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Home , Acanthocephalus (plant), Aeromonas salmonicida, Aquaparamyxovirus, Aquareovirus, Ceratonova shasta, Common dab

DISEASES OF WILD AND CULTURED IN

Theodore Meyers, Tamara Burton, Collette Bentz, Jayde Ferguson, Davis Stewart, and Norman Starkey

July 2019 Alaska Department of and Fish Pathology Laboratories The Alaska Department of Fish and Game printed this publication at a cost of $9.83 in Anchorage, Alaska, USA. About This Field Guide

This field guide is a product of the Diagnostics, Educational and Outreach Program which was initiated and funded by the Yukon River Panel’s Restoration and Enhancement fund and facilitated by the Yukon River Drainage Association in conjunction with the Alaska Department of Fish and Game. The original impetus driving the production of this guide was from a concern that Yukon River fishers were discarding Canadian-origin Chinook believed to be infected by Ichthyophonus. It was decided to develop an educational program that included the creation of a field guide containing photographs and descriptions of frequently encountered parasites within Yukon River fish.

This field guide is to serve as a brief illustrated reference that lists many of the common (and not so common) parasitic, infectious, and noninfectious diseases of wild and cultured fishes encountered in Alaska. The content is directed towards lay users, as well as fish culturists at facilities and field biologists and is not a comprehensive treatise nor should it be considered a scientific document. Interested users of this guide are directed to the listed fish disease references for additional information.

Information contained within this field guide is published from the laboratory records of the Alaska Department of Fish and Game, Fish Pathology Section that has regulatory oversight of finfish health in the State of Alaska. This third printing includes several new entries, some new photographs and updated information on previous diseases and parasites. This version may be downloaded as a PDF from the ADF&G website at the following web address: http://www.adfg.alaska.gov/static/species/disease/pdfs/fish_disease_book.pdf

3 Text written and provided by: Theodore Meyers, Tamara Burton, Collette Bentz, and Jayde Ferguson, Alaska Department of Fish and Game, Fish Pathology Laboratories, 333 Raspberry Road, Anchorage, Alaska 99518; P.O. Box 115526 (physical 3333 Glacier Highway), Juneau, Alaska 99811-5526.

Manuscript Photographs: Alaska Department of Fish and Game, Fish Pathology Laboratory photo archives except where indicated.

Publication design by Southfork Graphic Services.

Cover Photograph: Ichthyophonus growing in laboratory culture.

©2019 Alaska Department of Fish and Game, third printing

The original printing of this publication was produced with funding and support from the Yukon River Panel and its members and the Yukon River Drainage Fisheries Association. Current funding is provided by the ADF&G, Commercial Fisheries and Sport Fish Divisions.

The Alaska Department of Fish and Game (ADF&G) administers all programs and activities free from discrimination based on race, color, national origin, age, sex, religion, marital status, pregnancy, parenthood, or disability. The department administers all programs and activities in compliance with Title VI of the Civil Rights Act of 1964, Section 504 of the Rehabilitation Act of 1973, Title II of the Americans with Disabilities Act of 1990, the Age Discrimination Act of 1975, and Title IX of the Education Amendments of 1972. If you believe you have been discriminated against in any program, activity, or facility please write ADF&G ADA Coordinator, P.O. Box 115526, Juneau, AK 99811-5526; U.S. Fish and Wildlife Service, 4401 N. Fairfax Drive, MS 2042, Arlington, VA 22203; or Office of Equal Opportunity, U.S. Department of the Interior, 1849 C Street NW MS 5230, DC 20240.

For information on alternative formats and questions on this publication, please contact the department’s ADA Coordinator at (VOICE) 907-465-6077, (Statewide Telecommunication Device for the Deaf) 1-800-478-3648, (Juneau TDD) 907-465-3646, or (FAX) 907-465-6078. Table of Contents

Viruses ...... 62 Aquareovirus ...... 2 neurotropus ...... 64 Erythrocytic Inclusion Body Syndrome (EIBS) ...... 4 Myxobolus squamalis ...... 66 Erythrocytic Necrosis (VENV) ...... 6 bryosalmonae (PKD) ...... 68 Infectious Hematopoietic Necrosis Virus (IHNV) ...... 8 Helminths (Worms) North American Viral Hemorrhagic Acanthocephalans (spiny headed worms) ...... 70 Septicemia Virus (NA-VHSV) ...... 10 Anisakid Larvae () ...... 72 Pacifc Salmon Paramyxovirus ...... 12 Philometra (nematode) ...... 74 (PRV) ...... 14 Philonema (nematode) ...... 76 Black Spot Disease (trematode) ...... 78 Bacterial Coldwater Disease (BCWD) ...... 16 Encysted Digenean Metacercariae (trematode) ...... 80 Bacterial Gill Disease ...... 18 Larval Diplostomulum of the Eye (trematode) ...... 82 Bacterial Kidney Disease (BKD) ...... 20 Gyrodactylus and (monogene) ...... 84 (ERM) ...... 22 Piscicola () ...... 86 Furunculosis ...... 24 (cestode) ...... 88 Fusobacteria-like Agent ...... 26 Schistocephalus (cestode) ...... 90 Marine Tenacibaculosis ...... 28 Triaenophorus (cestode) ...... 92 Motile and Pseudomonas Septicemia ...... 30 Mycobacteriosis of Fish ...... 32 External Parasitic ...... 94 Vibriosis...... 34 Salmincola () ...... 96 Fungi Sarcotaces (copepod) ...... 98 Phaeohyphomycosis of Safron ...... 36 Non-infectious Diseases Phoma herbarum ...... 38 Bloat (Water Belly) ...... 100 Blue Sac Disease of Fry ...... 102 Epistylis (Heteropolaria) ...... 40 Coagulated Yolk Disease (White Spot Disease) ...... 104 Hexamita...... 42 Drop-out Disease ...... 106 Ichthyobodiasis (Costiasis) ...... 44 Gas Bubble Disease (GBD)...... 108 Ichthyophonus ...... 46 Mushy Syndrome ...... 110 Saprolegniasis – Cotton Wool Disease ...... 48 Neoplasia (Tumors) ...... 112 Trichodiniasis ...... 50 Organ and Tissue Anomalies ...... 116 Trichophrya (Capriniana) ...... 52 Pigment Aberrations in Fish ...... 118 White Spot Disease ...... 54 Sunburn (Back-Peel) ...... 120 X-Cell Tumors ...... 56 Reference Glossary of Terms ...... 122 Ceratonova () shasta ...... 58 Fish Disease References ...... 127 Henneguya ...... 60 Aquareovirus

I. Causative Agent and Disease associated with epizootic fish mortal- Aquareovirus is a in the virus ity producing severe hemorrhaging in family . These icosahedral fingerlings and yearlings resulting in up (60-80 nm) 11 segmented double- to 80% mortality. stranded RNA viruses (over 50) have been isolated from a variety of marine IV. Transmission and freshwater aquatic world- Transmission is horizontal via water wide including finfish, and bivalve mol- or from fish to fish. Isolates from bivalve luscs. Genetic analyses have identified 7 mollusks likely represent virus that has different genotypes or (A-G) of been shed into the from a aquareoviruses. Most of these viruses fish and then bioaccumulated into produce self-limiting infections of low shellfish tissues by filter feeding. pathogenicity and are not associated with extensive disease or mortality. V. Diagnosis Exceptions include isolates from 7 fish Detection of Aquareovirus is by species that have been associated with isolation of the virus in cultures of fish mortality, most notably the grass susceptible fish cell lines inoculated aquareovirus (G). The viral agents with infected tissue. The virus causes a are most often isolated from asymp- unique cytopathic effect (CPE) charac- tomatic adult carrier fish during routine terized by focal areas of cellular fusion screening examinations. (syncytia) and cytoplasmic destruction creating a vacuolated or foamy appear- II. Host Species ance. The exception is species In the states of G that produces a diffuse CPE. Presump- Washington, and , tive identifications are made based on adult appear to be the the typical CPE and are confirmed by most frequent species infected with serology, electron microscopy or poly- aquareovirus A or B. The virus has also merase chain reaction (PCR). been isolated from adult coho and and steelhead. Rainbow VI. Prognosis for Host have been experimentally infected with The prognosis for the fish host is the virus resulting in mild hepatitis with good in the majority of cases where the no overt disease or mortality. In Alaska, virus is not a primary pathogen. There aquareoviruses have been isolated are no corrective therapies for viral from Chinook salmon (species B) and infections in fish except avoidance. geoduck clams (species A). VII. Human Health Signifcance III. Clinical Signs There are no human health concerns Fish naturally infected with aquareo- associated with aquareoviruses. viruses generally do not exhibit clinical signs of disease. Experimental infections can produce focal necrotic lesions in the livers of , chum salmon and fry. Other pathogenic exceptions include the grass carp species G that is

2 VIRUSES

Large rounded plaques of syncytial cell CPE (arrow) of Aquareovirus in bluegill fry cells.

Double morphology of Aquareovirus particles (arrow) in negative stain; transmission electron microscopy, X 91,000.

3 VIRUSES Erythrocytic Inclusion Body Syndrome (EIBS)

I. Causative Agent and Disease V. Diagnosis Erythrocytic inclusion body syn- Isolation and replication of the drome (EIBS) is caused by an unclassi- virus in available fish cell lines has fied icosahedral virus (70-80 nm) that been unsuccessful. Thus, diagnosis is infects erythrocytes of several salmonid by observation of the small pale blue fishes in fresh and seawater. Typically, inclusion bodies in the cytoplasm of EIBS presents with single or multiple infected erythrocytes with confirmation pale, basophilic inclusions (0.4-1.6 by transmission electron microscopy um) in the cytoplasm of erythrocytes (TEM). The virus is found free in the in stained peripheral blood smears. cytoplasm or more commonly occurs in Affected fish may be asymptomatic, membrane bound cytoplasmic inclusion but more often have varying degrees bodies within erythrocytes. of anemia and secondary bacterial and fungal infections. In severe cases of VI. Prognosis for Host uncomplicated anemia, cumulative fish Severe fish losses caused directly mortality over 20% has been reported by EIBS are rare. However, fish become with hematocrits less than 20%. weakened from the anemia and mortal- ity from other associated environmental II. Host Species stressors or secondary pathogens can be EIBS has been found in Chinook, significant. The disease generally is self- coho and in the Pa- limiting with recovery and immunity in cific Northwest, , and the survivors. British Isles. Other salmonid species showing variable susceptibilities by ex- VII. Human Health Signifcance perimental injection with infected blood There are no human health concerns homogenates include , with the EIBS virus. masou salmon and chum salmon. NOTE: In Alaska, only one case of EIBS III. Clinical Signs has been reported in 2004 affecting Fish are lethargic, anorexic and juvenile Chinook salmon in seawa- anemic with chronic mortality often ter netpens. Subsequent studies have associated with secondary infections shown that EIBS in Japanese farmed by other pathogens. Five stages of EIBS may be caused by a strain have been described: preinclusion, inclu- of Piscine Orthoreovirus (PRV-2). sion body formation, cell lysis with low Molecular studies have determined that hematocrits, recovery with increasing PRV is present in Alaskan coho and hematocrits and full recovery. Chinook salmon. See PRV chapter for more detail. IV. Transmission The disease can be transmitted horizontally while surviving fish gener- ally recover and develop an acquired immunity against reinfection that is transferable by passive immunization.

4

VIRUSES 

Erythrocytes of Chinook salmon with small basophilic cytoplasmic inclusion bodies (arrow) typical of EIBS, X 1000.

EIBS inclusion body (not membrane-bound) composed of virus particles in the cytoplasm of an erythrocyte; transmission electron microscopy, X 56,400.

5 VIRUSES Erythrocytic Necrosis Virus (VENV)

I. Causative Agent and Disease IV. Transmission Erythrocytic necrosis or viral Transmission of this virus is likely erythrocytic necrosis (VEN) is caused horizontal from fish to fish based on the by several similar iridoviruses having few experimental studies using water- double-stranded DNA and a hexagonal borne exposure. Adult carrier fish of shape ranging in size from 130-330 nm. susceptible species are likely reservoirs The viruses infect erythrocytes causing of the virus that is transmitted to juve- a hemolytic disease often resulting in nile fish. Anadromous fish likely become anemia and secondary infections by infected during their marine phase of other pathogens including VHSV Type life. There is some suggestion that the IVa virus is vector-borne and one instance of infection in juvenile salmonids in II. Host Species freshwater suggesting vertical transmis- There are likely several different sion from adult anadromous parent fish. strains of the virus worldwide in the marine environment infecting a large V. Diagnosis variety of more than 20 anadromous and Diagnosis is made with blood smears marine fish species. In Alaska, VENV showing characteristic eosinophilic has been detected in Pacific inclusion bodies (1-4 um) present in the from several locations but has not yet cytoplasm of erythrocytes when stained been observed in salmonids. Results with Giemsa or Wright stains. Impres- from experimental infections and occur- sion smears of hematopoietic head rence of epizootics in young-of-the-year kidney can be substituted for blood. The Pacific herring indicate that juveniles are virus is confirmed by the observation more susceptible than older fish. of iridovirus particles associated with inclusion bodies using electron micros- III. Clinical Signs copy (TEM). VEN viruses have not been Adult herring generally show no successfully cultured in available fish clinical signs of disease. In juvenile cell lines, however an unvalidated PCR Pacific herring, fish are anemic exhibit- is available for the virus in Pacific her- ing nearly white gills and pale visceral ring. organs. color may be green due to breakdown of blood hemoglobin VI. Prognosis for Host releasing excess biliverdin. Hemotocrits The virus in Alaskan juvenile Pacific may be as low as 2 to 10%, erythrocytes herring caused one of the first natural are fragile causing hemolysis of blood epizootics reportedly associated with samples, and immature erythrocytes mass fish mortality. Chronic to subacute predominate in peripheral blood. High mortality in juvenile Pacific herring can mortality with dead fish on the shoreline also occur, especially when stressed. accompanied by extensive congregations of predator birds may occur in areas VII. Human Health Signifcance where juvenile herring are weakened by No human health concerns are as- the disease. sociated with VEN virus.

6 VIRUSES

Anemic Pacifc herring with very pale gills and green livers from excessive biliverdin commonly seen with VEN

Erythrocytes of Pacifc herring with large eosinophilic cytoplasmic inclusion bodies (arrow), some surrounded by pink

lattices composed of virus particles; Dif Quik, X 400. 

TEM of infected erythrocyte showing large virus particles (arrow) comprising the lattice surrounding inclusion bodies in stained smears, X 15,600.

7 VIRUSES Infectious Hematopoietic Necrosis Virus (IHNV)

I. Causative Agent and Disease III. Clinical Signs Infectious hematopoietic necro- Infected fish may exhibit: lethargy, sis virus (IHNV) is a bullet-shaped whirling behavior, cranial swelling, ab- that is enzootic to the dominal swelling, exophthalmia, anemia North American Pacific Northwest but and darkened body coloration; hemor- was inadvertently established in the US rhaging of musculature and base of fins; Valley in and in sev- fecal casts; pre-emergence in sac-fry; eral countries of Asia and Europe. The pale liver, spleen and kidney; stomach/ three genetic clades of IHNV (U,M,L) intestine filled with milky or watery can infect several salmonid species and fluid with petechial hemorrhaging of have had severe economic impacts on mesenteries or visceral tissues. Gills are intensively cultured salmon and trout. pale, moderately hyperplastic and blood IHNV in Alaska (U clade) has been smears often contain necrobiotic bodies. limited primarily to and rarely Chinook and chum salmon when IV. Transmission infected sockeye are present in their wa- Horizontal transmission through wa- ter supplies. Culture of sockeye salmon ter via feces or sex products or carcass in Alaska by avoidance of IHNV has degradation is the most common route been successful through the rigorous use of infection. Virus occurs commonly in of the ADF&G sockeye salmon culture ovarian fluids and on the surface of eggs. policy. The disease, infectious hemato- Rarely, vertical transmission can occur poietic necrosis (IHN), is an acute, sys- within eggs (internal) and possibly with temic infection causing necrosis of the adhesion of virus particles to sperm dur- kidney tissues and other visceral organs ing fertilization. Incubation and course resulting in extensive mortality in hatch- of the disease can be strongly influenced ery reared sockeye salmon juveniles as by water temperature as reported in the well as in wild stocks of out-migrating Lower 48. Optimum temperature is 10- sockeye salmon smolts. 12°C but IHN losses have been reported above 15°C. Mortalities occur within II. Host Species 4-6 days post-exposure peaking at 8-14 Fish species susceptible to infection days. In Alaska, the disease can cause and disease by IHNV include: sockeye, up to 100% mortality in sockeye salmon Chinook, chum, amago, yamame and at water temperatures as low as 1-2°C Atlantic salmon; cutthroat trout and rain- where exponential mortality may take bow/steelhead trout. Brook and brown longer to occur. No natural reservoirs of trout are experimentally susceptible to IHNV have been confirmed other than infection and mortality while those susceptible fish species that are are intermediate in susceptibility. Arctic carriers of the virus. However, transient char and grayling are resistant while detections of IHNV have been reported coho salmon are also resistant but can in organic sediments, , and carry the virus when in the presence of some forage species of marine fish when other susceptible virus-infected fish spe- associated with ongoing or recent IHNV cies. Mortality is highest in young fish epizootics in susceptible salmonid spe- and resistance to infection and disease cies increases with age.

8 VIRUSES

V. Diagnosis In Alaskan hatcheries, all infected lots of Susceptible fish cell cultures are in- fish are destroyed. The occurrence of the oculated with kidney and spleen tissues disease is avoided through preventative (whole fry if small) or ovarian fluids measures including a virus-free water from fish suspected of having IHNV. supply, rigorous disinfection, isolation Presumptive diagnosis results from dif- of egg and fish lots and containment of fuse or plaqued lysis of inoculated cell diseased fish. There is an effective DNA monolayers (cytopathic effect). Virus is vaccine used in that is also li- definitively identified by PCR. censed in the US but has been restricted commercially due to unlikely safety VI. Prognosis for Host concerns regarding GMO products. Prognosis for infected fish is poor. Survivors of epizootics and subclinical VII. Human Health Signifcance infections become lifelong carriers of There are no human health concerns the virus. There is no known therapy for associated with IHN virus. fish that have been infected with IHNV.

Hemorrhaging at the base of the fns is sometimes observed in IHN disease. Exaggerated (top, middle) cephalic bumps on sockeye salmon fry commonly occur with IHN disease.

Scoliosis in sockeye salmon smolt surviving IHN.  

 IHN virus particles (arrow) budding from cell Necrotic macrophages or kidney cells membrane of an EPC cultured fsh cell; TEM, (necrobiotic bodies-arrows) with debris in X 34,000. peripheral blood, X 1000.

