicemia viruses (VHSV) and infectious hematopoietic necrosis viruses (IHNV) - hemorrhagic septicemia in salmonids and other teleosts.
10
Q
Describe the effects of Infectious Hematopoietic Necrosis (IHN) in fish.
What type of virus is this?
What are other names of this disease?
What is the epidemiology of this disease? Where is it endemic, where is it introduced? What fish are most susceptible? What temperatures are risk factors?
How is it transmitted?
What are the typical clinical signs?
What lesions are seen on necropsy?
How is it diagnosed?
How are outbreaks controlled?
A
Infectious hematopoietic necrosis (IHN) – rhabdovirus (Noga)
- AKA Chinook Salmon Disease Virus, Sacramento River Chinook Disease, Columbia River Sockeye Disease, Oregon Sockeye Disease
- Epidemiology - major cause of mortality in salmonids (CF and CM)
- Endemic in PNW, introduced and established in Japan, Taiwan, Italy, France, Germany, and other areas in US
- Natural IHN outbreaks in rainbow trout and salmon (Atlantic, chinook, pink, sockeye)
- Refractory: Coho salmon, brook trout, brown trout, cutthroat trout
- Major disease in cultured rainbow trout in freshwater, but salmon in seawater can also have large mortalities
- Only young fish (<2 y) clinically affected with high mortality <6 mo
- Temperature
- Peak mortality: 10 C
- Fewer, more chronic mortalities: <10 C
- Fewer, more acute mortalities: >10 C
- No disease: >15 C
- Vertical and horizontal transmission; also isolated from leeches, copepods and mayflies
- Survivors release virus for ~45 days with strong protective immunity (carriers)
- Exam: lethargy, sporadic hyperactivity, long thick white feces, dorsal darkening, coelomic distension, exophthalmos, hemorrhage/pale gills and mucoid fluid in the stomach
- Larger individuals die first
- Fry avoid current, move to the edge of the raceway
- Fecal pseudocast is long, thick and offwhite
- Visceral pallor and petechiation
- Sockeye salmon survivors: 5% or more may have spinal deformities
- Anemia, leukopenia, necrobiotic bodies in smears of kidney (less frequent in peripheral blood
- Adult carriers are asymptomatic
- Histopathology
- Necrosis: kidney, hematopoietic tissue, pancreas, GIT, interrenal tissue; spleen and kidneys usually affected first and most severely
- Pleomorphic intracytoplasmic and intranuclear inclusions in pancreatic acinar and islet cells
- Necrosis of eosinophilic granule cells of the intestinal submucosa
- Older fingerlings - gill lesions including branchial hyperplasia and fusion
- Definitive diagnosis: culture and identification of virus from target tissues with appropriate clinical signs; can be isolated from dead eggs
- Differentials: IPN, VHS, herpesvirus salmonis disease; white feces thicker and longer than IPN
- Degeneration and necrosis of the granular cells of the stratum compactum and stratum granulosum are pathognomonic
- Carriers: post spawning examination of ovarian fluid or kidney and spleen in spawning males
- Disinfect and quarantine; raise temperature above 15 C, treat eggs with povidone iodine
- Infection incidence among feral American Pacific salmon stocks is 5-94% and higher in females - avoidance not possible with pathogen free water
- Screen and cull broodstock to significantly reduce incidence (does not eliminate and labor intensive)
- Increasing temperature can stop epidemics, but is not effective for all strains and is less effective in fish showing clinical signs
- Inactivated by 25 ppm iodine for 5 minutes - treating eggs with iodophor decreases risk of vertical transmission
- Decrease stress and ectoparasites (potential reservoirs)
11
Q
Describe the effects of viral hemorrhagic septicemia in fish.
What type of virus is this?
What species are affected?
How is it transmitted?
What are the typical clinical signs? What is the mortality rate like?
How do acute versus chronic cases differ?
What findings are typically present on necropsy?
How is this definitively diagnosed?
How are outbreaks controlled?