9 VIRUSES North American Viral Hemorrhagic Septicemia Virus (NA-VHSV)

I. Causative Agent and Disease 100% of exposed with lower North American viral hemorrhagic chronic mortality occurring in adults. septicemia virus (NA-VHSV) Type IVa Infected juvenile herring develop hemor- is a bullet-shaped RNA novirhabdovirus. rhages of the skin around the mouth and It is molecularly distinct from the similar isthmus and/or at the base of fins while Type IVb in the Great Lakes, USA that occasional hemorrhages occur in adult is pathogenic for a large number of fish along the flanks that may progress nonsalmonid species. It is also different to ulcers. Fin erosion and lethargic from Type IVc in marine/freshwater spe- swimming behavior may also be present. cies of Atlantic Canada and most VHSV Experimentally infected juvenile rain- strains in Asia (IVa occurs in Japan/ bow trout exhibited darkened body color Korea) and Europe (Types I, II, III) that and hemorrhaging at the base of fins and are pathogenic for some marine species vent associated with low mortality. and rainbow trout. IV. Transmission II. Host Species Transmission of VHSV is horizontal NA-VHSV Type IVa infects many through ambient seawater from fish to marine fish species in the northern fish and likely by ingestion of infected Pacific including anadromous fish. Individual infected juvenile Pacific coho and Chinook salmon. In Alaska, herring can shed up to 106.5 plaque form- the virus is reported from Pacific ing units (PFU) of virus per ml. Primary herring, , Pacific hake and virus infection is through the epidermis . Two isolates from pink and possibly gill tissues followed by salmon have been the only occurrences systemic infection (viremia). Because of VHSV from a free ranging Alaskan VHSV in the Pacific Northwest is indig- salmonid. The virus is enzootic in enous to Pacific herring and other forage populations of Northern Pacific herring species utilized by salmon, these prey and causing epizootic mortal- are a likely source of VHSV periodi- ity. Experimental studies indicate that cally detected in adult coho and Chinook juvenile Alaskan Chinook, coho, in Washington State. and sockeye salmon are refractory to the virus by waterborne exposure. V. Diagnosis Cultures of susceptible fish cell III. Clinical Signs lines are inoculated with kidney, spleen, Detection of NA-VHSV from ana- liver, ovarian fluids or epidermal lesions dromous salmonids in Washington and from suspect fish. Presumptive diagno- Oregon has generally been at very low sis is made when characteristic cyto- levels and prevalences and not associ- pathic effect (CPE) or lysis occurs in cell ated with clinical disease. In Pacific cod, monolayers from virus infection. Virus secondary VHSV infection can be de- identification is confirmed by PCR. tected at low levels in skin erosions and ulcers caused by other primary patho- VI. Prognosis for Host gens. Septicemia with skin hemorrhages Susceptible juvenile herring sustain may also occur. In Pacific herring, the up to 100% mortality which may not virus can be acutely lethal for up to occur in adult fish or is lower and more

10 VIRUSES

chronic. Herring that survive virus in- variable but generally lower in other for- fection develop apparent immunity to re- age species. infection. Noteworthy, is that low levels of VHSV can occasionally be detected in VII. Human Health Signifcance a small percentage of apparently healthy There are no human health concerns herring from most populations. Clinical associated with NA-VHS virus. disease and mortality from the virus is

Skin hemorrhaging in infected Pacifc herring

Left: Pacifc herring with typical VHS hemorrhage; Right: Skin hemorrhaging in infected

Pacifc cod (photo: NMFS staf) 

Electron micrograph of VHSV particles (arrow) in a cultured EPC fsh cell, X 56,500

11 VIRUSES Pacific Salmon Paramyxovirus

I. Causative Agent and Disease This virus has the unique characteristic Pacific salmon paramyxovirus among fish viruses of hemagglutinating (PSPV) is a large, irregular shaped, erythrocytes from fish, some mammals enveloped, single-stranded RNA virus (human, , horse, and about 125-250 nm in diameter belonging swine), and birds. Hemagglutination in the family and the allows viral placement in the Paramyxo- genus Aquaparamyxovirus. The virus is viridae and confirmation of a para- of low virulence and not associated with myxovirus along with other procedures disease or mortality. The viral agent is including ultrastructural morphology generally isolated from asymptomatic by electron microscopy, fluorescent an- carrier fish during routine viral screen- tibody testing (), PCR and sequenc- ing. ing.

II. Host Species VI. Prognosis for Host The most common host in North The prognosis for the host is good America is adult Chinook salmon from regarding the non-pathogenic nature of Alaska, Oregon and Washington. Un- the North American isolates of PSPV. confirmed isolates have been reported The role of Norwegian ASPV in causing from other salmonids. In Norway, At- PGI is questionable since other agents lantic salmon paramyxovirus (ASPV) have been present confounding the has been isolated from seawater reared true etiology of fish mortality. In this Atlantic salmon. case perhaps corrective therapy would include optimizing the environment and III. Clinical Signs avoidance. Further study is warranted. No clinical signs of disease are associated with fish infected by PSPV. VII. Human Health Signifcance The ASPV paramyxovirus in Norway is There are no human health concerns reportedly associated with the disease associated with paramyxoviruses in fish. syndrome, proliferative gill inflamma- tion (PGI).

IV. Transmission The mode of transmission is hori- zontal by water or fish to fish. A marine reservoir for the virus is suspected.

V. Diagnosis Detection of paramyxovirus is by isolation in cultures of susceptible fish cell lines inoculated with infected tissue. The virus causes a cytopathic effect (CPE) characterized by retracted and rounded cells after an extensive incuba- tion period. Presumptive identifications are made by observing the typical CPE.

12

VIRUSES 

Chinook salmon, Ninilchik River, AK. Falsely colorized ultrastructure of PSPV in cultured infected CHSE-214 cell with three virus particles in diferent stages of budding from cell membrane (arrow = center particle); blue (B) = spiked envelope; purple (P) = nucleocapsid within particles from pool of subsurface nucleocapsid material in the cytoplasm. Inset: Same image not colorized. (From Meyers and Batts 2016).

20 um

Cytopathic efect of PSPV from Chinook salmon, Ninilchik River, AK in CHSE-214 cells at 14°C demonstrating clustered rounding and refractility of cells (Right) at 9 days post- inoculation of previously passaged material. Normal cell culture (Left). Phase contrast (From Meyers and Batts 2016).

13 VIRUSES Piscine Orthoreovirus (PRV)

I. Causative Agent and Disease species may be possible reservoirs. Piscine orthoreovirus (PRV), also known as Atlantic salmon reovirus, V. Diagnosis was identified in 2010 by next genera- HSMI disease is diagnosed by tion sequencing of tissues from farmed histological changes of mononuclear Atlantic salmon in Norway dying from inflammation and necrosis of the the disease “heart and and red skeletal muscle with absence of inflammation” (HSMI). The virus has pancreatic lesions. PRV replicates in the double-stranded RNA with 10 segments cytoplasm of red blood cells producing and is 72 nm in diameter. There are inclusion bodies similar to EIBS with or three strains of the virus (PRV1, 2, 3) without anemia. This finding suggests a possibly influencing disease outcome relationship of PRV with EIBS as well in different host species under different as HSMI. PRV does not replicate well environmental conditions. in available fish cell lines, requiring molecular detection and sequencing for II. Host Species confirmation of the virus and strain. PRV is reported from Norway, Denmark, Ireland, Chile, Japan and the VI. Prognosis for Host Pacific Northwest (WA, AK, BC, Can- Rarely, 20% mortality from HSMI ada) infecting Atlantic salmon, Pacific has occurred in Atlantic salmon smolts salmon and trout (cutthroat, steelhead, 5-9 months after transfer to seawater. sea-run brown). In Alaska, PRV was However, high levels of PRV genetic ma- sequenced from three stocks of coho and terial are detected in asymptomatic wild one stock of Chinook and unconfirmed and cultured salmonids with no evidence in one stock of chum salmon. of HSMI disease. In one experiment, PRV was infectious for Chinook and III. Clinical Signs sockeye salmon and persisted but did not HSMI, described from Norway in cause fish mortality or HSMI, or other 1999, causes anorexia, lethargy, and apparent disease. Testing of archived tis- ascites with inflammatory lesions of the sues from BC indicated PRV was present heart and skeletal muscle. It is a disease in asymptomatic wild and farmed Pacific of farmed Atlantic salmon (PRV-1) and salmon since 1987, possibly as early rainbow trout (PRV-3) in both freshwater as 1977 before Atlantic salmon were and seawater. PRV-1 has been associated imported for aquaculture. The ubiquity with jaundice, anemia and degenerative/ of PRV, apparent historic presence in necrotic lesions of the liver/kidney in wild Pacific salmon stocks in the PNW healthy farmed Chinook salmon and and lack of clear association with disease PRV-2 is associated with EIBS and suggest the virus is of low risk to wild jaundice/anemia in farmed coho salmon species of Pacific salmon. in Japan. Stress may precipitate clinical disease. VII. Human Health Signifcance There are no human health concerns IV. Transmission regarding infection of fish with PRV. PRV can be transmitted by injection and horizontally. Marine

14 VIRUSES

PRV and EIBS viruses are likely related if not the same virus. EIBS/PRV virus in Chinook salmon: (A) Peripheral blood smear with single and multiple cytoplasmic erythrocytic inclusion bodies (arrowhead), scale bar = 5 um; (B) TEM of a single virus inclusion body (arrowhead) in erythrocyte cytoplasm, scale bar = 0.5 um; (C) Higher magnifcation of virus particles (60-70 nm) in the inclusion body of (B), scale bar = 100 nm; (D) Extracellular virus particles associated with cell debris in peripheral blood, scale bar = 100 nm. (From Meyers 2007).

15 BACTERIA Bacterial Coldwater Disease (BCWD) and other freshwater flavobacteria

I. Causative Agent and Disease tissues surrounding the pyloric caeca. The causative agent of BCWD, Fla- Chronic BCWD can result in lordosis vobacterium psychrophilum, is a Gram- and scoliosis (“crinkle-back”) and an negative proteolytic bacterium causing abnormal swimming posture from the systemic disease in colder waters. Clini- destruction of muscle bundles adjacent to cal signs usually occur below 12°C and the vertebral column. Another sequella is in Alaska often occur at extremely cold bacterial invasion of the brainstem caus- water temperatures of 1°C. The bacte- ing erratic swimming, darkened posterior rium, originally classified to the genus body and sudden death from damage to Cytophaga, was changed to Flexibacter nervous tissues, vertebral cartilage and and later to . The species bone. Other flavobacteria cause erosive name means “cold loving”. BCWD is skin lesions that may penetrate deeply characterized by tissue necrosis of the into the underlying skeletal muscle. fins that progresses to complete destruc- tion of the caudal peduncle exposing the IV. Transmission vertebrae. Other common names for this Transmission of BCWD is horizontal condition are peduncle disease or low through the water column and vertically temperature disease. Infections by other through the eggs of infected adult sal- freshwater species of flavobacteria are monids. The bacteria have been isolated generally non-systemic causing similar from internal organs and gonadal fluids erosive skin lesions that may occur any- of returning adult salmon suggesting where on the surface of the fish host. they are carriers of the infection during their seawater phase but reinfection upon II. Host Species entering freshwater is also possible. All BCWD is found in temperate sal- other Flavobacterium species are com- monid producing regions worldwide. mon inhabitants of aquatic ecosystems Juvenile coho and Chinook salmon are allowing for horizontal transmission. particularly susceptible. External infec- tions by other freshwater flavobacteria V. Diagnosis also occur worldwide affecting several Presumptive diagnosis includes isola- species of fish. tion of long, filamentous, Gram-negative bacteria that are non-motile or have glid- III. Clinical Signs ing motility from kidney tissues or typi- BCWD begins with darkening of the cal skin lesions of fish. The bacteria grow peduncle region when water tempera- well on Cytophaga and TYES agars, with tures are between 4-12°C with up to 50% optimum growth at 15-16°C. Colonies mortality prior to the occurrence of more are bright yellow, entirely convex or with chronic peduncle erosion. When acute, convex centers and a spreading periphery lesions appear in the areas of increased resembling a “fried egg”. Colonies turn pigmentation on the peduncle region, orange-red when KOH is added indicat- or elsewhere. Ulcers are deep and the ing flexirubin pigment. Growth of F. caudal fin may erode completely expos- psychrophilum is inhibited by Congo red ing the vertebral column. When present, added to TYES agar or diffusion discs internal lesions may only consist of mild allowing rapid differentiation from other petechial hemorrhages within the adipose Flavobacterium species. Confirmatory

16 BACTERIA

diagnosis is done using PCR or mono- 1 hr treatments of formalin and for clonal direct FAT. BCWD antibiotic therapy may be necessary as well. VI. Prognosis for Host BCWD begins as an external infec- VII. Human Health Signifcance tion that becomes systemic. External There are no human health concerns flavobacteria generally remain as such associated with Flavobacterium psy- but either type of infection can result chrophilum or other flavobacteria. in fish mortality. Hatchery fish can be treated for the infections with external

Left: Deep ulcers with tissue liquefaction characteristic of favobacterial infections; Right: Complete erosion (bottom fsh) of caudal peduncle in coho salmon fngerling typical of bacterial coldwater disease .

Left: Typical yellow colonies of Flavobacterium psychrophilum on TYES agar; Right: Gram stain of flamentous bacteria from skin scrape of an external Flavobacterium sp. infection, X 400.

17 BACTERIA Bacterial Gill Disease

I. Causative Agent and Disease predispose fish to infection by these Bacterial gill disease (BGD) is bacteria that are present at low levels in most commonly caused by filamentous the aquatic environment. BGD typically bacteria within the genus Flavobacte- can occur in the spring with the feeding rium (most often F. branchiophilum). In of starter mash that irritates delicate gill previous these bacteria were tissues of swim-up fry. The resulting gill known as members of the Myxobacte- hyperplasia (excessive cell division and ria and were first placed in the genus thickness) interferes with normal gas ex- Cytophaga, later changed to Flexibacter change while secondary infections from and now Flavobacterium. The syndrome or other opportunistic pathogens of this disease includes swollen gill may occur. lamellae caused by proliferation of the epithelial cells sometimes resulting in IV. Transmission lamellar fusion. The epithelial prolifera- Transmission occurs horizontally tion is a response to irritation from the through the water from fish to fish. Pre- large numbers of filamentous bacteria disposing factors for epizootic outbreaks found attached to the gill surface. The are sub-optimal environmental condi- thickened epithelial layer results in tions and suspended solids or abrasive decreased gas exchange for respiration feeds. The incubation period can be as triggering explosive epizootics with high little as 24 hours or up to several weeks, fish mortality of up to 25%. most commonly during periods of colder water temperatures below 5°C. II. Host Species All cultured salmonids are suscep- V. Diagnosis tible and the disease is found worldwide. Fish with BGD have pale, swol- In Alaska, sockeye, Chinook and coho len gills, flared opercula, are listless salmon appear to be most susceptible. and do not feed well. Large numbers Adults and yearlings are less susceptible of filamentous rod-shaped bacteria are than fry and fingerlings. found attached to the gills causing epi- thelial hyperplasia and possibly fusion or III. Clinical Signs clubbing of gill lamellae. The causative Fish with BGD show a loss of ap- filamentous bacteria are Gram-negative, petite, orient to the water current for non-motile (or have gliding motility) and increased flow over the gills and exhibit grow on Cytophaga or TYES agars. exaggerated opercular movements. An increase in mucus on the head and upper VI. Prognosis for Host body may also be noted. BGD usually Early intervention in the progression affects fry or fingerling salmonids in of the disease may reduce fish mortality high density culture conditions. There- which can be significant. In a hatchery fore, the disease is often associated with setting external chemical treatments sub-optimal water and environmental with hydrogen peroxide may help control quality such as overcrowding that result the bacteria. If gill tissue is severely in excessive ammonia, low dissolved damaged, fish may not survive the treat- levels and excess suspended ments. Preventative measures for BGD organic matter. Such stressors can include maintaining the water supply

18 BACTERIA

free of fish (especially adults), mud and VII. Human Health Signifcance silt, reducing stress such as overcrowd- The causative bacteria of BGD are of

ing, avoiding low dissolved oxygen or no human health concern high ammonia levels and avoiding exces-

sive fish handling. 

Histological section of gill lamellar fusion (arrow) caused by external bacteria, X 100. 

Higher magnifcation showing flamentous bacteria (arrow) on gill, X 400.

19 BACTERIA Bacterial Kidney Disease (BKD)

I. Causative Agent and Disease bacterial pathogens of fish, R. salmoni- Bacterial kidney disease (BKD) is narum can also be transmitted vertically caused by Renibacterium salmoninarum within the egg. The bacteria gain access (Rs) that can replicate extracellularly during egg formation or more commonly and intracellularly within macrophages. enter the yolk through the micropyle af- BKD, also known as Dee Disease, is ter ovulation from contaminated ovarian a systemic bacterial infection caused fluids of the female parent. Transmission by a small, non-motile, Gram-positive from contaminated male seminal fluids coccobacillus. Typically, the course of during fertilization is another possible the disease results in slow chronic fish route. The organism may survive free in mortality that occurs in Alaska at much the environment for long periods of time. colder water temperatures of 1-2°C than reported elsewhere (11°C). V. Diagnosis Presumptive diagnosis of BKD is II. Host Species sometimes possible by observation All salmonids are considered suscep- of the gross pathology and the pres- tible and the disease usually occurs in ence of intracellular and extracellular fish 6 months or older, i.e., juvenile and Gram-positive, small, non-acid-fast, adult fish. non-sporeforming coccobacilli in Gram stained impression smears of infected III. Clinical Signs tissues. The organism does not grow on In the acute stage, fish may die TSA but requires a specialized KDM2 without exhibiting any clinical signs of media at 15-20°C for 10 to 21 days of disease. In the more typical chronic form incubation. Organisms can be confirmed of BKD fish may exhibit exophthalmia, with a specific fluorescent antibody test, petechial hemorrhages and/or vesicles of enzyme linked immunoabsorbent assay the skin, and abdominal distention due (ELISA) or by polymerase chain reaction to the accumulation of ascitic fluid in (PCR). the abdominal and pericardial cavities. The kidney, which is the target organ, is VI. Prognosis for Host often enlarged and edematous and may BKD results in chronic fish mortality exhibit off-white nodules varying in in both fresh and seawater and can have size. The whole kidney may appear gray, a detrimental impact on fish popula- corrugated and swollen. White foci may tions, generally during the later stages also be present in other organs, chiefly of rearing. Infected fish become carriers the liver and spleen. for life. In Alaska, losses of coho and Chinook salmon fingerlings from BKD IV. Transmission can range from 2-5%/month during final The Rs bacteria can be transmitted months of rearing. Dietary erythromycin horizontally from fish to fish or from reduces mortality which resumes when a water supply containing infected the drug is withdrawn. In numerous fish. In early fish culture, feeding raw, watersheds within Alaska, Rs unpasteurized viscera of infected fish to has been detected by ELISA in both wild other fish increased the incidence of the and hatchery stocks of all 5 species of disease in hatcheries. Unlike many other Pacific salmon. Prevalence usually is

20 BACTERIA

less than 10%, but some systems have VII. Human Health Signifcance carrier rates up to 90%. Wild trout, char There are no human health concerns and grayling are reservoirs for Rs, often associated with R. salmoninarum. showing prevalences of up to 100%.

  

Left: White pustules (arrows) in the posterior kidney and liver of a juvenile coho salmon typical of BKD; Inset: Infected fsh with exophthalmia; Right: White kidney pustules (arrow) in adult Bear Lake sockeye salmon with BKD (photo: CIAA staf).

Left: Stained kidney smear with small Gram-positive coccobacilli typical of R. salmoninarum, X 1000; Right: BKD bacteria, Renibacterium salmoninarum, stained with a fuorescene dye (green), fuorescent antibody test, X 1000.

21 BACTERIA Enteric Redmouth Disease (ERM)

I. Causative Agent and Disease with watery fluid and petechiation Enteric redmouth disease (ERM) or may be present in the musculature and is caused by Gram-negative, visceral organs, most notably in the hind motile bacteria known as gut and liver. ruckeri. The name ERM is derived from the inflammation and petechial IV. Transmission hemorrhages of the lower hind gut and The bacterium is horizontally inside and around the mouth of infected transmitted from fish to fish via the fecal fish that are not unique signs of infection oral route and often becomes localized by this bacterium. ERM is an acute in the lower intestine of fish surviving septicemia in salmonids with bacterial a disease outbreak. Bacteria can remain foci, necrosis and inflammation in all viable for a limited time in ambient tissues. In Alaska, two serotypes of water to infect susceptible fish. Other the bacteria, known as O1 and O2, can reservoirs of the bacteria include fish- cause the disease. The two serotypes eating birds reported near aquaculture are differentiated from each other based facilities. on biochemical and/or serological tests. The virulence varies considerably V. Diagnosis within each serogroup but Y. ruckeri O1 Presumptive diagnosis is made by has been more pathogenic in Alaskan the cultivation of a Gram-negative, salmonids and elsewhere. The bacteria oxidase negative, motile bacterial rod are found worldwide where salmonids from blood, kidney, or lesions when are cultured and there are a total of 6 inoculated onto bacteriological media. serotypes with several subgroups. Diagnosis is confirmed with biochemical tests or fluorescent antibody tests II. Host Species specific for Yersinia ruckeri Types O1 Rainbow trout are the most sensitive and O2. Type O1 includes subgroups host, but all salmonids and several a and b while Type O2 is composed other fish species are susceptible to of 3 subgroups (a,b,c). The remaining infection. ERM is a major concern in serotypes are O3, O5, O7 and O8. The the Norwegian Atlantic salmon industry majority of epizootics in salmonids are causing fish mortality in both fresh and caused by motile serotype O1a. That seawater pens. said, the current serotyping scheme is inconsistent and not as helpful as genetic III. Clinical Signs sequencing in determining relatedness Externally, clinical signs can be in clonal clustering that may influence similar to other bacterial septicemias. epidemiological differences. Infected fish are often lethargic and dark in color. Inflammation and petechiation VI. Prognosis for Host are prominent in and around the mouth, Under aquaculture conditions, the isthmus and on the opercula. diseased fish generally die if there is no Petechial hemorrhages are commonly antibiotic intervention. Prognosis for at the base of the fins. Fish often exhibit the population is good if the condition exophthalmia and a distended abdomen. is recognized early so that antibiotic Internally, the stomach is often filled therapy can be initiated.

22 BACTERIA

VII. Human Health Signifcance There are no human health concerns associated with Yersinia ruckeri.

Petechial hemorrhages of the liver present in enteric redmouth disease. 

Difuse internal petechial hemorrhaging (arrow) typically present with bacterial septicemias like enteric redmouth disease.

23 BACTERIA Furunculosis

I. Causative Agent and Disease IV. Transmission Furunculosis is caused by a Gram- Horizontal transmission to suscepti- negative bacterium known as Aeromo- ble fish is via the water column or by the nas salmonicida and is probably the fecal-oral route. Diseased or carrier fish most commonly encountered bacterial are point sources of infection. Increasing pathogen in cultured salmonids. The water temperature exacerbates the inci- disease occurs worldwide in freshwater dence and intensity of infection. Vertical and has also been reported in the marine transmission of the bacteria has not been environment. It is known to occur in demonstrated. , Europe, Asia, and . Furunculosis is characterized V. Diagnosis by a generalized bacteremia with focal Presumptive diagnosis is made by necrotic swellings in the muscle tissue culture of a Gram-negative, oxidase called furuncles. positive (an oxidase negative isolate has been described), non-motile bacterial II. Host Species rod from blood, kidney, or lesions on All salmonid species are susceptible. TSA or furunculosis agar with the pro- Rainbow trout show some resistance. duction of a brown diffusible pigment. Young fish are the most susceptible, Some strains of bacteria may not pro- especially when the water temperatures duce pigment. Diagnosis is confirmed are > 8º C. In hatcheries, pink and chum by biochemical tests, slide agglutination salmon are less likely to develop furun- and fluorescent antibody tests specific culosis since they are not reared long for A. salmonicida. before being released to seawater. Many non-salmonid species of fish in both ma- VI. Prognosis for Host rine and freshwater are also susceptible In nature, the disease usually results to infection by A. salmonicida, some in mortality. In a hatchery, prognosis strains of which are atypical. for the fish population is good if the condition is caught early and antibiotic III. Clinical Signs therapy is initiated. In acute septicemia where rapid death may occur, gross clinical signs VII. Human Health Signifcance may not develop. In subacute and There are no human health concerns chronic infections, body darkening, associated with A. salmonicida. lethargy and loss of appetite are associ- ated with the typical focal necrosis in the muscle, often visible as a swelling under the skin. These lesions eventually ulcer- ate producing deep craters. Erythema, petechiation and exophthalmia may be present and the abdomen of the fish may be distended with internal ascitic fluid. Bloody fluid may be discharged from the anal vent and the kidney, liver and/or spleen may be enlarged.

24 BACTERIA

Typical furuncle lesion on adult sockeye salmon with furunculosis.

Early furuncular lesion on young salmonid fsh with furunculosis. 

Kidney impression showing Gram-negative (red) bacteria (arrow) of causing furunculosis, X 1000

25 BACTERIA Fusobacteria-like Agent

I. Causative Agent and Disease VI. Prognosis for Host An external skin and/or gill infection External infection by these bacteria is caused by long, non-motile, Gram- results in high fish mortality if there negative bacterial rods that are sharply is no intervening therapy. One or two pointed at both ends. The bacteria, external applications of formalin or commonly referred to as fusobacteria, hydrogen peroxide have been successful infect cultured salmonid fish in fresh treatments. water during periods of very cold water temperatures, usually less than 5°C. VII. Human Health Signifcance Infection produces excessive mucus There are no known human health externally and on the gills causing respi- concerns associated with this fusobacte- ratory distress. ria-like agent.

II. Host Species This organism has been detected on cultured salmonid fishes at various life stages from alevin to pre-smolt in the Pacific Northwest and Alaska. Chinook and coho salmon have been the most commonly affected species.

III. Clinical Signs The skin of infected fish has exces- sive mucus production and gill infec- tions result in lamellar hyperplasia and increased respiration.

IV. Transmission These bacteria are probably trans- mitted horizontally through the water from fish to fish.

V. Diagnosis Diagnosis includes observation of Gram-negative, non-motile, bacterial rods with a beaded appearance having characteristic attenuated ends on the skin and/or gills of infected fish. The biomass of bacteria is often extensive. This bacterial organism has not been cultured successfully on conventional bacterial media but minor temporary success has been achieved on swabs aerobically incubated in 50% MEM and lake water at low pH (4.5).

26 BACTERIA

Fusobacteria stained with Giemsa showing typical fusiform shape with pointed ends and beaded appearance, X 1000.

Gram stain of skin scrape showing high biomass of fusobacteria, X 1000.

27 BACTERIA Marine Tenacibaculosis

I. Causative Agent and Disease external trauma or other environmental Tenacibaculum maritimum is a fila- stressors. mentous, Gram-negative bacterium that moves by gliding motility. These marine V. Diagnosis bacteria are opportunistic pathogens Diagnosis of Tenacibaculum of fish producing external (sometimes infections is made by observing large systemic) infections such as bacterial numbers of filamentous bacteria in wet gill disease, , skin ulcers or eroded mounts of lesion material. The bacteria mouth disease. Infections are often can be cultured on seawater Cytophaga initiated by physical trauma, pinheading or TYES agars with added 1.5% NaCl and adverse environmental conditions. or 30 ppt to full strength seawater and Resulting fish mortality can be signifi- incubated at 15°C. The colonies, often cant. yellow in color, are and oxidase positive with no flexirubin pigment in II. Host Species cell walls. Identity confirmation of T. All marine fish worldwide are maritimum is by PCR and there are three potentially susceptible to infection by O serotypes. Tenacibaculum maritimum which has been isolated from a variety of - VI. Prognosis for Host nid fishes, Dover , sea , , This external bacterial infection can bream, halibut and sardines. In Alaska, cause significant mortality, especially this bacterial pathogen has caused if fish are stressed. Treatment has been mortality of juvenile Pacific salmon in successful with oral antibiotic therapy. seawater netpens during the winter and early spring. VII. Human Health Signifcance There are no human health concerns III. Clinical Signs associated with Tenacibaculum mariti- Diseased fish have ulcerated skin mum. lesions, frayed or eroded fins and tail. Moderate to severe erosions of the head and mouth may also occur. Infected epidermal tissue may appear pale yellow to white due to the presence of large numbers of bacteria. Infected gills of fish may produce excessive mucus, have pale color and exhibit lamellar hyper- plasia. Secondary systemic infections by other bacteria commonly occur through open lesions.

IV. Transmission Tenacibaculum is a naturally occur- ring marine bacterium and is transmit- ted horizontally through the water from fish to fish, generally requiring minor

28 BACTERIA

Caudal fn lesion on a halibut caused by infection with a marine Tenacibaculum.

Severely eroded head and upper jaw of a coho salmon smolt due to marine Tenacibaculum infection.

29 BACTERIA Motile Aeromonas and Pseudomonas Septicemia

I. Causative Agent and Disease hemorrhaging and necrosis of the fins is Motile bacterial septicemias are common. Exophthalmia and abdominal caused by Gram-negative bacteria distention with ascitic fluid may also be including Aeromonas and Pseudomonas present. Internally, the kidney may be with the -complex soft and swollen and the spleen enlarged. and Pseudomonas fluorescens being Petechial hemorrhages may be present the most common species. The A. hy- internally in many tissues and the intes- drophila (liquefaciens) complex contains tines may be inflamed and filled with numerous biotypes and serotypes of yellow mucus or bloody fluid. A. hydrophila as well as A. sobria , A. caviae, A. shuberti and A. veronii. These IV. Transmission bacteria are ubiquitous in the aquatic These bacteria are among the normal environment and are found around the flora of healthy fish and are ubiquitous world in both fresh and brackish water, in the aquatic environment. They are but more commonly in freshwater. These particularly abundant in organically bacteria generally cause a systemic, polluted waters while infected carrier hemorrhagic disease in fish. Most of fish and other aquatic animals can serve these bacteria are considered opportu- as reservoirs. Transmission is horizontal nistic pathogens causing disease in fish from fish to fish or from contaminated compromised by stress or other patho- water. Water temperatures 10°C or above gens. Some species, most commonly P. favor these opportunistic pathogens. fluorescens and A. hydrophila, have been reported as primary fish pathogens in V. Diagnosis systems of high intensity fish culture. A presumptive diagnosis is made when fish exhibit characteristic clinical II. Host Species signs with tissue imprints, squashes or When less than optimum condi- blood smears containing Gram-negative, tions prevail, all species motile rod-shaped bacteria. A definitive are likely susceptible to these bacteria. diagnosis is made by isolation of the Among salmonids, rainbow trout and organism on appropriate bacteriological Chinook salmon are probably the most media followed by identification from susceptible to the A. hydrophila com- biochemical tests. plex. Both Aeromonas and Pseudomonas are pathogenic for other cold-blooded VI. Prognosis for Host including frogs and reptiles Severely affected fish will die. and will infect mammals including man However, these bacteria are generally through wounds or when they are im- weak pathogens. Poor environmental munocompromised. conditions predispose fish to disease out- breaks which are self-resolving without III. Clinical Signs intervention by antibiotic therapy when Lethargy, low-level mortality and the source of stress is removed. When occasional cutaneous lesions on the body necessary, antibiotic therapy can be ef- surface may occur. Inflammation and fective, except some pseudomonads are erosion in and around the mouth with resistant to available aquaculture drugs.

30 BACTERIA

VII. Human Health Signifcance Some bacteria in these genera can cause disease in humans through wounds or when immunocompromised.

Petechial hemorrhages on ventral surface of a salmonid fsh with bacterial septicemia. 

Petechial hemorrhages of liver, pyloric caeca, gut and visceral fat (arrow) of a juvenile salmonid fsh with bacterial septicemia.

31 BACTERIA Mycobacteriosis of Fish

I. Causative Agent and Disease cal (transovarian) transmission in live Mycobacteriosis is caused by a bearing fishes has also been reported. pleomorphic, Gram-variable, acid-fast, Other aquatic organisms can be infected aerobic, non-motile group of bacteria and act as vectors. in the family Mycobacteriaceae, genus Mycobacterium, that includes the human V. Diagnosis pathogen M. tuberculosis. There are over Presumptive diagnosis is made by 190 species and 11 subspecies that are histologic examination of tissues show- rods 0.2–0.6 um in diameter and 1–10 ing typical inflammatory granulomas um long. The most common species in with concentric layers of noncompressed fish areM. marinum, fortuitum, chelonae and compressed (spindle cell layer) and shottsii that cause a chronic sys- epithelioid cells forming discrete spheri- temic granulomatous disease affecting cal lesions. The centers are necrotic, any or all tissues and organs. Most often containing mycobacteria visible by mycobacteria can survive within host acid-fast stains. Fast and slow growing macrophages. mycobacteria can be cultured on selec- tive liquid and agar media providing II. Host Species phenotypic characteristics with defini- Distribution is worldwide in amphib- tive identification by PCR. ians, reptiles and 151 species of wild and cultured fish representing 40 families VI. Prognosis for Host including many freshwater Mycobacteriosis in fish is a chronic species, salmonids and marine fishes. disease often precipitated by stress. The disease causes serious problems in Acute mortality in wild fish is uncom- cultured species, especially aquarium mon. Long-term population declines fish. In Alaska, the disease has occurred attributed to mycobacteria are possible in sablefish, pollock and and as suspected for Chesapeake Bay striped is likely more widespread in other fish bass, likely exacerbated by environ- species. mental decline. There is no effective treatment for infected fish which should III. Clinical Signs be culled if in a culture environment. Gross clinical signs of mycobact- eriosis may be non-specific scale loss, VII. Human Health Signifcance dermal ulceration, emaciation, spinal Aquatic mycobacteria pose signifi- defects and ascites. Internal signs cant zoonotic concerns, especially in include enlarged spleen, kidney and/ immunocompromised people. M. mari- or liver and characteristic gray or white num, fortuitum and chelonae are known nodules in internal organs. human pathogens producing granuloma- tous skin lesions and sometimes deeper IV. Transmission infections of peripheral tissues (with The epizootiology in fish includes marinum). Infections are treatable by horizontal transmission by contact and antibiotic therapy. ingestion as established experimentally in zebrafish and early salmonid culture when raw fish were used as feed. Verti-

32 BACTERIA

C

Left: Large round white granulomas (pointer) in the kidney and peritoneum of a sablefsh (photo: Eric Forrer) caused by Mycobacterium sp.; Right: Histology of mycobacteria nodules in a Siamese fghting fsh showing concentric layers of epithelioid cells with necrotic centers (C), X 400.

B

Left: Histology of sablefsh granuloma in post-mortem kidney with mycobacterial colony (B) in necrotic center, X 200; Right: Histological acid-fast stain of mycobacteria (red) in sablefsh granuloma, X 1000.

33 BACTERIA Vibriosis

I. Causative Agent and Disease lesions that ulcerate, releasing blood. The genus Vibrio contains signifi- There may also be corneal opacity cant bacterial pathogens of marine fish followed by evulsion of the orbital that cause vibriosis, an acute bacterial contents. Internally, the intestine may septicemia. The primary pathogens be distended with a clear, viscous fluid. include V. (Listonella) anguillarum, V. Hemorrhaging is common in the viscera ordalii and V. salmonicida. In addi- and around the intestines, with swelling tion, may occur as and necrosis of the kidney and spleen. a secondary invader and V. vulnificus is generally restricted to European and IV. Transmission Japanese waters. Vibrio salmonicida Horizontal transmission occurs from is reported from Atlantic Canada and organisms in the water or contact be- Maine in North America and in Norway, tween fish. Outbreaks have occurred in Shetland Islands and Faroe Islands in freshwater fish fed carcasses of marine Europe causing cold water vibriosis or fish. In Alaska, disease does not usually Hitra disease mostly in Atlantic salmon. occur until seawater temperatures reach These bacteria are ubiquitous in the 8°C. marine environment causing typical Gram-negative acute septicemias with V. Diagnosis bacterial foci, necrosis, hemorrhaging Presumptive diagnosis is made by and inflammation in most fish tissues. observing motile, curved Gram-negative bacterial rods in spleen squashes or II. Host Species peripheral blood smears of marine Because vibriosis has occurred in an or anadromous fish. Bacteria can be extensive number of fish species world- isolated on tryptic soy agar, sometimes wide, most marine fish species are likely requiring 1.5% NaCl. Confirmatory to be susceptible. All species of Pacific diagnosis is made using biochemical or salmon and trout are susceptible to vib- slide agglutination tests. riosis that often involves V. anguillarum. Coho salmon seem to be more resistant VI. Prognosis for Host while chum and Chinook salmon are Epizootics of vibriosis in wild fish very susceptible. V. ordalii and V. sal- populations are rare but result in signifi- monicida are principally associated with cant fish mortality. When cultured sal- Pacific and Atlantic salmon, respective- monids are reared in seawater net pens ly, while V. vulnificus most often infects the disease is common resulting in high causing red pest disease. mortality if not treated with antibiotics. Several licensed vaccine preparations for III. Clinical Signs aquaculture have been effective in the Characteristic clinical signs of vib- control of vibriosis. riosis include inflammation and redden- ing along the ventral and lateral areas VII. Human Health Signifcance of the fish with petechial hemorrhaging The Vibrio species associated with that develops at the base of fins, vent and most fish diseases such as V. anguil- within the mouth. Acute cases exhibit a larum, V. ordalii and V. salmonicida are darkened body with swollen, cutaneous not considered to be human pathogens.

34 BACTERIA

However, several other vibrios are of human health concern including V. chol- erae, V. vulnificus, V. parahaemolyticus and occasionally V. alginolyticus.

Bloody ascites (arrow) in abdominal cavity typically present in fsh with vibriosis.

Coho salmon smolt with small posterior external hemorrhage due to

vibriosis. 

Gram-negative curved Vibrio bacteria (arrow) stained from skin scrape of infected chum salmon juvenile, X 1000.

35 FUNGI Phaeohyphomycosis of Saffron Cod and Other Fish Species

I. Causative Agent and Disease IV. Transmission Fungal infections caused by a The external nature of the fungal variety of dark-colored (dematiaceous) infections suggests that transmission is fungi define phaeohyphomycosis. Large by ascospores contained in ambient sea- black, oval, external lesions of the water or sediments, possibly increased skin and smaller foci on the gills have by rain, flooding and stress that require been reported by subsistence users in previous mechanical tissue injury as a saffron cod and other fish species from portal of entry into the host. However, the Norton Sound area of Alaska since the actual mode of transmission is 2005. The lesions are caused by at least 8 unknown. Reports of these black lesions different opportunistic ascomycete fungi on fish most commonly occur during including; Alternaria sp., Cladosporium the late fall and early winter months of herbarum, Chaetomium globosum, October through December. Cadophora luteo-olivacea, Penicillium sp., Phoma herbarum, Pseudophacidium V. Diagnosis ledi and Valsa sordida. These fungi Diagnosis is based on typical clinical typically infect the surface of the skin signs of shallow, circular, black rugose with invasion of the underlying skeletal plaques or foci on the skin and/or gills muscle. Mortality has not been reported with hyphae present in wet mounts. This but estimated prevalence is 1 in 200 is followed by isolation and characteriza- fish. These brown to black pigmented tion of the fungus on artificial media and fungi are filamentous and ubiquitous in confirmation of fungal genus and species the soil. They occur as pathogens, by PCR. on paper products, wood, natural fiber textiles, in the air and on plant debris. VI. Prognosis for Host The prognosis for infected fish is II. Host Species unknown but the large skin plaques and/ The black external lesions have been or involvement of the gill tissues suggest confirmed from saffron cod and also a chronic debilitating mycosis that may photographed in from result in mortality. Norton Sound including estuarine wa- ters of the Unalakleet, Nome and Snake VII. Human Health Signifcance Rivers. Several of these fungi are opportu- nistic human pathogens in immunocom- III. Clinical Signs promised hosts. These fungi have caused Skin lesions caused by these fungi fatal deep mycoses as well as brain are typically large (1 X 2 cm), black, abscess, sinusitis, peritonitis, cutaneous slightly raised circumscribed plaques lesions, and onychomycosis that are firm with rugose textured (nail infections). Chaetomium globosum centers. Gill infection results in smaller produces mycotoxins such as chaeto- black foci within the soft tissues of the min and chaetoglobosin and commonly filaments. Rarely are internal tissues grows inside homes on water damaged invaded and often there is food in the gut roofs, ceilings, walls and carpets, pos- indicating that infected fish are feeding sibly representing an allergenic threat to normally. human health.