A
Viral hemorrhagic septicemia (VHS, EGTVED Disease) – Novirhabdovirus - Noga
- Epidemiology:
- Typically cold freshwater and marine - wide host range
- Die off of temperate warm water fish (white bass, bluegill)
- Major cause of mortality in salmonids in freshwater especially rainbow and brown trout
- Europe, Puget Sound, Alaska
- Non Salmonids
- Great Lakes 2005 - diseased muskelunge, drum, round goby
- Isolated from over 50 species (mostly marine) - salmonids + herring and anchovy, gadids, flatfish, smelt, perch, scorpionfish, eel, topminnow, stickleback
- Susceptible: turbot fry, Japanese flounder, wild Pacific herring and hake, walleye pollock (AK, WA), pilchard, black cod, ratfish, shiner perch, yellow perch, smallmouth bass, crapie, bluegill, shad, walleye, suckers
- North America, Asia, Europe
- Prodromal period 1-2 wks usually, but 3-4 weeks at low temperatures (2 C)
- Temperature
- Epidemics: 3-12 C, often in spring with fluctuating temperatures
- Highest mortalities: 8-10 C
- Outbreaks rare: >15 C
- Never > 18 C
- Shedding only occurs at low temperatures (typically winter)
- Horizontal transmission (urine and gills -> skin and gills)
- Susceptibility varies greatly between individuals
- Survivors can be carriers but it is not consistently detectable until sexually mature
- Endemic in some areas
- Typically cold freshwater and marine - wide host range
- Examination: Neurological signs; lethargy; darkening; exophthalmos; swollen coelom; hemorrhage, anemia, leukopenia, thrombocytopenia
- High mortality in fry (up to 100%)
- 30-70% mortality in older fish during epidemics
- Phases - severity of infection
- Acute (15-18 C): rapid initially high mortality, but lower cumulative mortality, darkening, congregate away from current, reddening at base of fins and gills (injection of vessels and punctate hemorrhage), coelomic hemorrhage, leukopenia
- Chronic (1-5 C): moderate protracted deaths cumulating to high mortality, fish black, anemia, exophthalmos, swollen coelom, organ pallor and hemorrhage, kidney and liver may be swollen
- Nervous: low mortality, looping swimming, darting through water, spiraling at bottom
- Turbot and Japanese flounder: swollen coelom, exophthalmos, hemorrhage
- Similar to Japanese flounder rhabdovirus disease, but more prominent fluid accumulation in peritoneal and pericardial cavities; necrotizing myocarditis diagnostic
- Pacific herring - skin ulcers and reddening gross lesions
- Histopathology:
- Degeneration and necrosis are most common histopath findings - kidney, liver (vacuolation)
- Acute: focal hemorrhage, necrosis and lymphocytic inflammation in all tissues
- Chronic: heavy hemosiderin deposition in melanomacrophages, hematopoietic hyperplasia and degeneration
- Choroidal retrobulbar hemorrhage
- Definitive Diagnosis: isolation of virus from target tissues
- <4 cm fish: whole larvae/fish
- 4-6 cm: entire viscera (kidney)
- >6 cm: kidney and spleen have highest titers in acute and chronic phase; brain should also be sampled
- Stable for months in frozen viscera
- Presumptive: lack of pancreatic damage compared to IHN or IPN, relatively normal intestine and gills
- Carriers: most sensitive tissues are ovarian fluid (post spawning), then pyloric ceca, then kidney, brain
- Disinfection and quarantine; egg wash
- Lime not effective, but susceptible to most disinfectants
- Obtain fish from certified VHSV-free stock is best method to avoid disease
- Iodophor treatment will eliminate virus from eggs of carriers
- Eradicated from some parts of europe
- Aquaculture challenges
- Endemic in many areas
- Do not cultivate rainbow trout and flatfish together in mariculture
- Avoid introduction of farmed fish from seawater to freshwater for susceptible fish
- Great lakes isolate causes moderate mortality in salmonids typically not affected by other isolates (Chinook salmon, lake trout, steelhead trout)
-
Viral hemorrhagic septicemia virus (VHSV) - ZP
- Farmed fish, rainbow trout and turbot.
- Has since been described in over 50 spp of marine and FW fish.
- Salmonids (brown and rainbow trout), muskellunge, smallmouth bass, walleye lake whitefish, FW drum, atl herring.
- Rhabdovirus, Novirhabdovirus genus.
- Can cross species barriers.
- Transmission through predation or scavenging of diseased or dead fish, thorugh contamination of water with urine or feces, mechanical human or bird vecros, leeches, prey species i.e. amphipods.
- Three forms:
- Acute, chronic, nervous.
- Acute – sudden death up to 100% fry.
- Darkening of skin, lethargy, exophthalmia, ascites, abdominal distention.
- Petechiae at base of fins, gills, mouth, eyes, and multifocally along skin.
- Branchial pallor, abnormal swimming.
- Chronic – swimming behavior more lethargic.
- Nervous – hyperactive, abnormal spiraling patterns, flashing and jumping from the water.
- Gross lesions – hemorrhage, renal congestion, hepatic pallor.
- Chronic stage similar changes, mortality is decreased.
- Endothelium is primary target cell.
- Lytic parenchymal necrosis in liver, kidney, heart.
- Vasculitis.
- Aerocystitis.
- Bullet shaped virions.
- Confirmation with immunohistochemistry, VI, RTPCR, IFAT, ELISA.
12
Q
Describe the effects of Spring Viremia of Carp.
What type of virus is this? Does it have any other names?
What species are commonly affected?
Where does this usually occur? How is it transmitted? Outbreaks occur in what temperature range?
What are the typical clinical signs? What secondary infections are common? What is the mortality rate like?
What lesions are typically seen on necropsy?
How is it diagnosed? What samples should be submitted?
How is it controlled?