36

FUNGI 

Left: Safron cod with phaeohyphomycotic fungal lesion (arrow) caught from mouth of the Tununak River near Nightmute, AK (photo: Peter Pitka); Right: Similar black skin lesion on rainbow smelt from Bethel, AK (photo: Mary Matthias).

Left: Wet mount of branching fungal hyphae of Chaetomium globosum from safron cod lesion, X 400; Right: GMS histological stain of similar skin lesion showing fungal hyphae (stained black) infltrating the dermal tissues, X 100.

37 FUNGI Phoma herbarum

I. Causative Agent fore, transmission of infectious stages Phoma herbarum causes a systemic is suspected to be oral with food or with mycotic infection in salmonids and is gulping air to inflate the air bladder. normally a pathogen of . This fungus is a member of the fungi imper- V. Diagnosis fecti with unknown sexual reproductive Diagnosis is based on typical gross stages in the order Pleosporales. The clinical signs and septate fungal hyphae fungus infection is characterized by present in the lumen of the air bladder mycelial invasion of the air bladder and/ or gut and/or the presence of visceral or digestive tract. The fungus invades hyphae. The fungus is cultured by other organs becoming systemic result- aseptically removing material from the ing in gut obstruction and peritonitis. abdominal cavity of an infected fish and plating onto sabouraud dextrose or II. Host Species potato agar and incubating at 16-20°C. The disease has been found in cul- Colonies appear as light buff turning to tured fry and fingerling coho, Chinook light pink and finally to greenish-gray to and sockeye salmon, lake trout, steel- black as pycnidia are formed. Pycnidia head/rainbow trout and Arctic grayling produce hyaline unicellular conidia. in Alaska and the Pacific Northwest. Hyphae are fine in diameter and septate (have cross walls). III. Clinical Signs Affected fish may swim on one side VI. Prognosis for Host or in a vertical position with tail down or There is no known treatment for may rest on one side at the bottom of the systemic mycosis in fish. In most cases rearing container. Fish often have swol- only a small percentage of the popula- len and hemorrhagic vents and the ab- tion will become infected. Those fish dominal area can be laterally compressed that are infected will eventually die. In into a “pinched abdomen”. Fish may also natural infections, cumulative mortality exhibit hemorrhage of the caudal fin and/ is generally low (<2-5%) but can be up to or petechial hemorrhages on the lateral 20%. and ventral body surfaces, fluid-filled air bladder, visceral necrosis and adhesions VII. Human Health Signifcance with severe hemorrhaging, perforated There are no human health concerns body wall and secondary Pseudomonas associated with Phoma. septicemia.

IV. Transmission Phoma herbarum is a weakly infec- tious facultative fish pathogen that likely invades either by entrance of conidia or hyphae into the air bladder via the pneu- matic duct connecting the esophagus, or by entering with food into the lower where the primary focus of infection may develop. There-

38 FUNGI

Perforated body wall near vent and “pinched abdomens” in fry with Phoma infection.

Anal prolapse (arrow) and hemorrhage of sockeye salmon fry infected with Phoma.

Left: Hyphae of Phoma (black) invading fsh muscle, Grocotts fungus stain, X 200; Right: Phoma hyphae exhibiting typical septa or crosswalls, X 1000.

39 PROTOZOA Epistylis (Heteropolaria)

I. Causative Agent and Disease VI. Prognosis for Host Epistylis is a sessile, ciliated The prognosis for an infested fish is freshwater protozoan that propagates as good if organism numbers are low and colonies at the ends of non-contractile fish are not stressed. Heavy colonial stalks on the skin and sometimes the growth in a hatchery setting must be gills of fish. This organism is not a true treated with salt or chemicals (formalin parasite but an epibiont utilizing fish as a or hydrogen peroxide) to reduce numbers substrate for attachment that will cause of protozoa and prevent secondary tissue necrosis from secreted proteolytic infections by bacteria and water molds. enzymes. This biofouling and tissue Infestation is a sign of poor water quality damage results in osmoregulatory stress that should be improved. and secondary invasion by opportunistic bacteria and water molds. This proto- VII. Human Health Signifcance zoan exists worldwide. There are no human health concerns associated with Epistylis. II. Host Species All species of salmonids are suscep- tible, but infestations are more common in and other warmwater fish spe- cies including their egg masses.

III. Clinical Signs Flashing is a nonspecific sign of external attachment by any parasite or epibiont. Infested fish may also produce excessive external mucus and exhibit white or hemorrhagic lesions.

IV. Transmission This organism reproduces by binary fission and is horizontally transmitted from fish to fish by transformation of the zooid (bell shaped body) into a disc- shaped ciliated telotroch. Slow water flows with high organic loads and abun- dant bacteria on which it feeds favor the colonization of this protozoan.

V. Diagnosis Diagnosis is made by observation of the live protozoan in wet mounts of skin scrapes. The colonies appear like a cluster of bluebells growing on stalks at- tached to the fish by a disc. Epistylis has branched non-contractile stalks.

40 PROTOZOA

Stalked of the genus Epistylis, X 1000. 

Skin smear from a juvenile sockeye salmon with Epistylis ciliates (arrow) among host epithelial cells, X 400.

41 PROTOZOA Hexamita

I. Causative Agent and Disease VI. Prognosis for Host Hexamita is a pyriform-shaped Prognosis for fish host is dependent protozoan (6-12 um long by 3-5 um wide) upon tissue affected and degree of infes- with eight (6 anterior and 2 posterior) tation. Mortalities are associated with flagella. This is largely an intestinal heavy, systemic infestations of Hexam- parasite of salmonids which can cause ita. Damage to the intestinal epithe- fatal tissue and systemic visceral infesta- lium, intestinal obstruction and anemia tions (hexamitosis) in other fish species. contribute to pathological changes in the fish host. Dietary administration of 3% II. Host Species sulfate has been an effective Members of the genus Hexamita treatment for purging the organism from parasitize wild, farmed and aquarium the intestine in salmonids. freshwater fish and amphibians world- wide. In cold and temperate waters VII. Human Health Signifcance many fish families are potential hosts. Hexamita is not known to be a hu- H. salmonis most commonly parasitizes man health concern. salmon species.

III. Clinical Signs Fish parasitized with Hexamita may not have any clinical signs. However, when parasites are numerous fish may show signs of anorexia, emaciation, weakness, listlessness, pale gills, ab- dominal distention, fecal casts, a hemor- rhagic vent, exophthalmia and/or dark body coloration.

IV. Transmission Transmission occurs horizontally in the water by the fecal-oral route where ingestion of cysts or vegetative stages (trophozoites) occurs by a fish host.

V. Diagnosis Diagnosis is made by observation of the protozoan in fecal contents of the gastrointestinal tract or, if systemic, from visceral smears of parasitized fish. Confirmation is by morphological identification of the parasite based on body shape, size, number and location of flagella using phase contrast or bright field microscopy.

42 PROTOZOA

Single Hexamita stained with Giemsa, X 400.

Two Hexamita stained with iodine showing posterior and anterior fagella, X 400.

43 PROTOZOA Ichthyobodiasis (Costiasis)

I. Causative Agent and Disease daughter cells, each with 2 flagella, that Ichthyobodiasis is caused by a parasitize the same or different host. Mo- flagellated protozoan of the genus tile forms attach by means of a flat disc Ichthyobodo, formally known as Costia. with two small microtubules extending These parasites are very small (5-10 um) into the host cell but retain flagella. In- with both free swimming and attached festation of a host must occur within one stages that can easily be overlooked in hour after division or the parasite dies. an examination. I. necator is an obligate parasite infesting the skin and/or gills V. Diagnosis of fishes including salmonids. When Definitive diagnosis is made by wet present on gills, Ichthyobodo seriously mount preparations of skin and/or gills. reduces the ability of young salmon to The organisms exhibit a characteristic adapt to seawater. asymmetrical, oval, flat-bodied attached form with a smaller number of free- II. Host Species swimming forms that are more ellip- This organism lacks host specificity soidal in outline. Two unequal flagella and parasitizes a wide variety of warm are occasionally visible arising from and cold water fish species and amphib- the anterior end and lie along a funnel- ians worldwide. Although primarily in shaped groove on the organism’s ventral freshwater, there have been reports of side. The parasites can also be observed marine or strains/species. as attached forms in stained histological Fingerlings and fry are especially sus- sections. ceptible, although older fish also become parasitized. VI. Prognosis for Host Ichthyobodo is considered one of the III. Clinical Signs most pathogenic protozoans Fish infested with Ichthyobodo are of salmonid culture causing significant often anorexic and listless and will mortality, especially in smaller juvenile typically exhibit flashing behavior. In fish. In the hatchery environment, Ich- advanced cases a blue-gray film ap- thyobodo must be removed by chemical pears on the surface of fish caused by treatment, generally formalin. Seawater increased mucus production and general does not have any effect on the parasite hyperplasia of epidermal . and the severity of the disease may in- Gill hyperplasia and lamellar fusion crease among lightly parasitized fish that (clubbing) can occur if gills are infested. survive seawater transition but are held Secondary bacterial and fungal infec- for further rearing. tions are common. VII. Human Health Signifcance IV. Transmission There are no human health concerns This organism is horizontally trans- associated with Ichthyobodo. mitted from fish to fish. Subclinically parasitized fish are the reservoirs for the parasite in the environment. Ichthyo- bodo reproduces by asexual longitudinal fission where one cell produces 2 motile

44

PROTOZOA 

Wet mount of salmonid gills showing numerous Ichthyobodo (arrow)

attached along the periphery of lamellae, X 200. 

Higher magnifcation of attached Ichthyobodo (arrow), X 1000.

Ichthyobodo attached to gill lamellae (arrow), histological section, X 100.

45 PROTOZOA Ichthyophonus

I. Causative Agent and Disease be infected horizontally by cohabitation. , the causative Similar transmission studies with plank- agent reported for the disease ichthyo- tivorous species, such as Pacific herring, phoniasis, may comprise several dif- have failed by both routes. ferent populations or strains. Although once considered a member of the fungi, V. Diagnosis Ichthyophonus was recently reclassi- Microscopic diagnosis is made by fied as a protozoan member of the class wet mounts of infected tissues, usu- , a highly diverse group ally lesions of the heart or muscle. of organisms having characteristics of Tissue explant cultures using a liquid both animals and fungi. The severity Ichthyophonus medium can increase of disease is dependent on the general detection in lightly infected fish that stress and health of the fish host. Disease are not clinically diseased. Microscopic can be acute with mortality, chronic with or histological examination of infected reduced performance or subclinical. Ich- tissues demonstrate the characteristic thyophonus is a systemic pathogen local- variously sized macrospores (schizonts) izing in major organ systems including and hyphae (germination tubes) of the the heart. Infected fish are carriers for organism. PCR is useful to confirm life. cultures, diagnose severe infections of Ichthyophonus or when the organisms II. Host Species are no longer viable for culture. Ichthyophonus has infected a wide range of freshwater, marine and anadro- VI. Prognosis for Host mous fish (80 species), amphibians and Some species, such as Atlantic her- reptiles worldwide. ring, are more susceptible to Ichthyopho- nus infections and have sustained mass III. Clinical Signs mortality from the disease. Other species The gross clinical signs of Ich- and some stocks within a species have thyophonus can be confused with other more resistance to exposure and may be- similar conditions. A strong inflamma- come infected with the parasite without tory response against the parasite often serious consequences. In experimental results in visible granulomas encapsulat- studies with juvenile herring, death from ing the macrospores of the organism. injection of Ichthyophonus macrospores These granulomas contain host lym- can occur in 80% of the fish within 60 phocytes, macrophages, neutrophils and days. Other field studies of adult Pacific fibrous connective tissue that appear as herring have suggested the pathogen can white, yellow or brown foci in infected persist for long periods without initiating tissues such as the spleen, liver, kidney, rapid disease or mortality. skeletal muscle and especially the heart. VII. Human Health Signifcance IV. Transmission This parasite is a pathogen only for Ichthyophonus is an obligate patho- poikilothermic animals. Therefore, there gen likely of marine origin. Piscivorous are no human health concerns associated fishes are infected through consumption with Ichthyophonus. of infected prey while rainbow trout can

46 PROTOZOA

Left: Difuse white coalescing granulomas containing Ichthyophonus in a salmon fllet; Right: Various sized schizonts in a wet smear of a granuloma, X 200.

Left: White granulomas of Ichthyophonus in the kidney of a coho salmon; Right: Culture of round various-sized schizonts (largest lower left) surrounded by elaborate branched germination tubes (hyphae), X 400.

47 PROTOZOA Saprolegniasis – Cotton Wool Disease

I. Causative Agent and Disease to perforation of the abdominal wall. The disease saprolegniasis is caused by water molds () mostly in IV. Transmission the genus . Genetic sequenc- External mold infections are ing places oomycetes in the class Oomy- transmitted through ambient water by cota, Heterokontophyta, related infectious biflagellated re- to photosynthetic brown , leased from hyphal sporangia. Systemic and apicomplexan protozoa. They are infections in cultured fish occur by filamentous based on production ingestion of uneaten food that has been of oospores, diploid chromosomes, cell colonized by mold hyphae. Environ- walls of beta glucans and cellulose, two mental stress plays an important role types of flagella and tubular in the etiology of the external disease. cristae in the mitochondria. Saproleg- Outbreaks occur primarily after minor niasis describes any cotton-like growth injury from handling or during crowded adherent to skin or gills that include sev- conditions when environmental quality eral genera of molds. Water molds occur is suboptimal. Adult salmon migrating in fresh and brackish water less than to spawning areas have weakened im- 2.8 ppt salinity. Most are saprophytes mune systems and often have external occurring naturally in the environment infections of Saprolegnia. Also, cold and are opportunistic pathogens, usu- water temperatures predispose fish to ally requiring prior injury of external mold disease because development of tissues from mechanical abrasion or zoospores and sexual stages are favored other primary pathogens. Some species while host tissue repair and the inflam- of Saprolegnia (parasitica) are primary matory response are slowed by the lower pathogens producing a systemic disease. host metabolism.

II. Host Species V. Diagnosis All freshwater fish species, incu- Diagnosis is based on typical gross bating eggs and other lower aquatic clinical signs of white, cottony tufts vertebrates/invertebrates worldwide are of hyphae on the skin, gills and other susceptible to saprolegniasis. surfaces of infected fish or eggs. Wet mounts of mycelium from lesions show III. Clinical Signs large, branching, non-septate hyphae. The mold produces white/brown Terminal ends of older hyphae form cotton-like foci on the surface of the club-shaped sporangia containing skin and/or gills. Early foci are pale with biflagellated zoospores. The mold can be peripheral areas of erythema and central isolated on cornmeal or potato agar. zones of lifted scales that frequently ulcerate, exposing underlying muscu- VI. Prognosis for Host lature. Systemic infections produce When external infections are exten- mycelial masses in the gut and viscera sive and/or involve the gills, death of the causing peritonitis, extensive hemor- host is likely from fluid imbalance and rhage, necrosis and adhesions. In smaller peripheral circulatory failure (shock). juvenile fish, external signs of bloating In the hatchery environment external caused by gut obstruction may progress fungus infections can be treated success-

48 PROTOZOA

fully with 1hr formalin drips. There is VI. Human Health Signifcance no treatment for systemic molds that are There are no human health concerns rapidly fatal. associated with Saprolegnia.

Tail rot on a juvenile salmonid infected by Saprolegnia mold.

Typical lesion with peripheral hemorrhaging due to Saprolegnia mold on the skin of a slender bitterling. 

Wet mount of Saprolegnia mold: large hyphae with no cross-walls and a sporangium (arrow) containing zoospores, X 1000.

49 PROTOZOA Trichodiniasis

I. Causative Agent and Disease the skin and fins. Excessive mucus is Trichodiniasis is caused by ciliated produced causing a white to bluish sheen protozoans of the family Trichodinidae of the skin. Fins are generally frayed and in which the most common of 6 genera fish exhibit flashing behavior by scrap- is Trichodina represented by over 30 ing their bodies against hard surfaces. If species. This protozoan is probably the the gills are heavily infested opercular most frequently encountered external movements may be labored. obligate parasite in cultured freshwater fishes worldwide. Some species in this IV. Transmission family also parasitize fish and shellfish Fish are infested with Trichodina in the marine environment. Trichodina through direct transmission from fish to (40-60 um in diameter) is saucer-shaped fish or from organisms in the water and moves along the surface of the skin, originating from a subclinically infested fins and gills of fish by means of its cilia. reservoir host. The organisms reproduce It feeds on the detritus and other debris by binary fission whereby daughter found on the surface of the fish using organisms either attach immediately to tooth-like structures called denticles. the original host or seek a new host in These denticles scrape the debris from the water column. the surface of the fish to the mouth of the parasite. When abundant, the V. Diagnosis scraping and movement of these organ- Diagnosis is easily made by micro- isms irritate the skin and gill surfaces scopic observation of the highly motile causing hyperplasia of the epithelium. spinning protozoan in a wet mount prep- Extreme cases of hyperplasia can result aration of skin scrapes or gill tissues. in reduced gas exchange or reduced When abundant, the organisms may be osmoregulation in the fish host. When visible gliding on the skin surface with environmental conditions are suboptimal the naked eye. Genus and species iden- or when fish tissues are mechanically tification require microscopic examina- damaged, more severe infestations may tion of the shape and arrangement of the occur. denticles on the chitin disc surrounding the mouth of the parasite. II. Host Species Protozoa of this family are found VI. Prognosis for Host parasitizing freshwater and marine fish Trichodinid protozoa are relatively species worldwide. Rainbow and steel- weak pathogens when compared to other head trout, coho and Chinook salmon external protozoans infesting fish. The appear more susceptible than other spe- prognosis for parasitized fish is good cies of salmonids. Young fish (yearlings when parasite numbers are low, and or younger) are most susceptible. The fish are not stressed. However, some of parasite has also been reported from these protozoa are serious pathogens amphibian tadpoles. causing high fish mortality, especially in hatchery cultured species. Under these III. Clinical Signs conditions external chemical treatment Fish parasitized by Trichodina often with formalin is necessary and effective have white patches and/or mottling of in controlling the parasite.

50 PROTOZOA

VII. Human Health Signifcance There are no human health concerns associated with trichodiniasis.

Trichodina protozoan showing cilia and denticles, phase contrast microscopy, X 400.

Many Trichodina from skin scrape, X 100.

51 PROTOZOA Trichophrya (Capriniana)

I. Causative Agent and Disease retract into the cell if disturbed. Overall, Trichophrya is a protozoan (30-40 Trichophrya resembles a pincushion. um) in the subclass Suctoria that attach- es to the gills, skin or fins of a fish host. VI. Prognosis for Host The protozoan has suctorial tentacles, Prognosis for the host is good when which are used to feed on and infestations are light, and the fish are other ciliates in the water and on fish not otherwise stressed. When present mucus and epithelial cells. When present in large numbers gill hyperplasia can in very large numbers, the ciliates can interfere with respiration and predispose cause pathological changes in the gills fish to infections by bacteria and fungi. including hyperplasia and necrosis that Trichophrya in Alaska has been resistant interfere with respiration. to formalin treatments while exposure to seawater when fish are transferred to II. Host Species marine net pens has been more effective This protozoan is commonly found in eliminating the parasite. on the gills of many freshwater in North America and Eurasia. VII. Human Health Signifcance There are no human health concerns III. Clinical Signs associated with Trichophrya. Nonspecific gill hyperplasia is the principal clinical sign of infestation often accompanied by flashing behavior typical of any external parasite infesta- tion. The parasite may be observed on the gill lamellae by microscopic exami- nation. In Alaska, the occurrence of this parasite is generally incidental to other more significant etiologies.

IV. Transmission This is horizontally transmit- ted from fish to fish. Water with high organic loads, as occurs in lake rearing, favors growth of this organism.

V. Diagnosis Diagnosis is made by observing wet mounts of skin scrapes or gill tissues. The organism has an oval or irregularly elongated body which adheres to the gill lamella with a flattened broad at- tachment surface and the upper surface exhibits tentacles. The body of the parasite appears orange to brown. The dorsal tentacles are prominent and can

52 PROTOZOA

Trichophrya protozoan showing suctorial tentacles, sometimes appearing as a pin cushion; phase contrast microscopy, X 200.

Trichophrya attached to gill tissue, X 400.

53 PROTOZOA White Spot Disease

I. Causative Agent and Disease IV. Transmission White Spot Disease in marine fish The parasites divide by simple is caused by a large ciliated protozoan, fission, are highly contagious and are irritans. The disease also transmitted horizontally fish to fish. occurs in freshwater fish but is caused There are three stages of the parasites: by a distantly related larger ciliate, Ich- encysted trophont (feeding stage) that thyophthirius multifiliis. Infections by drops from the fish to become a tomont both parasites cause significant disease cyst (reproductive stage) producing problems for marine and freshwater tomites; tomites escape the cyst becom- aquarists and commercial aquaculture ing theronts (free-swimming infective worldwide. Both protozoa are obligate stage). Depending on the fish host, strain parasites infecting mostly the epidermis of parasite and water temperature, the of the skin, fins and gills causing rapid life cycle may take from days to weeks. mortality. Major differences between the The freshwater life cycle is completed in parasites exist regarding salinity toler- 5 to 7 d at 21°C and 30 to 40 d at 10°C. ance and duration of life cycle. Water temperatures of 32°C kill the Ich theront. About 10% of the Ich trophonts II. Host Species on a fish may reproduce within the host Both parasites are distributed world- epithelium adding to the infection inten- wide and infect a broad spectrum of sity. Marine white spot occurs between wild and cultured marine and freshwater 15 and 30°C with an average life cycle fish species. In Alaska, Cryptocaryon of 1 to 2 wks, but may range from 6 d to has been reported at two large aquarium 11 wks. facilities parasitizing captive greenling, sculpins, wolf eels and rockfish. These V. Diagnosis infections occurred at colder seawater External white spots on the skin or temperatures of 8°C suggesting a strain gills are examined by wet mounts that of the parasite better adapted to lower demonstrate the large ciliated trophont temperatures. In the late 1970s, Ichthy- stage (48-452 um for marine form; ophthirius caused pre-spawning mortal- 500-1000 um for freshwater form) with ity in Alaskan sockeye salmon and in a lobed macronucleus for Cryptocaryon 3-spine . More recently, Ich and one that is horseshoe-shaped for has been reported in captive , Ichthyophthirius. pike and in feral Arctic grayling. VI. Prognosis for Host III. Clinical Signs Wild fish generally have light Both protozoa produce coalesc- infections with negligible mortality, ing white spots, nodules or patches on acquire at least partial resistance and the surface of the skin, gills and fins. are reservoirs for the parasites. Culture Excessive mucus production or changes conditions allow explosive parasite re- in skin color may be accompanied by production causing extensive and rapid flashing behavior and increasing fish fish mortality. External treatment with mortality. copper sulfate pentahydrate is the most effective therapy against the theronts but must be repeated for 3-6 wks to prevent

54 PROTOZOA

reinfection by theronts still to come VII. Human Health Signifcance from the remaining resistant trophonts There are no human health concerns embedded in surviving fish tissues and with white spot disease in fish. tomont cysts in the substrate.

Marine white spot on the dorsal skin and pectoral fns of a captive copper rockfsh (photo: Lynn Wilbur).

C

C

Left: Wet mount of rockfsh white spot lesion with two Cryptocaryon trophonts (C), X 400; Center: Histology section of parasitized rockfsh epidermis with encysted Cryptocaryon trophonts (C), X 400; Right: Wet mount of freshwater white spot lesion from pike with Ichthyophthirius trophont showing horseshoe-shaped macronucleus, X 1000.

55 PROTOZOA X-Cell Tumors

I. Causative Agent and Disease V. Diagnosis X-cell tumors are xenomas com- The presence of apparent tissue posed of enlarged host cells containing a masses on the skin, fins or in the bran- replicating protozoan parasite belong- chial cavities of species ing to the superphylum Alveolata and is suggestive of X-cell tumors. Three phylum as determined by types of X-cell xenomas are described molecular studies. There are at least two indicating tissue and host specificities: highly distinct X-cell clades of protozoa Type 1- pseudotumors on the branchial in the Family Xcellidae comprising the lamellae in the from the genera Gadixcellia and Xcellia. The Atlantic; Type 2- lesions primarily on former genus includes pseudobranchial the pseudobranchs of cod and related parasites of Gadiformes (cod and blue species in the Atlantic and Pacific; Type whiting), and the other is composed 3- lesions on the skin reported for vari- of gill and epidermal X-cells from ous species of , a gobiid fish and Pleuronecti- in the Pacific and in a hardhead catfish formes. Both genera together are sister (LA, USA). Histologic/ultrastructural to Perkinsus spp., pathogens of bivalve features of X-cells are uniform consist- mollusks, and are the first such perkin- ing of large rounded to polygonal cells sids known to cause pathology in fish. having faint eosinophilic cytoplasm, a centrally located enlarged nucleus with II. Host Species a prominent nucleolus. Host granula- X-cell disease is reported worldwide tion tissue may infiltrate the X-cell mass in one freshwater fish species (hardhead where the cells may be irregular in size catfish) and various marine demersal fish and multinucleated plasmodial X-cells including: dab, cod, rockfish, walleye have been observed in the xenomas of pollock, flatfishes, gobiids, and icefish in Atlantic and Pacific cod. the Antarctic. VI. Prognosis for Host III. Clinical Signs X-cell xenomas are not reported to Papillomatous or fibroma-like be fatal, however, ulceration can lead to growths on the fins, skin or as tissue secondary infection by other pathogens masses involving the pseudobranchs or and involvement of gill and pseudo- gill filaments and lamellae. Ulceration branch tissues seriously debilitates res- may occur but generally all forms are piration in fish hosts. There is evidence limited to the dermal/epidermal layers that host cell response may cause regres- of the skin. Molecular probes have occa- sion of X-cell xenomas in some infected sionally shown a few X-cells in visceral fish. organs including liver or kidney where they do not appear to proliferate. VII. Human Health Signifcance This parasite infects only fish. There IV. Transmission are no human health concerns associated The current mode of transmission is with X-cell tumors. unknown. Infection by co-habitation and transplantation of xenomas have been unsuccessful.

56 PROTOZOA

Left: X-cell xenomas forming white plaques in and around the branchial chamber of a black rockfsh; Right: close-up view of xenomas causing white thickened gill tissues of a dusky rockfsh.

X

P E

Left: Ulcerated X-cell xenomas on skin of Pacifc cod (photo: Ruth Fairell); Center: Histologic section of cod lesion with epidermis (E) and focus of degenerative X-cells (X) in dermis beneath, X 200; Right: Multinucleated plasmodial X-cells (P), X 1000.

57 CNIDARIA Ceratonova (Ceratomyxa) shasta

I. Causative Agent and Disease absent in parasitized wild fish nor has The parasite is the parasite been found in any hatchery not a protozoan but a metazoan in the stocks of Alaskan salmonids. class in the phylum Cni- daria (anemones, , corals) based III. Clinical Signs on molecular studies and the feature of Parasitized fish typically appear discharging cells (cnidocytes) known as darkened in color with swollen or hem- polar capsules. The parasite produces orrhaged vents and abdomens distended crescent shaped 14-23 um long by ascites. Although lesions are variable by 6-8 um wide at the suture line. A by age and fish species, the entire diges- single contains two refractile polar tive tract may be affected with granu- capsules, each with an extensible coiled lomas and abscesses (boils) causing filament. Vegetative trophozoites and tissue necrosis that may spread to major spores produce necrotic lesions within visceral organs and skeletal muscula- various tissues of salmonid fishes but the ture. These lesions contain developing parasite has a tropism for the gastroin- multicellular trophozoites and spores. testinal tract, especially the intestine. Each trophozoite forms a pansporoblast High mortality may occur in susceptible usually containing two spores. juvenile fish and the parasite contributes to significant pre-spawning mortality IV. Transmission of infected adult salmon. Depending Ceratonova shasta is transmitted on the host species and stock, natural to fish through the gills by infectious exposure to the parasite may allow some actinosporean tetractinomyxon stages fish populations to develop resistance in the water that are shed by parasitized to infection and severity of the disease. freshwater worms of the Ceratonova occurs seasonally (May to species Manayunkia speciosa that serve November) becoming more intense when as the alternate host. The worms become water temperatures reach or exceed parasitized by ingestion of mature spores 10°C. released by parasitized live or decom- posing fish hosts. However, unlike other II. Host Species myxozoans, the parasite develops within This organism parasitizes several the alternate host epidermis rather than different species of freshwater and ana- within the intestinal epithelium. dromous salmonids and is restricted to the Pacific Northwest (PNW) and British V. Diagnosis Columbia. Ceratonova shasta is present Tissue lesions or intestinal scrapes in wild adult chum, coho and sockeye are examined for spores having the typi- salmon, rainbow trout and Dolly Varden cal size and morphology of this parasite. in Alaska within several south central Identity is confirmed with fluorescein or and interior drainages including; Yetna, enzyme conjugated antibody tests and Yukon, Naknek, Wood, King Salmon, by PCR specific for Ceratonova shasta. Togiak and Sushana Rivers and Lower Talarik, Mortenson and Russell Creeks. VI. Prognosis for Host Clinical signs of disease, except for Depending on the fish species, stock white gill nodules in sockeye, have been and water temperature, prognosis may

58 CNIDARIA

be poor with high fish mortality. Major parasite is the only effective method of epizootics of juvenile salmonids in PNW control. hatcheries have commonly occurred when exposed to surface waters where VII. Human Health Signifcance the parasite is enzootic. Resistant fish Although parasitized fish tissues may in enzootic areas can become subclini- be aesthetically displeasing, there are no cal carriers of Ceratonova shasta with human health concerns with Ceratonova spores occurring in the lower intestinal shasta. tract. Prevention of exposure to the

10 um Wet mount of Ceratonova shasta spore with two  polar capsules.

Stained spore of Ceratonova shasta showing polar capsules (arrow) and the medial suture line, X 1000.

Coho salmon with swollen prolapsed vent due to the parasite Ceratonova shasta (photo: R. Holt, Oregon Dept. of Fish and Wildlife).

Bloating due to ascites in fsh parasitized with Ceratonova shasta (photo: R. Holt, Oregon Dept. of Fish and Wildlife).

59 CNIDARIA Henneguya

I. Causative Agent and Disease sporoblast or cyst formed of host tissue. Henneguya is not a protozoan but a When post-spawned salmon decompose, metazoan in the class Myxosporea in the the cysts rupture and release spores into phylum Cnidaria (anemones, jellyfish, the water where they likely are ingested corals) based on molecular studies and by an alternate host such as the feature of discharging cells (cnido- a tubificid worm. Infectious stages (ac- cytes) known as polar capsules. The ge- tinospores) for juvenile salmon develop nus has about 120 different species, some in the invertebrate host and are released are very host and tissue specific. The into the water column. parasite is found in fish as an ovoid spore (11 x 9 um) with two anterior polar cap- V. Diagnosis sules and two long caudal appendages White cysts in the flesh are examined (26-40 um). The most common species microscopically for the typical 2-tailed in Alaska is H. salminicola. The spores spores characteristic of Henneguya. of this parasite occur in the muscle and The condition can also be diagnosed by under the skin of Pacific salmon causing histological examination of tissues to a condition known as “milky flesh” dis- verify presence of the parasite. Species ease because of the creamy white fluid is determined by further spore morphol- containing spores that oozes from the ogy. cysts (pansporoblasts) during filleting. It is also known as “tapioca” disease from VI. Prognosis for Host the many small round spore containing Many fish parasites are well tolerated cysts in the flesh. depending on the target tissue affected. Fish mortality from Henneguya target- II. Host Species ing the flesh has not been reported. Many species of anadromous, marine and freshwater fishes are susceptible to VII. Human Health Signifcance the several different species of Henne- Although the cysts in the flesh are guya distributed worldwide. unsightly when present in large num- bers, there are no human health concerns III. Clinical Signs associated with Henneguya. Fish infected with Henneguya have numerous white pansporoblasts (cysts) in the target tissues that may contain thousands of spores.

IV. Transmission Henneguya salminicola is transmit- ted by an infectious stage in freshwa- ter. Pacific salmon become infected as juveniles and the parasites reach the muscle via the circulatory system passing through several developmental stages that eventually become spores. The spores are enclosed in a visible pan-

60 CNIDARIA

White pansporoblasts of Henneguya scattered within muscle of sockeye salmon.

Single white pansporoblast of Henneguya containing myriad numbers of spores.

Wet smear from pansporoblast showing Henneguya spores with two polar capsules and two caudal appendages, X 1000.

61 CNIDARIA Kudoa

I. Causative Agent and Disease tebrate as described for other myxo- Kudoa species are metazoans in sporeans. After infection, the parasites the class Myxosporea in the phylum reach the skeletal muscle by the circula- Cnidaria (anemones, jellyfish, corals) tory system passing through several based on molecular studies and the developmental stages that eventually feature of discharging cells (cnidocytes) become spores enclosed in a visible known as polar capsules. The genus has pseudocyst within the host skeletal over 90 different species among which muscle fiber. When the fish host dies and K. is most commonly reported decomposes, the pseudocysts rupture re- in over 30 marine and estuarine fish leasing spores into the water where they species worldwide. Many Kudoa species likely are ingested by the invertebrate infect skeletal muscle tissues producing alternate host, probably an oligochaete pseudocysts containing stellate-shaped or polychaete worm. Infectious stages spores with 4 or more valves and polar (actinospores) for fish develop in the capsules. Infections produce inflam- invertebrate host and are released into mation but no significant disease. High the water column. intensities of Kudoa cause unfit product quality from post-mortem myoliquefac- V. Diagnosis tion of fish flesh (soft flesh syndrome) White pseudocysts or inflamma- due to release of proteolytic enzymes tory foci in the flesh are examined in from the parasite. wet mounts for spores having 4 or more valves with polar capsules character- II. Host Species istic of Kudoa. Species is determined Many species of marine and by further spore morphology and PCR. estuarine fishes from several families Due to its very wide geographic and host are reported hosts of Kudoa species distribution, the reports of K. thyrsites worldwide. In Alaska, Kudoa has rarely from around the world may represent occurred in coho, Chinook and pink several indistinguishable species. Also salmon, and in . Sexually confounding a diagnosis; post-mortem mature fish appear to be more suscep- liquefaction may occur from developing tible to infection. parasite stages, prior to the visual pres- ence of mature pseudocysts and spores. III. Clinical Signs Fish infected with Kudoa have white VI. Prognosis for Host pseudocysts in the skeletal muscle fibers Kudoa is well tolerated containing hundreds of spores. Muscle and fish mortality has not been reported. tissue may exhibit liquefaction with However, there are species parasitizing varying intensities of the parasite that the heart muscle which may negatively may go visually unnoticed. Heavily affect cardiac performance. infected fish exhibit soft flesh when held on ice for 3-6 d or if cold smoked. VII. Human Health Signifcance Although the pseudocysts and/ IV. Transmission or the myoliquefaction of the flesh are Kudoa is likely transmitted by an unacceptable for consumption, there are infectious stage from a marine inver- no human health concerns reported for

62 CNIDARIA

most Kudoa. A self-limiting foodborne

illness can occur in raw olive

infected with K. septempunctata. 

25 um

Pseudocyst containing many 4 valved spores (arrow) of Kudoa sp. within the muscle of a Pacifc halibut.

Wet mount of two 4 valved Kudoa spores from red infammatory foci in the muscle of a pink salmon, X 1000.  

Stained smear of a Kudoa-like (arrows) containing many sporoblasts with dividing sporogonic cells; liquefed fllet muscle of soft-feshed Chinook salmon, X 400.

63 CNIDARIA Myxobolus neurotropus

I. Causative Agent and Disease clude spinal deformities, darkened body Myxobolus neurotropus is a meta- color and circular swimming behavior. zoan in the class Myxosporea in the phylum Cnidaria (anemones, jellyfish, IV. Transmission corals) based on molecular studies and Like most myxozoans, transmission the feature of discharging cells (cnido- likely requires a benthic invertebrate as cytes) known as polar capsules. This an alternate host, in this case occurring species was found in the brain and spinal in freshwater. After infection of the fish cord tissues of a wild rainbow trout in host, the parasites reach the central ner- Alaska which was a new geographic vous tissues via the circulatory system record. Currently there are at least eight passing through several developmental Myxobolus species that infect neural stages that eventually become spores tissue of salmonids, but some may rep- enclosed in sporocysts within the host resent more than one species or may ul- brain and spinal cord. When the fish timately be identified as synonyms. The host dies and decomposes, the spores are affected trout exhibited a deformed spine released into the water where they are and circular swimming behavior similar ingested by the invertebrate host, likely to signs of Whirling Disease caused by a tubificid oligochaete worm. Infectious another Myxobolus species, M. cerebra- stages (triactinomyxons) for fish develop lis. However, the latter parasite infects in the invertebrate host and are released the cartilage of the head rather than the into the water column. soft nervous tissues. Also, it has never been visually observed, caused disease V. Diagnosis nor has been confirmed in Alaska despite Brain or spinal cord tissues are marginally positive PCR results of one examined in stained smears for typical study from rainbow trout in 2005-2006. round to oval spores 11-13 um in length x 10-12 um in width with polar capsules II. Host Species 4 x 6 um in width and length containing This is a recently discovered parasite coiled filaments with 6-8 turns. Species reported in rainbow, cutthroat and bull identification is determined by further trout, Chinook and sockeye salmon from spore morphology and PCR. Idaho, Washington, , Oregon, Cali- fornia, and now in rainbow trout from VI. Prognosis for Host the Alaska Peninsula. The distribution Parasitisms by many species of in Alaska is unknown but could be an myxosporeans are well tolerated by fish emerging parasite more widespread than hosts unless infections cause dysfunction suggested from this single case due to of major organs and tissues. Infection of improved detection by PCR. the brain and spinal cord by M. neuro- tropus has potential to cause neuro- III. Clinical Signs logical dysfunction and fish mortality if M. neurotropus is not associated with infection intensity is high. tissue changes and is likely apathogenic so infected fish have few or no clinical VII. Human Health Signifcance signs unless parasite intensities are high. There are no human health concerns In such cases, signs could potentially in- associated with M. neurotropus.