A
Spring viremia of carp (Rhabdovirus carpio) - Noga
- AKA Swim Bladder Inflammation
- Cold freshwater: cyprinids (common carp, koi, goldfish, etc), non cyprinids (northern pike, pumpkinseed, guppy) experimentally susceptible
- Common carp most susceptible and main host
- Epidemiology
- Europe, Asia, US
- Similar virus isolated from shrimp in Hawaii
- Horizontal transmission, suspected vertical transmission but may not significant source
- Spreads in winter with low temperature and suppressed immunity then outbreak in spring when most severe when temperatures begin to reach 15-18 C
- Fewer, chronic mortalities above or below range
- Clinical disease less likely to develop at 20-22 C
- Mortality 30-70%, more severe in young fish
- Examination: Lethargy; lying on bottom of pond; trailing mucus cast from anus
- Seek slow moving water
- Dark, sluggish, nonresponsive, swim on their side and rest
- Exophthalmos, coelomic distention, hemorrhage from skin, gill or eyes
- Internal hemorrhage, especially in swim bladder; intestine, muscle, peritoneum
- Secondary infection - Aeromonas hydrophila common (carp erythrodermatitis)
- Acute: infectious dropsy of carp
- Peracute:no gross lesions
- Histopathology
- Swim bladder: epithelial monolayered become multilayer and submucosal blood vessels dilated and inflamed
- Necrosis of liver, kidney, spleen, intestine
- Purkinje cells in brain cortex may have eosinophilic inclusions
- Diagnosis:
- Definitive - culture and identification confirmation with histopathology
- Sampling
- <4cm: whole fish
- 4-6 cm: entire viscera including kidney and brain
- >6 cm: liver, kidney, spleen, brain
- Differentials - other swim bladder infections (Sphaerospora renicola)
- Disinfect and Quarantine
- Antibiotics can control the Aeromonas aspects to disease complex
- Carriers have strong protective immunity
- Povidone iodine wash of eggs
- Chemical and physical disinfection of ponds and equipment
- Minimize stress/overcrowding - reduce stocking density in winter and early spring
- Raising fish at 19-20 C - high cost of heating water
13
Q
Describe the effects of infectious pancreatic necrosis virus?
What type of virus is this?
What fish are commonly affected? What age group is susceptible? What age group can be carriers?
Hois it transmitted?
What are the typical clinical signs?
What differentials should be considered?
How is it diagnosed? What samples should be collected?
A
-
Birnaviruses
- Infectious pancreatic necrosis virus (IPNV)
- Young salmonids in aquaculture, especially rainbow trout
- Causes acute septecemic disease and can be challenging to eliminate
- Etiology: Nonenveloped RNA virus
- Tranamission
- Highly contagious – horizontal and verticle transmission and can be carried inside the eggs
- Very hardy – weeks on water surface and months in frozen tissues
- Carriers – fish with resolved clinical signs and brook trout, striped bass and hybrids.
- Signalment
- Only pathogenic in salmonids, especially in fry and fingerlings
- Risk factors
- Water temp 50-57F, high number of salmonid farms and identification of IPNV in the previous production cycle.
- Signs
- Acute clinical course with spiraling/erratic swimming, skin darkening/hemorrhages and coelomic distention common. May see white fecal casts, exophthalmos, or gill pallor. Appetite normal
- Differentials for septicemic disease in salmonids: IPN, infectious hematopoietic necrosis virus, viral hemorrhagic septicemia, salmonids alphavirus, infectious salmon anemia, Aeromonas salmonicida, and Yersinia ruckeri
- Diagnosis
- VI posterior kidney or pyloric ceca
- Necropsy – tissue pallor, white or clear mucus in stomach and intestines. Pancreatic necrosis and basophilic intracytoplasmic inclusions. Necrosis of anterior intestines and renal tubules.
- Resistant to air drying and requires high UV doses. Management typically depopulation and disinfection
- Disinfection of eggs with iodophors does not eliminate infection since it can be carried inside the eggs.
Infectious Pancreatic Necrosis (IPN) and other Birnaviruses (Noga)
- Prevalence: Salmonids (cold freshwater and marine); birnaviuses in non salmonids as well
- Brook and rainbow trout most susceptible
- Older fish can become carriers
- IPNV in North America, South America, Asia, and Europe, but not Oceana; however other birnaviruses isolated from non salmonids in Australia and New Zealand
- Striped bass known to harbor IPN
- Aquabirnaviruses can infect at least one member of 38 fish families as well as invertebrates (mollusks, crustaceans, rotifers, digenean trematodes) - majority no proven pathogenicity
- Japanese eels (young)
- muscle spasms, retracted abdomen, anal fin congestion, congestion of gills or ceolom
- food absent from gut, ascites, hypertrophied kidneys, exudative glomerulonephritis, nephrosis (hyaline droplet degeneration), renal interstitium congestion, tubule cells sloughing, focal necrosis of liver and spleen
- Yellowtail in Japan
- Fry and fingerlings- acute pancreatic-hepatic necrosis with ascites
- Marine aquabirnavirus (MABV) or yellowtail ascites virus (YTAV)
- Epidemics May-June at 18-22 C
- Flatfish - clinical disease in cultured turbot, dab, and atlantic halibut
- Other - suspected in red sea bream, tiger puffer, European sea bass, Atlantic menhaden, striped bass, and others
- Japanese eels (young)
- History: usually acute but sometimes chronic morbidity/mortality
- Only young fish become ill - mortality in fish over 6 mo is rare