64 CNIDARIA

Rainbow trout infected with Myxobolus neurotropus from Margo Creek on the Alaska Peninsula - darkened body coloration and spinal deformity.

Wet mount of M. neurotropus unstained spores from the spinal cord of the rainbow trout above, X 200. Inset scale bar = 10 um (from Bentz et al. 2012).

Malachite green-stained smear of M. neurotropus spores with oviform polar capsules of nearly equal size, X 1000.

65 CNIDARIA Myxobolus squamalis

I. Causative Agent and Disease through the skin. The parasite undergoes Myxobolus squamalis is not a several divisions toward final develop- protozoan but a metazoan in the class ment and travels to the specific target Myxosporea in the phylum Cnidaria tissues under the scales. (anemones, jellyfish, corals) based on molecular studies and the feature of V. Diagnosis discharging cells (cnidocytes) known White cysts under the scales of para- as polar capsules. The species produces sitized fish are examined microscopically round spores having two polar capsules for spores characteristic of Myxobolus at one end. Parasitized tissues are char- squamalis. Spores are typically 8-9 um acterized by cyst-like pansporoblasts in diameter with polar capsules of 3 x 4 under the scales that contain developing um in width and length. However myxo- spore stages of the parasite. The scales spore morphology is unreliable because are pushed up and often appear as M. squamalis is similar to several other bumps on the side of the fish. myxobolids that share host species and geographic ranges. Molecular methods, II. Host Species including sequencing, may be necessary This parasite is found mostly affect- for confirmative identification. ing anadromous Pacific salmon within the Pacific Northwest. In Alaska, M. VI. Prognosis for Host squamalis is observed most commonly in The effects from Myxobolus squama- coho salmon. lis are benign and mortality of the host due to the parasite has not been reported III. Clinical Signs Fish parasitized by Myxobolus squa- VII. Human Health Signifcance malis have numerous white pansporo- Although the cysts in the skin are vi- blasts under the scales. These spore- sually unappealing when present in large filled cysts raise the scales causing a numbers, there are no human health discolored pitted appearance of the skin. concerns associated with Myxobolus squamalis. IV. Transmission Transmission of M. squamalis most likely occurs in freshwater and is based on known life cycles of similar parasites in this class of organisms. Following the death of an infected fish, the cysts under the scales rupture releasing the spores into the bottom sediments where they are eaten by an alternate host, probably an oligochaete worm. Infectious stages for fish (triactinomyxons) develop in the gut of the alternate worm host. The triactin- omyxons are released to ambient water in large numbers with the feces of the worm and infect juvenile fish by entering

66 CNIDARIA

Skin lesions typical of infection by Myxobolus squamalis in a coho salmon.

Wet mount (Left) and stained smear (Right) of Myxobolus spores with polar flaments discharged from the polar capsules (cnidocytes), X 1000.

67 CNIDARIA Tetracapsuloides bryosalmonae (PKD)

I. Causative Agent and Disease cospores, are released with the urine to Proliferative kidney disease (PKD) is infect more . Vertical transmis- caused by the PKX cnidarian myxozoan sion allows T. bryosalmonae to persist (Malacosporea), Tetracapsuloides bryo- in the bryozoan host. are salmonae, that is a parasite of freshwater known to be subclinical carriers for at bryozoans ( sp., least 5 yrs. sp.) and salmonid fish. Waterborne spores of T. bryosalmonae are released V. Diagnosis from the bryozoan host where they in- Microscopic diagnosis is made by: fect the fish host, primarily through the Giemsa-stained imprints showing amoe- gills. The parasite travels via the blood boid PKX cells (10-20 um) with foamy to the kidney and other vascular organs cytoplasm, distinctive cell membrane where it proliferates, causing chronic and 1 mother cell (primary) nucleus with inflammation often accompanied by 1-7 daughter cells; histological exam secondary pathogen infections. indicating proliferative and granulo- matous nephritis, vascular necrosis and II. Host Species thrombi with eosinophilic PKX cells PKD has been reported in both wild among the kidney interstitial cells, often and captive salmonids and several other surrounded by attached host macro- species including whitefish and northern phages. Parasite DNA can be detected in pike in the Pacific Northwest and New- all organs by PCR and PKX cells can be foundland; trout, Atlantic salmon and observed in kidney, spleen and liver of grayling in Europe, including Finland infected fish by immunohistochemistry. and Sweden; in Iceland. In Alaska, the parasite has been reported in VI. Prognosis for Host lake-reared juvenile sockeye salmon and Temperature increase induces transi- two adult returning chum salmon. tion from covert into overt infection where infectious stages of T. bryosalmo- III. Clinical Signs nae develop and are released into the The gross clinical signs of PKD water. Variable mortality (5-90%) occurs include pale gills, a uniformly swollen at elevated water temperatures (12-15°C) kidney (may be gray/mottled) and spleen while fish that show less severe clini- with exophthalmia, ascites and anemia. cal signs of disease largely survive the infection when water temperature is IV. Transmission lower (< 12°C). Surviving fish develop Spores, released from freshwater immunity and may clear the infection bryozoans, infect salmonids through with regeneration of damaged tissues. the skin and gills releasing ameboid The decline of wild salmonid popula- sporoplasms. A single spore is sufficient tions in several rivers has been attributed to infect a fish and cause clinical PKD. to PKD which will become an emerging These travel to the kidney and undergo fish pathogen as global warming contin- extra-sporogonic multiplication in the ues. interstitium and differentiate through sporogenesis in the kidney tubules. Resulting spores, designated fish mala-

68 CNIDARIA

VII. Human Health Signifcance This parasite is a pathogen for fish. There are no human health concerns as- sociated with PKD.

  

Histology of eosinophilic PKX cells (arrows) in the kidney interstitium of steelhead trout containing large primary cell nuclei (dense red) next to translucent daughter cell nuclei. PKX cells are surrounded by basophilic (blue) host infammatory cells (arrowheads); H&E, X 1000.

A 

PKD in rainbow trout exhibiting bloody ascites (A) and swollen nodular posterior kidney (arrow) due to infammation and proliferation of PKX cells (photo: M. L. Kent and R. P. Hedrick, Univ. of Calif., Davis).

69 HELMINTHS Acanthocephalans (Spiny-Headed Worms)

I. Causative Agent and Disease An egg will hatch in the intermediate Acanthocephalans are endoparasitic host releasing an acanthor that penetrates worms characterized by a retractable the gut and develops into an acanthella/ proboscis armed with rows of hooks used cystocanth. The life cycle is complete to attach to the intestines of fish. Many when a fish eats a parasitized microcrus- genera have been described as adults in tacean and the adult worm develops in the intestines of fish while some larval the alimentary tract of the fish host. In forms have also been identified in the some cases, fish are the second interme- viscera. Genera commonly found in diate host as well as the final host. Alaskan fishes are Neoechinorhynchus, and Corynosoma. Gut V. Diagnosis infestation by numerous acanthocepha- Diagnosis is made by the visual de- lans can cause fibrotic nodules on the tection of adult acanthocephalans in the surface of the intestine. The intestine intestine or invasive larvae in the body may become inflamed with the destruc- cavity of a parasitized fish. The shape of tion of intestinal villi and resulting the proboscis, the arrangement and the necrotic and degenerative changes in number of proboscis hooks are important mucosal epithelium. Intestinal absorptive characteristics used to definitively iden- efficiency may be compromised leading tify the species of acanthocephalan. PCR to decreased growth and emaciation. has been useful in confirming species Acanthocephalans occasionally perfo- that has resulted in changing taxonomy. rate the intestinal wall which can lead to peritonitis and death of the host. VI. Prognosis for Host The principal effects on the final host II. Host Species can include mechanical damage to the Acanthocephalans have been found intestinal wall and emaciation. Signifi- in both marine and freshwater fishes cant fish mortality or emaciation due to worldwide. infestation by acanthocephalans are rare unless the worms are present in large III. Clinical Signs numbers. Parasitized fish may be emaciated with inflamed intestinal tracts and tissue VII. Human Health Signifcance necrosis in areas where worms are at- There are no human health concerns tached to the intestinal wall. associated with these parasites.

IV. Transmission Acanthocephalans require a ver- tebrate as a definitive host and arthropods as an intermediate host. Fish usually are the final host for aquatic acanthocephalans and microcrustaceans (amphipod, copepod, isopod or ostracod) are generally the intermediate host. Inter- mediate hosts are infected by eating eggs eliminated in the feces of parasitized fish.

70 HELMINTHS

Acanthocephalan worm of the genus Pomphorhynchus.

Pomphorhynchus: a higher magnifcation of the spiny head (proboscis) showing numerous hooks, X 200.

Highly armed proboscis of Echinorhynchus.

71 HELMINTHS Anisakid Larvae

I Causative Agent and Disease cycle is completed when ingested by the The larval form (third stage juvenile) final host, usually a marine mammal but of several nematode species within the sometimes a bird or fish. Incidental para- subfamily Anisakinae are found coiled sitism of a human host usually results in the flesh and viscera of parasitized in re-encystment of the juvenile worm. fish. Common genera include , The nematode matures in the gut of the Paranisakis, Porrocaecum, Pseudoter- marine mammal host and releases eggs ranova and Contracaecum. The larvae into the sea to continue the cycle. Some are relatively non-pathogenic to the fish anisakid larvae can also be transmitted host, although visceral adhesions from from fish to fish through . migrating larval worms do occur. V. Diagnosis II. Host Species Presumptive diagnosis is made by Anisakid larvae are common in visual examination of the body cavity, marine and anadromous fishes worldwide organs and flesh of the fish for typi- and have also been reported in cal coiled worms. Examination under and cuttlefish. In Alaska, among other a dissecting microscope can verify the fish species, these worms are commonly identity of the larval based on found in Pacific salmon and cod, walleye morphological characteristics. PCR has pollock, Pacific halibut and Pacific her- been useful in confirming species that ring (herring worm). has resulted in changing taxonomy.

III. Clinical Signs VI. Prognosis for Host Parasitized fish contain reddish or Prognosis for the fish host is good. In white, tightly coiled larval worms found most cases the worms are well tolerated most commonly in skeletal muscle and and there have been few reported cases visceral organs. These areas may exhibit of fish mortality due to juvenile anisakid mild inflammation, encapsulation and/or parasitism. granuloma formation. Visceral adhesion may occur in fish when many juvenile VII. Human Health Signifcance worms are present in the visceral cavity. Anisakiasis in humans can be ac- This condition causes production of quired by eating viable worms in raw or fibrous connective tissue by the fish host partially cooked fish. The Food and Drug in response to irritation from migrating Administration recommends cooking worms. fish at 67ºC for 5 minutes or freezing at -20ºC for at least 7 d before eating to kill IV. Transmission juvenile anisakid worms. Anisakid worms have a complex life cycle involving several hosts. Eggs eliminated in the feces from the final host hatch in the sea where the larvae are consumed by (usually Euphausids), which in turn are eaten by fish. The larva burrows into the gut or flesh of the fish and encysts until its life

72 HELMINTHS

Anisakis Life Cycle

Humans contract by consumption of raw or undercooked Marine mammal

fish (abnormal host) final host for the adult nematode Anisakis

Eggs and second stage larva

Fish and Squid

Free swimming larva ingested by crustaceans (Euphausids)

Anisakis third stage juvenile worms tightly coiled in liver.

Anisakis third stage juvenile worm being pulled from salmonid muscle.

73 HELMINTHS Philometra

I. Causative Agent and Disease of the host or the female migrates to the Philometra is a nematode parasi- skin surface to release larvae. tizing the body cavities or tissues of fish. Larval stages of this worm migrate to V. Diagnosis the final resting sites in the subcutaneous Diagnosis is made by observation of tissues (fins, head, and body) or body typical Philometra worms in fish host cavities of . The migration body cavities or subcutaneous tissues, of the parasite within the host can result particularly the fins, snout, and head in inflammation of visceral organs, or areas of raised scales. Dissection of mechanical damage of blood vessels nodules expose the long, smooth, fili- with hemorrhaging and destruction of form worms characteristic of the genera. skeletal joints resulting in poor growth Worms are usually red in color and the and emaciation. immensely larger females contain live larvae and burst easily when placed in II. Host Species water. Many species of marine and fresh- water fish, including salmonids, are VI. Prognosis for Host susceptible to this parasite that is found Prognosis for the host is dependent worldwide. on the degree of infestation and other environmental stressors that may be III. Clinical Signs present. Generally, Philometra is well Nodules under the flesh containing tolerated causing no significant harm to juvenile or adult worms cause raised fish hosts. scales or are visible between the fin rays of the fish host. Larger nodules contain VII. Human Health Signifcance gravid females that eventually extrude Philometra is not of human health through the skin and disintegrate to concern. release live larvae. This is followed by complete healing of the host flesh leav- ing little sign of previous infestation.

IV. Transmission Philometra has a two-host life cycle. Larval worms are transmitted through an intermediate host (copepods) to the fi- nal fish host. Predatory fish may acquire the parasite by eating infested cope- pods or forage fish that have preyed on infested copepods. In skin infestations the much larger female parasites excyst and burst releasing larvae into the water to be ingested by copepods where the larvae undergo a series of molts. When parasitizing a body cavity, larvae are released through the gut with the feces

74 HELMINTHS

Adult Philometra worm (red) between the caudal fn rays of a freshwater slender bitterling.

Same Philometra worm dissected from fn rays above.

75 HELMINTHS Philonema

I. Causative Agent and Disease migrate into the body cavity where Philonema (oncorhynchi and agu- worms molt into sub-adults and eventu- bernaculum) is a nematode (roundworm) ally adults that produce more larvae. found in the visceral cavity of fish that rarely migrates to the musculature. V. Diagnosis Larval, sub-adult and adult worms (17 Diagnosis is made by necropsy of mm to 86 mm) can be present. The diseased fish and the visual identification worms generally do not cause significant of the nematode. Philonema is a filiform pathology in the fish host but a condition worm having a rounded anterior end known as visceral adhesion occasion- and a posterior tail tapering into a sharp ally occurs in severely parasitized fish. point. These and other morphological Visceral adhesion is characterized by the features are used to identify the worm. production of fibrous connective tissue by the fish host in response to tissue ir- VI. Prognosis for Host ritation from migrating worms. In severe Prognosis for the host is good unless cases, internal organs are bound together infestation is severe or other stressors by the scar tissue. further debilitate the fish. Severe parasitism can cause visceral adhesions II. Host Species that interfere with spawning ability and The parasite occurs in all anadro- may cause serious organ dysfunction. mous Pacific salmon, resident trout and However, the literature indicates this char in upper North America and the condition is probably transitory and does Northern Pacific including Russia and not cause significant fish mortality. Japan. VII. Human Health Signifcance III. Clinical Signs Philonema is not infectious for hu- Usually there are no clinical signs of mans. nematode infestation. Highly parasitized fish may have extensive visceral adhe- sion discovered only by necropsy.

IV. Transmission Juvenile fish acquire the parasites in freshwater but the adult worms may develop while the fish are at sea. The life cycle includes live larvae released from gravid female worms extruded with fish eggs from adult spawning fish. The larval worms infest a freshwater cope- pod where they develop into third stage larvae that are infectious for juvenile salmonids. Fish are infested by eating the parasitized copepods and the larvae

76 HELMINTHS

Many juvenile Philonema found in the visceral cavity of an adult coho salmon, X 200.

Juvenile Philonema nematode with posterior tail tapering into a fne point, X 400.

77 HELMINTHS Black Spot Disease (Neascus and Heterophyids)

I. Causative Agent and Disease sections. Tissue sections reveal a thick, Black spot is caused by digenean fibrinous capsule around the encysted trematodes (flukes) in the families metacercariae with the periphery of the Diplostomatidae and Heterophyidae. capsule containing numerous mela- The cercarial forms of the trematodes nocytes. Neascus is a collective larval penetrate the skin of a fish, where they genus for several genera and species of encyst and develop into metacercariae. trematodes having characteristics of the The fish surrounds the cyst with black family Diplostomatidae. More precise pigmented melanin in response to the genus and species identification is based foreign organism. The black spots are on marine or freshwater habitat, tissue often visible to the naked eye. These site of encystment and other morpho- worms are present in both freshwater logical characteristics of the encysted (Uvulifer ambloplitis, Crassiphiala metacercariae. bulboglossa, Apophallus donicus) and marine (Cryptocotyle lingua) fish. VI. Prognosis for Host Most metacercarial infestations of II. Host Species the skin and fins are relatively nonpatho- Salmonids and other freshwater and genic. marine fish are second intermediate hosts worldwide. VII. Human Health Signifcance Generally these worms are reported III. Clinical Signs to infect only poikilotherms, but experi- Infested fish exhibit black, raised mental studies have indicated that meta- nodules in the skin which are often less cercariae of Apophallus donicus from than 1mm in diameter. freshwater fish can parasitize various mammals including humans. The Center IV. Transmission for Disease Control recommends cook- Fish are parasitized by exposure ing fish at 67ºC for 5 minutes or freezing to water containing parasitized snails. fish at -20ºC for at least 7 d to kill worm The actively swimming cercariae from parasites before ingestion. the snails penetrate the skin of the fish where they develop into metacercariae. The definitive hosts are fish eating birds and mammals that complete the life cycle by releasing eggs into the water with feces. The eggs hatch into mira- cidia which parasitize the snail hosts.

V. Diagnosis Presumptive diagnosis is made by the observation of small, multifo- cal, slightly raised black spots in the fish skin. Confirmation is obtained by observing metacercariae in the cysts in wet mount preparations or histological

78 HELMINTHS

Typical black spots composed of melanin that surround encysted metacercariae of the larval genus Neascus in an Arctic grayling.

Marine form of black-spot heterophyid circumscribed by blue- green pigment on the caudal fn of a Bering cisco (photo: B. Collyard, ADF&G).

Encysted metacercaria of Neascus, X 1000.

79 HELMINTHS Encysted Digenean Metacercariae (white and yellow grubs)

I. Causative Agent and Disease tebrate hosts. The inclusion of many White and yellow grubs, caused by other trematode species, especially in several species of digenean trematodes the marine environment, involves more (flukes) have cercarial forms that pene- hosts including birds and mammals as trate the skin of fish, where they encyst final hosts while fish can be a second and develop into metacercariae, appear- intermediate host, paratenic host or the ing as white or yellow nodules in the final host. flesh. The most common worms present in freshwater are Clinostomum spp. V. Diagnosis (yellow grub) and Posthodiplostomum Presumptive diagnosis is by the minimum (white grub). In the marine observation of white or yellow cysts ecosystem there are many species of containing metacercariae in the skin, trematodes that produce white and yel- fins or viscera of fish. Freshwater white low cysts in fish. grubs are 1-1.5 mm and yellow grubs are 3-8 mm. The smaller white grub encysts II. Host Species in visceral organs, especially kidney, Many North American fish species liver and heart. The yellow grub is more are second intermediate hosts for the common in skin, fins and musculature. freshwater white and yellow grubs. Sim- In marine fish the nodules may vary ilar or the same species occur in Europe, considerably in location and size due to South America and Asia. Also, numer- the many different trematode species. ous species of marine fish worldwide can Confirmation is by observing metacer- be parasitized with metacercariae that cariae in the cysts of wet mount prepara- produce white and yellow cysts. tions or histological sections. Tetracotyle is a collective larval genus for several III. Clinical Signs genera and species of trematodes having Infested fish exhibit white or yellow characteristics of the family Strigeidae. nodules in the flesh that can vary greatly More precise genus and species identifi- in size. cation is based on tissue site of encyst- ment and morphological characteristics IV. Transmission of the metacercariae. DNA sequencing Fish are infested by exposure to has also become an important method fresh or seawater containing parasit- for identifying these parasites ized snails or other invertebrates. The actively swimming cercariae shed by VI. Prognosis for Host the invertebrate penetrate the skin of the Most metacercarial infestations are fish and/or travel to other target tissues relatively non-pathogenic. Encystment where they develop into metacercariae. in visceral organs may cause significant The definitive hosts for freshwater white pathology and fish mortality when infes- and yellow grubs are fish eating birds tation intensity is high. Grub-infested where adult worms occur in the mouth, flesh also produces inferior product throat or intestine. The life cycle is com- quality in commercial and farmed fish. pleted by release of eggs into the water with saliva or feces. The eggs hatch into VII. Human Health Signifcance miracidia which parasitize the inver- Generally, these worms are consid-

80 HELMINTHS

ered to infect only poikilotherms, but Disease Control recommends cooking there have been cases in Japan, Korea fish at 67ºC for 5 minutes or freezing and SE Asia where metacercariae of C. fish at -20ºC for at least 7 d to kill worm complanatum have parasitized humans parasites before ingestion. from eating affected fish. The Center for 

Left: Yellow grub-like encysted metacercariae (arrow) in the pericardial cavity of a sheefsh; Right: Strigeid-type trematode larva teased from a cyst on the left, resembles a Tetracotyle of an Ichthyocotylurus sp., X 10.