- Mortality highest at high temperatures (10-14 C), but less mortality >14C and at lower temperatures
- Exam: neurological signs, trailing white feces, dorsal darkening, coelomic distension, exophthalmos, hemorrhage, pale gills, catarrhal exudate in stomach
- Larger more robust fish die first
- Corkscrew swimming, whirling - especially if fish are startled
- Necropsy: petechial visceral hemorrhages in older fingering trout vs pale viscera with few petechiae in larger trout; catarrhal exudate in stomach/intestine produces cohesive fecal pseudocast
- Histopathology:
- acute necrosis of pancreatic acinar cells (primary target) with basophilic intracytoplasmic inclusions, damage of adjacent adipose tissue
- McKnight cells (epithelial cells of pyloric ceca) swell and have a fragmented nucleus with eosinophilic cytoplasm shed into the lumen
- Renal tubular, hematopoietic tissue, liver may be necrotic
- Definitive diagnosis: isolation of high titers (10^6-10^9 infective units/gram of tissue)
- Large fish (>6 cm): posterior kidney is best; pyloric ceca, spleen, liver useful
- Small fish: sample entire fish including kidney
- Sampled within 24 hours - store on ice
- Homogenates - best to freeze at lowest possible temperature
- ID subclinical carriers by sacrificing fish for culture of posterior kidney
- Immunohistochemistry can be used
- Differentials: IHN, VHS, HVS, alphavirus
- Unique feature of IPN is fragile white feces and clear to milky mucus in the stomach/intestine
- Clinical signs on day 3-5 after exposure in fry or day 8-10 after exposure in fingerlings
- Peak mortality 12-18 days after exposure
- Fish that survive outbreaks often stunted (pancreatic fibrosis) and most become carriers (shed virus in feces/urine for >2 years)
- Transmission:
- Horizontal (especially fecal pseudocast) and vertical (transport fluids or egg - suspected contributor to embryo mortality)
- Shed in feces of piscivorous birds
- Disinfect, quarantine, raise fish in virus-free water for first 6 months of life
- Disinfection: 40 mg/l chlorine for 30 min; 20,000 ppm formalin 5 minutes, 35 ppm iodine for 5 minutes, pH 12.5 for 10 min, 90 ppm ozone for 0.5-10 minutes
- One of the most stable fish viruses - survives for months frozen, 3 months in sterile water, one month at air drying at 10C, lasts a while in brackish water, resistant to UV (partial inactivation), not controlled with egg baths
- Virus free water - spring or well water
- Lowering temperature can reduce severity of outbreaks
-
Infectious pancreatic necrosis (IPN) - ZP
- Highly contagious, young salmonids, worldwide.
- Bisegmented, ds RNA, Birnaviridae family
- Most commonly rainbow trout, brook trout, brown trout, atl salmon, pacific salmon.
- Halibut, flounder, cod, yellowtail, turbot.
- Many others asymptomatic carriers.
- Species susceptibility reported to decrease with age, correlate with population rearing intensity, temperature, transfer from FW to SW.
- In FW – corckscrew or spiral swimming behavior, dyspnea, severe abdominal swelling, pigmentary darkening of the body.
- Post-transfer to SW – anorexia, lethargy, abnormal swimming patterns, unable to maintain buoyancy.
- Darkening of skin along tail and abdomen, pale yellow liver, GI tract containing pale yellow catarrhal exudate.
- Histo – severe pancreatic acinar cell necrosis, epithelial necrosis of intestinal mucosa.
- Pancreatic tissue replaced by fibrous connective tissue.
- Cytoplasmic viral-specific tubules and paracrystaline arrays of virions on TEM.
- Sampling – Virus isolation (liver, spleen, kidney, brain, ovarian fluid during spawning.
- Can be isolated from asymptomatic fish that may be reservoirs.
- Economic impact of IPN:
- Millions of dollars, concern for impact on wild populations.
14
Q
Describe the effects of Carp Edema Virus.
What type of virus is this? Does it have another name?
How is it transmitted?
What are the typical clinical signs?
What differentials should be considered?
How is it diagnosed?
How is it treated?
A
- Pox Viruses
- Carp edema virus – affects common carp and subspecies such as koi
- Etiology: Poxviridae, double stranded DNA viruses
- Transmission – horizontal
- Fish with resolved clinical signs are likely carriers. Positive for up to 5-6 months
- Outbreaks more common at 60-77F, but disease has been seen at lower temperatures in Europe
- Signs
- Severe lethargy, often laterally recumbent on substrate with minimal response to stimulation. May congregate at surface or sides of a pond. Inappetence common. May see skin edema, generalized edema, pale edematous gills with white/grey areas of necrosis (similar to KHV), dyspnea, ulcerative/hemorrhagic skin lesions especially around mouth and base of fins, increased mucus, enophthalmos
- Differentials for systemic inflammation in carp: CEV, spring viremia of carp. KHV, viral hemorrhagic septicemia, motile aeromonad septicemia, and vibriosis
- Diagnosis
- Gill wet mount – hyperplasia, edema, increased mucus. No gross internal lesions
- Branchitis with epithelial hyperplasia, edema, and lamellar fusion. Intracytoplasmic inclusions common
- PCR gill tissue
- Treatment – increase salinity to 5 g/L can reduce morbidity and mortality. PCR test before release from qt.
15
Q
Describe the effects of lymphocytiviruses in fish.
What type of virus is this?
What species are commonly affected?
How is it transmitted?
What are the typical signs?
What differentials should be considered?
How is it diagnosed? What samples should be taken? What types of inclusion bodies are present?
How is it managed?