Left: Yellow grub-like metacercariae encysted in the peritoneal lining and musculature of a rainbow trout; Right: Metacercariae encysted in the skin of a starry founder causing numerous raised nodules.

81 HELMINTHS Larval Diplostomulum of the Eye

I. Causative Agent and Disease VI. Prognosis for Host Eye fluke is caused by digenean If parasitized bilaterally, complete larval trematodes of the genus Diplos- blindness may result, and the fish host tomulum that parasitize the eye of many will probably die from predation or in- fish species. A common trematode found ability to find food. When only one eye in the lens is D. spathaceum while other is parasitized, the host fish may survive species are found in the vitreous cham- for an indefinite period of time. ber of the eye. The parasites can remain in the eye for a long time often resulting VII. Human Health Signifcance in cataracts and blindness in the fish There are no human health concerns host. associated with this parasite.

II. Host Species Many salmonids and other fish are susceptible throughout North America and Europe.

III. Clinical Signs The fish may have cataracts and the eye appears opaque.

IV. Transmission As with other digenean trematodes, the fish becomes parasitized horizontally through the water from infested snails. The invasive cercariae from a snail (first intermediate host) penetrate the fish (second intermediate host), usually through the skin, and migrate to the eye where they develop into the metacer- carial form. The life cycle is completed when the fish host is eaten by a piscivo- rous bird where the adult fluke develops in the gut and releases eggs into the water.

V. Diagnosis This condition is diagnosed by wet mount observation of metacercariae in the lens or vitreous humor of the eye in a parasitized fish. Typical metacercariae can also be identified using histological methods.

82 HELMINTHS

Diplostomulum Life Cycle

Metacercaria from lens Fish eating birds final host for adult trematode Diplostomulum

Mature egg

Fish with parasitized eye

Ciliated larvae – miracidium

Free swimming cercaria Infected snail

Metacercarial form of the eye fuke Diplostomulum from an Arctic grayling, X 200.

83 HELMINTHS Gyrodactylus and Dactylogyrus

I. Causative Agent and Disease behavior and lethargy. Gill infestations The genus Gyrodactylus contains of Dactylogyrus produce clinical signs many species but G. salmonis is a com- very similar to Gyrodactylus. mon parasite of salmonids in North America. This small (0.2 mm) monoge- IV. Transmission nean fluke attaches to gills, fins and skin Horizontal transmission occurs epithelium using an attachment organ or between fish by physical contact in opisthaptor armed with a pair of large crowded environments or when the hooks and 16 marginal hooklets. The flukes are present in the water seeking head of the worm is bi-lobed, lacks eye a fish host. Both genera are hermaphro- spots and the worm produces live young. ditic. Gyrodactylus produces live young Heavy infestations by the parasite can that attach to the same or different host. result in destruction of the gills or skin Dactylogyrus releases fertilized eggs epithelium due to mechanical damage that hatch in the water column producing caused by the attachment organ. The juveniles that likely attach to a different genus Dactylogyrus is found on the gills host. of mostly cyprinid fishes and is also very small (0.3 mm). Dactylogyrus is V. Diagnosis recognized by a four-lobed head with Diagnosis is made by observing the four eye spots and produces eggs. The parasites in wet mounts of skin scrapes opisthaptor consists of one conspicuous or gill tissues. Gyrodactylus has no eye- pair of large hooks and up to 12 smaller spots and is viviparous having hooklets. When the worm is present with well-developed hooks visible inside in large numbers, gill hyperplasia and the body of the adults. Dactylogyrid necrosis may result. flukes have 4 eye spots and contain vis- ible eggs. II. Host Species The genus Gyrodactylus has many VI. Prognosis for Host species in Eurasia and North America Prognosis for the host is good if in- that parasitize both marine and freshwa- festations are not excessive. If extensive ter fish. In Alaska, the worm is common- mechanical damage occurs to the fins, ly observed as an external parasite of skin and/or gills the fish become very wild and hatchery salmonids. The genus susceptible to secondary infections with Dactylogyrus is found worldwide para- opportunistic pathogens. Formalin treat- sitizing mostly cyprinids in freshwater. ments are used in the hatchery environ- ment to eliminate these external flukes III. Clinical Signs from fish. The skin of fish infested with Gyro- dactylus may become mottled, necrotic VII. Human Health Signifcance and dark with excess mucus production. There are no human health concerns Infestation of the gills often results in associated with either Gyrodactylus or lamellar hyperplasia, also accompanied Dactylogyrus. by excessive mucus production and rapid respiratory movements. Heavy body in- festations cause fin erosion with flashing

84 HELMINTHS

Gyrodactylus attached to gill lamellae by hooks, X 100. 

Gyrodactylus having visible internal embryos with hooks (arrow), X 200.

Left: Adult Gyrodactylus; Right: Stained Dactylogyrus with 4 eye spots (arrow), X 200.

85 HELMINTHS Piscicola

I. Causative Agent and Disease a blood meal, a leech either attaches Piscicola is a freshwater leech to a fish for another feeding cycle or belonging to the phylum Annelida it produces eggs. Eggs are encased in (segmented worms) that can be abundant oval “cocoons” that are attached to the in some freshwater lakes, ponds and substrate at the bottom of the lake or streams. Piscicola attaches to the skin of river. Juvenile leeches hatch from the freshwater fish and is nourished by suck- eggs and enter the water column to find a ing blood and other tissue fluids from the fish host. Parasitic juvenile leeches usu- host. Members of the genus Piscicola ally require several blood meals before usually remain attached to a fish for sev- becoming mature adults. Leeches of this eral days while feeding and then drop off genus have been implicated as possible and sink to the bottom where the food is vectors of the fish virus, IHNV. digested. Piscicola has well developed oral and caudal suckers with a subcylin- V. Diagnosis drical and elongate body. Leeches usu- Leeches are obvious by visual ally do not cause serious harm to their examination of the host. Observation of hosts since most tissue damage is local- the worm under a dissecting microscope ized at the sites of attachment. However, for various morphological character- when present in large numbers parasitic istics including color and pattern of leeches can cause extensive tissue dam- pigmentation, number and arrangement age to fishes including epidermal erosion of eye spots on the oral sucker and other and ulceration, hemorrhaging, necrosis external features help identify the genus and anemia. External epidermal erosions Piscicola. may serve as portals of entry for second- ary bacterial or fungal pathogens. VI. Prognosis for Host Leeches usually do not cause signifi- II. Host Species cant harm to their hosts unless present The parasite occurs on many species in large numbers. Prognosis for a host is of freshwater fishes in Europe and North good when infestations are low to mod- America. Salmonids are most commonly erate, but host inflammation may occur parasitized by P. salmositica in Alaska. locally at the site of attachment.

III. Clinical Signs VII. Human Health Signifcance Piscicola leeches are visible with the There are no human health concerns naked eye. Attachment of leeches may associated with Piscicola. occur anywhere on the host body and are often found on or under the opercula, in the mouth, along the jaw and at the bases of fins.

IV. Transmission The life cycle of leeches is relatively simple, consisting of an egg, a juvenile stage and a mature hermaphroditic adult that produces eggs. After digestion of

86 HELMINTHS

Piscicola Life Cycle

Adult Piscicola leeches attach to fish host Hatched, leeches seek fish host

Engorged leech falls off host producing eggs

Eggs encased in cocoons Eggs attach to vegetation or rocks in the substrate

Adult and juvenile Piscicola on rainbow trout producing typical epidermal attachment lesions (visible as round depressions).

Freshwater leech of the genus Piscicola (measurement in cm).

87 HELMINTHS Diphyllobothrium

I. Causative Agent and Disease predatory fish that become paratenic Six species of diphyllobothrid ces- hosts when other infested fish are eaten. todes (tapeworm) occur in Alaska, all of The life cycle is complete when the fish which use fish as a second intermediate host is eaten by a mammal or bird defini- and/or as a paratenic host. Three species tive host where the worm becomes an of larval Diphyllobothrium that most egg-producing adult. commonly occur in Alaskan salmonid fishes include D. ditremum, dendriticum V. Diagnosis and nihonkaiense. The cestode larvae Diagnosis is made by visual identi- can be found free in the visceral cavity fication of the cestode during necropsy or encysted in the viscera or muscle tis- of a parasitized fish. Plerocercoid stages sues. of Diphyllobothrium have a compressed scolex with characteristic bothria or II. Host Species grooves. The body is usually slightly Planktivorous and carnivorous fresh- wrinkled, suggesting segmentation. PCR water fishes are potential hosts in North/ has been useful in confirming species South America and Eurasia including that has resulted in changing taxonomy. salmonids, whitefish, , , sticklebacks, , and blackfish. VI. Prognosis for Host Prognosis for the host is good pro- III. Clinical Signs vided the infestation is low and there are The larval Diphyllobothrium can not other stressors involved. Juvenile fish be found (sometimes encysted) in the are more adversely affected than older muscles, viscera and connective tis- fish and can die from severe plerocercoid sues of the fish host causing adhesions, infestations. hemorrhaging (particularly the liver) and ascitic fluid resulting in abdominal dis- VII. Human Health Signifcance tension. Severe infestations in juvenile Species of this cestode group can fish can cause mortality. successfully parasitize humans. Most human infestations are accidental since IV. Transmission the natural hosts are fish eating birds Infestation of the fish host is part of and mammals. Infestation in man occurs a 3-host life cycle for this parasite. Adult by ingestion of raw or lightly smoked worms are found in the small intestine fish that contain viable plerocercoid of definitive hosts that are fish eating larvae. The Center for Disease Control birds or mammals (including humans). recommends cooking fish at 67ºC for 5 Eggs from adult worms are released into minutes or freezing fish at -20ºC for at the water with feces where they develop least 7 d to kill worm parasites before into a free swimming coracidium larval ingestion. stage that is ingested by copepods, the first intermediate host. The procercoid develops in the copepod and, when eaten by the fish second intermediate host, develops into the plerocercoid stage. Plerocercoids re-encyst near the gut of

88 HELMINTHS

Diphyllobothrium Life Cycle

Humans parasitized by consumption of raw or undercooked fish Fish eating birds and mamals are final hosts for adult cestode Diphyllobothrium

Eggs

Piscivorous fish Ciliated larvae (paratenic host) (coracidium)

Crustacean ingested by second Procercoid larvae in first intermediate host (fish) where intermediate host, larvae develop into plerocercoids a copepod

Left: Subsurface white cysts (center) in brook trout liver with plerocercoids of Diphyllobothrium sp.; Right: Diphyllobothrium sp. plerocercoid with wrinkled body suggesting segmentation.

 

Bothria (grooves) in plerocercoid scolex characteristic of Encysted plerocercoids in viscera of rainbow trout Diphyllobothrium sp. (black arrows).

89 HELMINTHS Schistocephalus

I. Causative Agent and Disease bothria (grooves) on the scolex. Fish will Schistocephalus is a cestode (tape- often contain multiple plerocercoids. worm) within the family Diphylloboth- riidae parasitizing fish hosts as plerocer- VI. Prognosis for Host coid larvae transmitted by ingestion of Prognosis for the host is dependent parasitized copepods. The worm in the on the degree of infestation. Pathology fish host occurs in the body cavity often caused by the plerocercoids includes causing abdominal distention due to growth retardation, abdominal disten- multiple infestations and the large size of sion, and physiological dysfunction of the plerocercoids. internal organs. The debilitation caused by the parasite increases the vulnerabil- II. Host Species ity of the fish host to predation by the Several freshwater fish species are final host. susceptible to this parasite in North America and Eurasia. In Alaska, this VII. Human Health Signifcance cestode is most often found in stickle- There are no known human health backs. concerns associated with Schistocepha- lus. III. Clinical Signs Fish with heavy infestations of this parasite are often bloated and mis- shapen since the parasite is quite large. Normal fish swimming behavior may be impaired.

IV. Transmission Transmission occurs through a com- plex life cycle utilizing two intermediate hosts. The first intermediate host is a co- pepod that is parasitized by a coracidium hatched from a cestode egg deposited in the water column. A procercoid stage develops in the gut of the copepod that is eaten by the second intermediate host, a freshwater fish. The plerocercoid devel- ops in the second intermediate fish host that is eaten by the final bird host where the adult worm develops and produces eggs in the intestinal tract.

V. Diagnosis Diagnosis is made by internal obser- vation of the plerocercoid larvae. The white larvae are 2-7 cm long, broader at one end and segmented with shallow

90 HELMINTHS

Plerocercoid stage of Schistocephalus from abdominal cavity of parasitized

Two plerocercoids of Schistocephalus removed from the body cavity of a stickleback.

91 HELMINTHS Triaenophorus

I. Causative Agent and Disease and develop into the plerocercoid stage. Triaenophorus crassus is a cestode The life cycle of the worm is completed (tapeworm) belonging to the family when the parasitized fish is eaten by the Triaenophoridae that parasitizes fish final fish host, commonly a northern as plerocercoid larvae (1 mm X 30 cm) pike. Eggs are produced after the worm found encysted in the musculature. develops into an adult in the intestinal These cestodes can also be found as tract of the final fish host. adults living in the guts of predatory fish. V. Diagnosis Diagnosis is made by observation of II. Host Species encysted or unencysted white plerocer- There are many fish intermediate coids in the skeletal musculature of a hosts for the plerocercoid (larval) stage parasitized fish. Identifying microscopic of Triaenophorus in North America and features of the plerocercoid scolex Europe. The definitive hosts are piscivo- (head) include dorsal and ventral pairs of rous fishes such as northern pike. trident shaped hooks on an apical disc. Adult worms are larger and found in the III. Clinical Signs intestinal tract. Triaenophorus often stimulates formation of yellow to white cysts of VI. Prognosis for Host host connective tissue that surround the Prognosis for the fish host depends plerocercoids in the muscle. Encysted on the degree of cestode infestation, or unencysted larvae can cause local- the age and size of the fish and expo- ized muscle discoloration and necrosis. sure to other stressors. Generally, these Liver dysfunction and blood loss can parasites have caused health problems occur from larval migration through with juvenile cultured fish but are well the viscera and may be associated with tolerated when occurring as natural hemorrhaging, necrosis, fibrosis, edema infestations of larger healthy fish. and tissue discoloration. Severe adult tapeworm infestations in the gut can VII. Human Health Signifcance cause perforations, mechanical block- Although this tapeworm is not age with distension and prevent nutrient known to occur in man or other warm- uptake causing emaciation and anemia. blooded animals, infested fish flesh is unsightly. IV. Transmission The life cycle of this tapeworm oc- curs in freshwater where eggs are shed from adult worms living in the intestinal tracts of the final hosts (usually preda- tory fish). The cestode eggs, containing a coracidium, are eaten by copepods and develop into procercoids. The copepods are eaten by the second intermediate fish host where the procercoids migrate from the intestinal tract to the muscle

92 HELMINTHS

Triaenophorus Life Cycle

Adult pike, a common final host for the adult cestode Triaenophorus

This fish eaten by piscivorous fish, the final host – with development of adult tapeworm

Eggs

Ciliated larvae (coracidium)

Crustacean ingested by second intermediate host (fish) where larvae develop into plerocercoids Procercoid larvae in first intermediate host, a copepod crustacean

Characteristic trident shaped hooks on scolex of Triaenophorus crassus plerocercoid found in fsh muscle, X 40.

93 ARTHROPODS External Parasitic Copepods

I. Causative Agent and Disease taches to the fish where it goes through a A variety of different parasitic number of larval stages before becoming copepods can cause external infesta- an adult. tions of freshwater and marine fish. Some members of the group are com- V. Diagnosis monly referred to as fish lice. They are The larger parasites can be seen with frequently found on the body, around the naked eye. Definitive identification the mouth, and on the gills. Members of is based on microscopic morphologies of the order Copepoda commonly found body parts and structures. in Alaska include the genera Lernaea (anchor worm) in both fresh and marine VI. Prognosis for Host waters, Salmincola (discussed in next The prognosis for the host depends section) in freshwater and Lepeoph- on the specific parasite, tissue loca- theirus (sealice) in marine waters. Fish tion and numbers present. If parasite infested with external parasitic copepods numbers are small, fish normally are often lethargic and may flash or rub survive with little adverse effects unless against substrate. In heavy infestations, the copepods are anchor worms that the skin may appear opaque due to the destroy one or both eyes. This can result production of mucus and the fins may in blindness and death of the host by be frayed. Epidermal and gill tissues starvation or predation. When present may become necrotic with secondary in large numbers, such as Lepeophthei- infections by fungi and bacteria. These rus in seawater netpens, significant fish parasites are found worldwide. losses may result. SLICE is a drug used in Canada and Europe for eliminating II. Host Species fish lice in seawater netpens and is ap- A variety of different freshwater and proved for use in the US under an INAD marine fishes are susceptible to infesta- permit. tions from these copepods. VII. Human Health Signifcance III. Clinical Signs There are no human health concerns Parasitized fish may act listless and associated with these organisms. lethargic. Mechanical abrasion due to the attachment and/or feeding by the cope- pods is common resulting in frayed fins, gill hyperplasia, and patchy epidermal damage and necrosis. Infections with secondary pathogens often occur.

IV. Transmission Most of these organisms have a direct life cycle involving a number of free-living and larval stages. Transmis- sion is through contact with an infective free-swimming stage of the organism in the water column. The infective stage at-

94 ARTHROPODS

Lepeophtheirus salmonis copepod from the surface of a salmonid fsh.

Left: Lepeophtheirus on coho salmon; Right: Phrixocephalus cincinnatus (anchor worm) embedded in the eye of an arrowtooth founder.