A
Lymphocystiviruses (CGFM)
- Lymphocystis disease viruses – hypertrophy of fibroblastic cells leading to plaques or nodules on the skin and sometimes viscera
- Tropical teleosts – cosmetic concern and indicator of stressors. Rarely causes systemic disease
- Etiology – Iridoviridae, DNA virus
- Transmission – horizontal and vertical (egg surfaces)
- Common in tropical and subtropical marine and freshwater teleosts (cardinalfish, groupers, amberjack, flounder, cichlids, guppies, platies)
- Many strains relatively host specific
- Signs
- White or tan plaques/nodules on the skin and fins, particularly on the rostrum, over operculum and near lateral line
- Systemic signs rare, but may increase susceptibility to secondary infections
- Differentials for plaques/nodules on skin: lymphocystivirus, carp pox, papillomas, granulomatous inflammation, chlamydia-like organisms, microsporidial xenomas, and calcinosis cutis
- Diagnosis
- Scrapes – round cells with thickened outer membranes
- Can have plaques or nodules on kidney and spleen.
- Encapsulated hypertrophied cells, no inflammatory response, Feulgen-positive intracytoplasmic inclusion bodies
- Management – reduction/resolution of stressors. Lesions regress over days to months if stressors removed. Can surgically debride to speed resolution
Problem 40 – Lymphocystis – Lymphocystivirus (Iridovirus)
- Host/location: Captive fish – both freshwater and marine – skin and gills
- Clinical Signs/Pathology: Typically self-limiting but can permanently disfigure a fish
- Pearly-white dermal nodule, usually on fins
- Hypertrophied dermal fibroblasts with irregular inclusions and an undisplaced nucleus
- Distinguished from Epitheliocycstis which has epithelial cells with a hypertrophic nucleus that is peripheral to basophilic inclusion bodies
- Transmission: Virus is viable in water for about 1 week. Incubation period is weeks to months.
- Diagnosis: Basophilic IC inclusions in fibroblasts
- Treatment: None, affected fish should be quarantined at least a month after recovery.
Lymphocystis (ZP)
- Cultured and wild, FW and SW
- Lymphocystis disease virus LDV (iridovirus)
- Icosahedral, diameter 200 nm
- LDV-1
- Flounder and place
- LDV-2
- Dab
- Iridoviruses isolated from other species have not been formally characterized.
- Incubation period – long, weeks to months.
- Clinical history related to stress.
- Transmission – horizontal, abrasions of lesions and release of iridovirus into environment.
- Self limiting.
- Gross lesions – variably sized, raised, white to tan masses, skin MM, gills.
- Pinpoint, discrete and nodular, or coalescent and multinodular.
- Microscopically – extreme cytomegaly of dermal fibroblasts, dermal infiltration by lymphocytes and histiocytes.
- Dx – microscopic examination of histologic sections or wet mount, cytomegalic dermal fibroblasts.
17
Q
Describe the effects of megalocytoviruses in fish.
What are some of these viruses?
What are their typical clinical signs?
How are they transmitted?
A
- Megalocytiviruses
- Includes infectious spleen and kidney necrosis virus (ISKNV), scale drop disease virus (SDDV) and red seabream iridovirus (RSIV)
- Freshwater and marine telesots, cause systemic inflammatory disease
- Family: Iridoviridae
- Horizontal transmission (suspected vertical as well)
- ISKNV epizootic reported in: teleosts (tetras, swordtails, mollies, platies, freshwater angelfish, Oscars), cultures food fish (Nile tilapia, cod) and marine fish (mandarin, cardinalfish, batfish)
- SDDV epizootics only reported in cultured barramundi
- RSIV infects marine and estuarine teleosts (red seabream, amberjack, grouper)
- Clinical signs:
- Asymptomatic, lethargy, abnormal swimming, abnormal position, inappetence, skin darkening or pallor, petechiae, ulcers (scale loss common with SDDV), exophthalmos, dyspnea/tachypnea, white feces, coelomic distention
- Diagnosis: characteristic inclusions on histology and virus isolation or PCR
- Clinical pathology may show hemolytic anemia, erythrocytes with large eosinophilic intracytoplasmic inclusions
- Necropsy: pallor, petechiae, splenomegaly, renomegaly
- Histopath: Necrosis and inflammation with disseminated mesenchymal cells with high cytoplasm to nuclear ratios and large basophilic or amorphous intracytoplasmic inclusion
- Spleen and kidney most commonly affected
- RSIV – reportable to OIE
- Slowly decrease water temperature to slow disease progression
-
Systemic iridoviruses (ZP)
- Genera Megalocytivirus and Ranavirus
- FW and marine, global distribution
- Megalocytoviruses
- Pathogens of fish
- RSIV – Red sea bream iridovirus
- ISKNV – Infectious spleen and kidney necrosis virus
- These two are the best known, OIE listed.
- BCCIV – Banggai cardinalfish iridovirus
- The only megalocytivirus reported in marine ornamental fish.
- CS – lethargy, anemia.
- Gross lesions – branchial hemorrhages, splenomegaly.
- Histo – cytomegalic cells in multiple organs.
- Granular basophilic viral inclusions that distend the cytoplasm and are often located beneath the endothelium of blood vessels.
- Genera Megalocytivirus and Ranavirus
- Megalocytivral Disease and Red Seabream Iridovirus (RSIV)
- Pagrus seabream (red seabream) and 30 other cultured marine fish species in Japan (Perciformes, Pleuronectiformes and Tetraodontiformes)
- Epidemiology
- Significant mortality in rock bream and Japanese flounder
- Mainly juveniles affected - lethargy, anemia, gill petechiae, splenomegaly
- Horizontal transmission
- Disease typically >20 C
- Form inclusion body - bearing cells (IBCs) in the spleen, hematopoietic tissue, gills and digestive tract
- Definitive diagnosis via virus identification from cell culture or tissue - kidney and spleen
- Vaccine under development
- Decreasing temperature may control infection
- Related iridovirus in brown spotted grouper in Thailand, ISKNV (infectious spleen and kidney necrosis virus in mandarin fish), Turbot Iridovirus (TBIV) in Korea
- Red sea bream resistant to ISKNV
- White Sturgeon Iridoviral Disease WSID
- Up to 95% mortality in juvenile (<1 yr) farmed white sturgeon in North America
- Vertical and horizontal transmission
- Lake sturgeon experimentally susceptible
- Similar virus in Russian sturgeon
- Emaciation is key clinical sign, secondary infections common due to skin and gill damage
- No internal lesions
- Focal to diffuse herplastictic epidermis with hypertrophied, amphiphilic to basophilic, Malpighian cells
18
Q
Describe the effects of infectious salmon anemia virus.
What type of virus is this?
What species are typically affected? Are there any vector or carrier species?
How is this virus transmitted?
What are the typical clinical signs?
What differentials should be considered?
How is this disease diagnosed? What samples need to be collected?
Is this a reportable disease?
What lesions are typically seen on necroposy?
How are outbreaks prevented?
A
Orthomyxoviruses (CGFM)
- Infectious salmon anemia virus (ISAV) – causes severe hemolytic anemia in the Atlantic salmon
- Enveloped RNA viruses, horizontal transmission reported with vertical transmission suspected
- Viruses survive for hours to days in seawater – vectors (sea lice) and carriers (brown trout, pollock and Atlantic cod)
- Fish that resolve clinical signs have lifelong immunity
- Natural infection limited to Atlantic salmon, mostly in salt water
- Signs:
- Clinical course is typically chronic with multiple Atlantic salmon usually affected; lethargy common. Affected fish in good condition
- Tachypnea, dyspnea, gill pallor (anemia) and exophthalmos, hyphema or coelomic distention may occur due to hemorrhage.
- Differentials for anemia and hemorrhage in Atlantic salmon ISAV, erythrocytic inclusion body syndrome, infectious hematopoietic necrosis virus, infectious pancreatic necrosis virus, Moritella viscosa, Yersinia ruckeri, and cardiomyopathy syndrome.
- Diagnosis – virus isolation and PCR on blood or heart from Atlantic salmon with severe anemia and hemorrhages
- Clinical pathology – severe anemia (PCV < 10%)
- Necropsy – visceral pallor, coelomic effusion, renomegaly, hepatomegaly with necrosis, petechia and hemorrhages
- Reportable to OIE – often depopulation and disinfection with movement restrictions imposed by the USDA
- Prevention – Atlantic sea pens kept far from wild stocks, farmed salmon and salmon processing plants. A USDA approved vaccine available but protection is variable. Reports that nucleotide analog ribavirin reduces mortality of experimental infection
Infectious salmon anemia (ISA - orthomyxovirus Isavirus) - Noga
- AKA Hemorrhagic Kidney Syndrome (HKS)
- Coldwater (marine only)
- Only known to cause disease in Atlantic salmon
- Isolated in diseased coho salmon in Chile
- Trout are asymptomatic carriers
- Epidemiology
- World-wide threat to Atlantic salmon farming
- Usually low mortality, but can be up to 100% - mean in Canadian epidemics is 12% over 60 days
- Usually fish that have been in seawater >1 year; spreads slowly in a farm
- Horizontal transmission (likely gills), sea louse (experimental)
- Virus active 20 hours in seawater and 4 days in blood or kidney at 6 C
- Latent carriers - stressed form treatment for sea lice or other infectious disease experienced outbreaks 2-3 weeks later
- Most often diagnosed in spring
- Examination: Lethargy; hanging head up; dyspnea; coelomic distension; exophthalmos; skin hemorrhage; pale gills
- Highly variable! Some nonspecific mortality and poor growth
- Peracute - no clinical signs
- Chronic (typical) - hang motionless at top before sinking to bottom, lethargy, dyspnea, anorexia
- Blood and endothelial cells (liver, heart) - severe anemia, vascular damage, hepatocellular degeneration, scale edema, pallor, ascites
- Nephromegaly, splenomegaly, darkening of the liver or petechiae
- Anemia
- Early moderate to severe anemia: HCT 15-25%
- Later very severe: HCT <10%
- Degenerate and vacuolated erythrocytes and erythroblasts with irregular nucleus
- Reduction in lymphocytes and thrombocytes to erythrocytes
- Histopathology
- Early: Focal congestion and dilation of hepatic sinusoids, rupture of sinusoidal epithelium and erythrocytes in space of Disse
- Late: multifocal hemorrhagic hepatic necrotic foci - zonal appearance with large areas around veins intact
- Kidney- tubular necrosis, eosinophilic casts, moderate sinusoidal congestion, interstitial hemorrhage, erythrophagia
- Spleen - congestion, erythrophagia
- Congestion and necrosis of intestine and pyloric caeca
- Branchial lamellar and filamental vessels congested
- Diagnosis - Definitive with virus identification (kidney best, liver, spleen, heart)
- Strong presumptive: gross lesions (ascites, splenomegaly, dark livers in at least some fish), hematology (HCT <10, degenerate erythrocytes), histopathology (hepatic necrosis and congestion)
- Dark livers also seen with cardiomyopathy syndrome, but will have gross and microscopic heart lesions
- Aquaculture (severe economic losses): specific OIE guidelines in cooperation with regulatory agency to officially confirm presence
- Clinical and necropsy findings confirmed with cell culture, antibody probe, or PCR or ISA cultured/identified in 2 separate samples or cultured from at least one sample with positive antibody or gene test
- Disinfect and quarantine
- Fish farms should be at least 5 km away from the next fish farm
- Disinfect effluent from salmon processing plants
- Autogenous vaccine - New Brunswick Canada
- Variable policies
- Norway: ISA-free zones
- Scotland: required slaughter of all fish on infected facilities
- Fallowing policies
-
Infectious salmon anemia virus (ISAV) - ZP
- Causes infectious salmon anemia (ISA)
- Marine, farm-raised atlantic salmon.
- Initially described in Norway, since identified in farmed salmon in FW and SW.
- Isavirus genus (only spp), only fish orthomyxovirus described to date.
- Enveloped, 8 ssRNA segments, negative polarity.
- Demonstrated to agglutinate erythrocytes from a range of different fish species.
- Virulence associated with highly-polymorphic region (HPR) or the hemagglutinin-esterase (HE) gene, and there is a marked difference in virulence of geographically different strains.
- Sea-run brown trout, rainbow trout, and Coho salmon subclinical disease, reservoirs.
- High mortality in experimentally infected rainbow trout.
- Transmission horizontal, carried in SQ contaminated with urine or feces.
- Sea lice implicated as a vector.
- Seasonality appears to play a role.
- Primary mortality between 6-10 months following the intro of naïve salmon to salt water pens.
- Acutely infected animals typically display evidence of abnormal swimming behavior and marked lethargy.
- Necropsy – ascites, exophthalmia, severe pallor of the gills and viscera.
- Petechiae, ecchymoses, liver and spleen often markedly congested.
- With chronicity, petechiation extends into the subcutaneous adipose.
- Necrohemorrhagic hepatitis, renal interstitial hemorrhage, and noninflammatory tubular epithelial degeneration and necrosis.
- Congestion of branchial filaments, gastric and foregut lamina propria, spleen.
- Viral antigen can be identified in tissue smears using immunoflorescent antibody tests (IFAT).
- Effective RT-PCR assays.
- Mos tsensitive diagnostic test followed by VI and IFAT.
- Large economic impact.
19
Q
What types of viruses cause vacuolating encephalopathy & retinopathy and viral nervous necrosis?
What fish are commonly affected?
What are the typical clinical signs?
How are these diseases diagnosed?
A
-
Betanodaviruses
- Known as vacuolating encephalopathy and retinopathy (VER) or viral nervous necrosis (VNN) – vacuolar lesions in brain and retina
- Identified particularly in marine teleosts – horizontal transmission reported, vertical likely.
- Can surviving freezing, low temperatures and extended periods in saltwater
- Invertebrate vectors (clams, brine shrimp, copepods) and carriers (gilthead sea bream)
- Wide host range – multiple marine teleosts (striped trumpeter, halibut, turbot, grouper, wrasses, bass), euryhaline fish (barramundi, grouper, Australian bass), and freshwater fish (sleepy cod and Nile tilapia)
- Sign
- Acute clinical course with abnormal swimming most common (spiral, dart, inverted), inappetence, blindness, progressive changes in coloration (pallor or darkening)
- Diagnosis
- Histology of neurologic system – vacuolating necrosis of neural cells of the spinal cord, brain, and retina. Intracytoplasmic inclusion bodies may be seen
- Recommend sampling brain and eye for histo, PCR, VI and sequencing
- Relatively resistant to UV and ozone. May need longer contact time for chemical disinfection. Prolonged drying is helpful (> 7 days)
- Histology of neurologic system – vacuolating necrosis of neural cells of the spinal cord, brain, and retina. Intracytoplasmic inclusion bodies may be seen
Nodaviral (Betanodavirus) diseases - Viral Nervous Necrosis (VNN), Vacuolating Encephalopathy and Retinopathy (VER) - Noga
- Marine (warm and cold water) - 30 fish species
- Groupers, sea bass, flatfish
- Worldwide except Africa
- Striped jack nervous necrosis virus (SJNNV)
- Tiger puffer nervous necrosis virus (TPNNV)
- Barfin flounder nervous necrosis virus (BFNNV)
- Red grouper nervous necrosis virus (RGNNV)
- Not host specific, horizontal and vertical transmission
- Disease mostly seen in larvae, but market size fish can be affected
- Examination: Abnormal swimming (whirling, belly - up); abnormally dark or light body color
- Mostly acute mortality, sometimes chronic
- Inappetance, blindness, changes in coloration, swim bladder hyperinflation
- Histopathology
- CNS vacuolation and necrosis - especially vacuoles in brain grey matter
- may have intracytoplasmic, ∼ 1-5 μm inclusions in brain cells
- Retinal damage
- Diagnosis
- Sample whole larvae; brain, spinal cord and eyes of larger fish; ovarian fluid at spawn may be helpful in asymptomatic carriers
- Presumptive diagnosis if histo shows vacuolating encephalopathy, necrosis and retinopathy
- Definitive with viral identification (PCR)
- Can look similar to tiger puffer virus disease in some fish
- Can screen for serum antibodies
- Biosecurity
- Disinfect and quarantine
- Screen broodstock and eliminate carriers (PCR)
- Ozone antisepsis of eggs successful in striped jack (0.2 ug/ml residual ozone) and Atlantic halibut (4.0 ug/ml residual ozone)
- Stocking larvae at low density (<10 per L) has been successful for some species
Image: Signs of vacuolation (*) and necrosis (arrowheads) on histology of the brain (a) and retina (b) from a Bartletts’ anthias (Pseudanthias bartlettorum), consistent with viral nervous necrosis. H&E x400 and x200.
20
Q
What types of viruses are salmon Pancreas Disease Virus and Sleeping Disease Virus?
What are the other names of these diseases?
What species do they affect?
What are the typical clinical signs? What are mortalities like?
What are the staged findings on necropsy?
How does Salmon Pancreas Disease differ from Infectious Pancreatic Necrosis?
How is it managed?
What are the differences with Sleeping Disease Virus?
A
Togaviridae - Alphavirus diseases (Pancreas Disease, Sudden Death Syndrome, Sleeping Disease) - Noga
- Cold marine and freshwater
- Salmon Pancreas Disease Virus (SPDV)/Salmonid alphavirus SAV 1,3,4,5,6
- Sea-cultured salmonids in Europe and North America (Pacific) - marine only
- Likely endemic in Atlantic salmon in Europe
- Atlantic salmon at any age most susceptible, sea reared rainbow trout in Norway
- Develop disease 6-12 weeks after transfer to seawater, any time of year
- Most favorable temperature for virus: 9-12 C; inhibited >15 C
- Clinical signs: Anorexia (spitting out feed), lethargy (swim around edges, whirling), emaciation, yellow cast-like feces
- Mortality in large fish - sudden death syndrome
- Fish lying motionless at bottom
- usually chronic (3-6 weeks) low mortality but can be up to 60-100%; poor growth rates and recovered fish poor doers
- Gross and Histopathology
- Sub-acute: loss of exocrine pancreas, variable cardiomyopathy, hyaline degeneration in skeletal muscle
- Acute: empty gut, yellow-white fecal casts, pyloric caecae surface hemorrhage (in pancreas), acute diffuse necrosis of pancreatic acinar tissue with disappearance of the exocrine pancreas tissue, acute necrosis of cardiac myocytes, epicarditis
- Chronic: decrease in coelomic fat, poor body condition, tissue atrophy between pyloric caecae, may see fibrosis of pancreas, foci of regenerating acinar tissue among fibrotic lesions, mitotic figures in cardiac myocytes, skeletal and heart muscle damage (similar to Vit E deficiency)
- Cardiac rupture occasionally observed in fish with no other gross lesions
- Pancreas, cardiac, skeletal abnormalities
- Definitive Diagnosis: virus isolation, PCR (serum, heart tissue), presence of specific neutralizing antibodies with clinical/histological findings
- Harder to diagnose after 40 days- surviving fish recovering
- May be underdiagnosed if concurrent infection with IPN
- Differences bt IPN and SPDV
- IPN usually within 3 months of transfer to sea
- Mortalities occur in acute phase of IPN rather than chronic with SPDV
- Inappetance more pronounced with SPDV
- IPN - pancreatic necrosis focal, catarrhal enteritis, no muscle lesions
- R/O Idiopathic diseases that cause muscle lesions in Atlantic salmon
- Cardiomyopathy syndrome (CMS) - first sea winter or close to harvest, histologic lesions in heart and liver, congestive heart failure
- Heart and skeletal muscle inflammation (HSMI) - more inflammatory; may be concurrent with with IPN
- Management
- All-in, all-out stocking and fallowing reduce impact
- Reduce stress
- Feeding smaller pellets may reduce anorexia and overall mortality
- Vitamin C and E supplementation may help with recovery
- Recovered fish do not experience another outbreak
- Sleeping disease virus (SDV); SAV 2 - Rainbow trout in freshwater
- Epidemics also seen in coho salmon
- Europe (France, UK, Italy, Spain, Germany)
- Fish recumbent on bottom; variable mortality, inappetance for several weeks (decreased growth)
- Exocrine pancreas: necrosis, rounding of acinar cells, then lymphocyte and fibrocyte infiltration, then heart (hyalinization, loss of striation) and skeletal muscle (loss of fibers, increased cellularity) effects
- Diagnosis: PCR, serum or heart tissue and presence of neutralizing antibodies