95 ARTHROPODS Salmincola

I. Causative Agent and Disease clusters of eggs twice during a 3-month Parasitic copepods of the genus life span. Eggs hatch into a larval form Salmincola are most often found at- that can survive free-swimming for tached to gill filaments, opercula, tissues several days. The larvae attach to gills within the mouth cavity, and fins of or fins of a fish host and molt into 4 suc- salmonid fishes. The parasites feed on cessive larval stages and degenerate into blood and epithelial tissues of their grub-like parasites. Males then detach hosts. Salmincola species are restricted and copulate with the females, after largely to freshwater but may survive on which the males die. Females molt into salmonids while at sea. The adult female the adult stage and produce two pairs of copepods are larger than the males and egg clusters. The female Salmincola dies attach permanently to the fish host with shortly after the second group of eggs a modified mouth part known as a bulla hatch. that is inserted into the host tissues. Host damage by parasitic copepods depends V. Diagnosis on the location of the attachment site, the Salmincola are large enough to ob- species of parasite, and the size and type serve grossly. Visual examination of fish of bulla. Gill attachment by Salmincola skin, fins, gills and mouth can reveal the can damage delicate epidermal tissues extent of copepod infestation. Micro- resulting in necrosis and loss of surface scopic examination of various morpho- area for respiration. Attachment may logical characteristics aid in identifying also provide portals of entry for second- the parasite to the genus and species. ary invaders such as bacteria and fungi. VI. Prognosis for Host II. Host Species Prognosis for the host is good when Salmincola has been reported more infestations are not severe and damage commonly from salmonid species in to gill tissue is minimal. Generally, in- North America and Europe. festations with this parasite do not cause significant fish mortality. III. Clinical Signs Salmincola copepods are visible to VII. Human Health Signifcance the naked eye when attached to fins, There are no human health concerns bases of fins, skin, opercula, gills and associated with Salmincola. branchial chamber. Gill damage caused by displacement from Salmincola can be extensive resulting in retarded filament growth and tissue necrosis. Gill hyper- plasia and hypertrophy may also lead to fusion of the filaments, thus reducing surface area for necessary gas exchange and respiration.

IV. Transmission Salmincola have a direct, but com- plicated life cycle. Females produce two

96 ARTHROPODS

Salmincola Life Cycle

Adult Salmincola attaches to fish host

← Egg sacs male Adult female copepod Copepodids are released with button-shaped bulla from egg sacs and male attached

Free swimming copepodids Copepodids molt several times while attached to fish host

Severe Salmincola infestation of rainbow trout gills; note necrotic areas at tips of gill lamellae.

97 ARTHROPODS Sarcotaces

I. Causative Agent and Disease V. Diagnosis Sarcotaces arcticus is an endopara- Diagnosis is made by internal exami- sitic copepod several centimeters long nation of the fish for characteristic pear- found encysted under the skin and in shaped cysts exuding black fluid and the muscle tissue of marine fish. The morphological identification of the larger juvenile copepod inserts its head into the female parasite. The body is oval with flesh and is eventually covered by the ill-defined transverse bands correspond- host skin except for the last pointed body ing to segments and a double rosette is segment that maintains connection with often visible around the mouthparts. the outside seawater. When the parasite dies, after growing to an enormous size, VI. Prognosis for Host the tissue forms a closed cyst. In Alaska, Prognosis for the host is good if in- this parasite is commonly found in festation is minimal and there are no sig- rockfish Sebastes( spp.) encysted near the nificant environmental stressors present. anus where surrounding intestinal tissue Infestations by Sarcotaces are associated forms a sac-like process. When fish are with lower fecundity in rockfish and fish filleted the ruptured cysts release black flesh becomes unappealing when fillets fluid, a breakdown product of blood that are tainted with the fluid leaking from the parasite has engorged. cysts.

II. Host Species VII. Human Health Signifcance This parasitic copepod is found most There are no human health concerns commonly in species of Sebastes spp. in with Sarcotaces. the northern Pacific Ocean and in other genera of teleosts in European waters.

III. Clinical Signs Sarcotaces parasites are difficult to detect externally because of the subder- mal location of the cyst. If the cyst lies over a bony surface, swelling of the skin may occur. In parasitized rockfish, the anal cysts are generally obvious.

IV. Transmission The life cycle is direct by horizontal transmission. Larval copepodids are released into ambient seawater from the encysted adult female after fertilization by a much smaller male that has entered through the open portal of the cyst. The juveniles seek out a new host to continue the life cycle.

98 ARTHROPODS

Left: Sarcotaces encysted in intestinal tissue protruding from anal area of a rockfsh; Right: Removed paired cysts.

Adult female Sarcotaces dissected from a cyst (in mm)

99 NON-INFECTIOUS DISEASES Bloat (Water Belly)

I. Causative Agent and Disease V. Diagnosis This is a non-infectious condition Bloat is usually diagnosed by the where the abdomen of salmonids is presence of excessive amounts of clear, abnormally distended by an enlarged, watery fluid in the stomach. The stomach water-filled stomach. The condition is wall is thinned from distension, but other most often seen in salmonids reared in significant histological changes are not seawater. The cause of this condition is present. not well understood, but potential vari- ables may include: a combined failure VI. Prognosis for Host of osmotic regulation, increased lipids, Although this condition can cause temperature and stress; increased drink- mortality, affected fish often survive for ing of seawater and nutrient overloading weeks. A reduced feeding regime after due to excessive feeding. In other words, fish have been starved for several days ingestion of nutrient-rich food may result or changing the composition of the food in slowed stomach emptying leading to will reduce the problem in captive fish. decreased absorption of water, thirst and increased drinking that further exacer- VII. Human Health Signifcance bates stomach distention. There are no human health concerns associated with this condition. II. Host Species This condition is reported frequently in Chinook, coho, chum and Atlantic salmon and also in rainbow trout. Bloat in Alaska is most common in juvenile coho, but also observed in chum, pink and Chinook salmon.

III. Clinical Signs Fish with bloat exhibit severe disten- tion of the abdominal wall. Necropsy reveals a massively enlarged stomach with a very thin wall. The stomach is filled with a clear, watery fluid mixed with feed.

IV. Transmission The disease is non-infectious and cannot be transmitted from fish to fish.

100 NON-INFECTIOUS DISEASES

Chum salmon fry with swollen abdomen typical of bloat.

Chinook salmon smolt with swollen abdomen typical of bloat.

101 NON-INFECTIOUS DISEASES Blue Sac Disease of Fry

I. Causative Agent and Disease V. Diagnosis Blue sac disease of fry is considered Diagnosis is based on the observation to be a non-infectious disease caused by of typical clinical signs of the condition. the accumulation of metabolic wastes and reduced dissolved oxygen result- VI. Prognosis for Host ing in excessive buildup of ammonia Blue sac disease is usually fatal due nitrogen. The disease was reproduced in to incomplete organogenesis and body several species of salmonid alevins by development. allowing metabolic wastes to accumu- late or by adding ammonia to the water. VII. Human Health Signifcance However, the condition has also been There are no human health concerns reproduced experimentally in rainbow associated with this condition. and brook trout by infection of eyed eggs with the bacteria Aeromonas hydrophila.

II. Host Species This condition has been reported primarily in salmonid fishes, especially brook trout and other char that tend to be the most susceptible species.

III. Clinical Signs The alevin/fry exhibit an abnormal accumulation of fluid, often bluish in color, at the posterior of the yolk sac often progressing to surround the entire yolk. Due to the increased fluid, fry cannot swim normally. Fry may have ex- ophthalmia, coagulated yolk, and appear smaller and pale. Petechial hemorrhages of the head, thoracic and vitelline blood vessels can occur in severe cases with hemorrhaging into the blue sac fluid and severe anemia.

IV. Transmission In most cases, the disease is due to suboptimal environmental conditions and is not transmissible. However, when poor environmental conditions can be ruled out, transmission of blue sac disease by A. hydrophila becomes a pos- sibility.

102 NON-INFECTIOUS DISEASES

Swollen yolk sacs of cultured lake trout caused by Blue Sac Disease.

103 NON-INFECTIOUS DISEASES Coagulated Yolk Disease (White Spot Disease)

I. Causative Agent and Disease the fish to maintain the replacement of Coagulated yolk disease is a epithelium covering the extremities; the noninfectious condition resulting from fins are the first to be affected but is self- unsatisfactory environmental conditions limiting, commonly observed in young during incubation. A wide variety of Chinook salmon shortly after transfer factors probably contribute towards the from incubators and troughs to rearing disease including gas supersaturation, ponds. unfavorably high water temperatures, heavy metals in the water supply (Cu, IV. Transmission Al, Zn), soft water, low water flows, low This disease is not infectious and dissolved oxygen, exposure to chemicals cannot be transmitted from fish to fish. or contaminants, excessive handling and otherwise inadequate or stressful incu- V. Diagnosis bation conditions. Yolk become Diagnosis is made by observing denatured and coagulate as manifested the abnormal white flecks or masses of by the appearance of white spots in incu- coagulated yolk in eggs, alevins or fry. bating eggs and the yolk sacs of hatched alevins. Yolk resorption is disrupted, VI. Prognosis for Host resulting in defective development of Most fish with coagulated yolk will vital organs. This causes physiological eventually die before reaching 1 gram in alterations in organ functions resulting size due to improper organ development. in death of eggs during incubation or af- Juveniles appear normal then suddenly terwards in alevins and larger juveniles. drop-out.

II. Host Species VII. Human Health Signifcance All fish eggs and alevins are suscep- There are no human health concerns tible. associated with this condition.

III. Clinical Signs White spots or flecks in eggs are typically at the surface of the yolk and randomly distributed. In alevins, the coagulated yolk appears a few days after hatching and may enlarge and coalesce with time. In fry that have completely absorbed the egg sac the coagulated yolk appears as a white mass in the visceral cavity, sometimes associated with clot- ted blood. Pinheading, anemic gills, and white or frayed fins are sometimes observed in affected fry. Non-infectious tail and fin erosion (especially pecto- ral fins) can be caused by unabsorbed coagulated yolk that remains in the body cavity that interferes with the ability of

104

NON-INFECTIOUS DISEASES 

Coagulated yolk (arrow) or white spot in salmonid alevins.

Mass of white coagulated yolk (arrow) extracted from body cavity of a juvenile chum salmon.

105 NON-INFECTIOUS DISEASES Drop-out Disease

I. Causative Agent and Disease II. Host Species Drop-out disease is commonly All salmonids are susceptible, but observed in hatchery reared juvenile the condition is seen most frequently salmonids but is not caused by an infec- in Chinook, coho and chum salmon in tious agent or a deficiency in the diet. Alaska. Affected fish may exhibit gill hyperpla- sia and severely clubbed gills, usually III. Clinical Signs stop feeding and become emaciated or Fish may stop feeding and become pinheaded. Other forms of drop-out are emaciated resulting in thin bodies and not associated with gill hyperplasia. Sec- large heads referred to as pinheading. ondary bacterial, fungal and protozoan Gill hyperplasia, sometimes very severe, infections often develop in affected fish. occurs in many instances but not all as indicated previously. Secondary infec- Drop-out associated gill hyperplasia tions commonly occur adding confusion causes include: to the primary diagnosis. 1. The fine particles in starter feeds irritate delicate gill epithelium. IV. Transmission 2. blooms of con- Since this is not an infectious dis- volutus can cause severe gill abrasion ease, transmission between fish does not in fish that are held in seawater occur. netpens. 3. Repeated therapeutic chemical treat- V. Diagnosis ments for external parasites and Diagnosis of drop-out and its bacteria can irritate gill epithelium. cause depends on whether the fish are pinheaded and have or do not have gill Drop-out NOT associated with gill hyperplasia and have been exposed to hyperplasia - causes include: one or more of the conditions listed. 1. An increase in feed pellet size may prevent a proportion of the smaller VI. Prognosis for Host fish from eating enough to maintain Mortality can be up to 20-30% of the good body weight and they become population or higher in the case of an al- pinheaded. gal bloom. Drop-out from gill hyperpla- 2. White spot or coagulated yolk causing sia can be corrected by removal or avoid- incomplete organ development can ance of the gill irritant(s). Drop-out from result in mortality of seemingly coagulated yolk or not enough yolk are healthy fish during early or later sequellae from preexisting conditions juvenile stages. Fish are not that cannot be changed in the current pinheaded. cohort of fish but could be prevented in 3. Not enough yolk (minimum 3-5% the next production cycle by improving body weight) remaining when alevins conditions or removing fish emerge from incubators. Mechanical earlier. removal may be necessary, especially with chum salmon. VII. Human Health Signifcance There are no human health concerns associated with this condition.

106 NON-INFECTIOUS DISEASES

Severe gill hyperplasia with fusion and clubbing commonly seen in drop-out disease due to irritation caused by feeding starter diets, X 100.

Wet mount of Chaetoceros convolutus diatoms that can cause gill irritation and abrasion, X 400.

107 NON-INFECTIOUS DISEASES Gas Bubble Disease (GBD)

I. Causative Agent and Disease old of 102-103% TDG before chronic Gas bubble disease is not infectious problems develop) while coho salmon and is caused by supersaturated levels of are least sensitive (average threshold total dissolved gas in the water. Lesions 115.7% TDG) in the fish are caused by the accumula- tion of gas bubbles in blood vasculature III. Clinical Signs and tissues. Either supersaturation of Fish with GBD often exhibit loss oxygen or nitrogen can result in the of equilibrium, abnormal buoyancy disease, however, the total dissolved gas and may float at the water surface. Fish (TDG) is more important than individual may also exhibit violent head shaking, gases or varying combined gas ratios. convulsions, flared opercula, release Supersaturation occurs when water of excessive gas from buccal cavity, contains more dissolved gas than it can blindness and may die with the mouth normally hold in solution at a given open. Alevins may show hemorrhage temperature and atmospheric pressure. of vitelline vessels, rupture of yolk- Under high pressure or at low tempera- sac membranes, and coagulated yolk. tures water can contain more gas. Gas Subcutaneous bubbles can accumulate in supersaturation in water can occur from tissues of the head, mouth, fin rays, and both natural and artificial causes. In gill arches. Air bubbles are often visible nature, supersaturation occurs in plunge in gill lamellar capillaries. Hemorrhage pools at the base of waterfalls, in natural of gills, fins, skin, muscle, gonads, and springs and wells where water is under intestinal epithelium can also occur. Fins pressure at depth, and in water that has may be eroded with whitened fin tips melted from glaciers or snow. During and exophthalmia may occur with blood the photosynthetic process water bodies present in the anterior chamber of eye. containing heavy aquatic plant growth can be saturated with oxygen and can TDG become supersaturated upon warming. 100-106% Embolic lesions will appear Artificially supersaturated water occurs with hemostasis in plunge pools from dams, when water ≥ 103% Certain species of salmonid is heated such as power plant effluent, fry are stressed and may and if air is entrained in pipes or pumps later develop conditions where pump pressure or gravity head leading to death (i.e., forces gas into solution. coagulated yolk, fin erosion, tail erosion, etc.) II. Host Species The disease can affect any fish or > 120% Acute levels, fry will invertebrate anywhere when in supersat- die before signs or lesions urated waters. Levels of gas supersatu- indicate a problem ration causing pathological changes or mortality vary for different fish species IV. Transmission and age of fish. Fry become susceptible Due to the environmental nature of post-hatch when they begin swimming this disease, transmission between fish up for food (at about 16 days). Steelhead does not occur. trout are most sensitive (average thresh

108 NON-INFECTIOUS DISEASES

V. Diagnosis waters where gas saturation is lower. Diagnosis is made by the observation There is no evidence that gas supersatu- of typical clinical signs and lesions. The ration adversely affects hatching success presence of gas emboli in capillaries of of salmonid embryos. GBD can be the the gills, fin rays, mouth and eyes are underlying cause of various diseases diagnostic. by predisposing fish to other secondary bacterial, viral or protozoan infections VI. Prognosis for Host that must be differentiated first before Gas bubble disease often results determining the primary problem. in chronic low-level fish mortality, especially in a hatchery environment. VII. Human Health Signifcance In natural waters, fish exposed to high There are no human health concerns TDG’s will seek greater depth or cooler associated with GBD in fish.

Visible gas bubbles in connective tissues of and eye typical of

acute gas bubble disease. 

Left: Gas bubbles (arrow) trapped in capillaries of a gill lamella typical of gas bubble disease; Right: Gas bubbles in and around connective tissue of the mouth.

109 NON-INFECTIOUS DISEASES Mushy Halibut Syndrome

I. Causative Agent and Disease VI. Prognosis for Host Smaller halibut of 15-20 lbs caught Reportedly, the Cook Inlet and Hom- by sportfishing charters near Homer er/Seward areas are nursery grounds and Soldotna, AK have had a condi- for large numbers of young halibut that tion locally known as “mushy halibut”. feed primarily on forage fish that have Typically, this condition consists of fish recently declined in numbers. Stomach having large areas of body muscle that contents of smaller halibut now contain is abnormally translucent and flaccid or mostly small species. Whether this jellylike. The overall body condition of forage is deficient, either in quantity or these fish is usually poor and often they in essential nutrients is not known. How- are released because of the potential for ever, mushy halibut syndrome is similar inferior quality. to that described for higher animals with nutritional deficiencies in E and II. Host Species . This muscle atrophy would Smaller Pacific halibut, mostly in further limit the ability of halibut to the Cook Inlet and Homer/Seward areas capture prey possibly leading to further but affected fish in other areas of Alaska malnutrition and increased severity of have been reported. the primary nutritional deficiency.

III. Clinical Signs VII. Human Health Signifcance Fish are asymptomatic except for Although aesthetically displeasing, poor body condition. Large areas of the there are no known human health con- fillets are abnormally translucent and cerns with mushy halibut syndrome. flaccid in texture. NOTE: mushy halibut is not to be IV. Transmission confused with chalky halibut, a condi- No infectious agents or parasites tion of opaque flesh with a cooked-like have been detected in affected fish, texture. Chalkiness is another flesh therefore, transmission from fish to fish quality problem caused by the buildup of is not likely. A nutritional deficiency is excessive lactic acid from overexertion suspected. of fish fighting capture for several hours on longline gear. V. Diagnosis Diagnosis is by gross observation of flaccid, translucent musculature with confirmation of a non-infectious degenerative myopathy by histological examination. There is severe muscle fiber atrophy, fragmentation and necrosis with loss of muscle mass. There may be accompanying inflammatory cells, fibro- sis and calcification of atrophied fibers. There is some attempt at regeneration as evidenced by internal nuclear chains within myofibers.

110 NON-INFECTIOUS DISEASES

Flaccid, glistening, translucent fesh typical of mushy halibut syndrome.  

Left: Skeletal muscle fber atrophy with fragmentation (arrow) necrosis and loss of muscle mass (empty spaces); Right: Early calcifcation (arrow) of atrophied muscle fbers.

Atrophied muscle fbers with fbrosis and infltration of infammatory cells (arrow).

111 NON-INFECTIOUS DISEASES Neoplasia (Tumors)

I. Causative Agent and Disease transmission does not occur. Generally, Tumors or neoplasms are tissue neoplastic growths are spontaneous growths of abnormal cells that prolifer- within an individual due to congenital ate uncontrollably. In bony fishes, neo- malformation, age or genetic predisposi- plasms of the connective tissues, such tion but could also be caused by environ- as fibroma and fibrosarcoma, are most mental conditions. common. Fish develop neoplasia or can- cer in much the same way as do higher V. Diagnosis/Classifcation animals. Known and suspected factors Definitive diagnosis is made by contributing to neoplasia in fish include observing the abnormal cells using his- viruses, environmental chemicals topathological methods. Neoplasms are (carcinogens), repeated physical trauma, classified according to the cell or tissue hormones, age, sex, genetic predisposi- of origin and are further grouped based tion and immunological competence of on benign or malignant characteristics. the host. Benign tumors are often well-differen- tiated, grow slowly, are well circum- II. Host Species scribed without invading surrounding normal tissue and do not metastasize. All fishes in any part of the Most benign neoplasms are not usually world could potentially develop neopla- life threatening and often end in the sia. For unknown reasons cancer has suffix “oma”. Exceptions are benign neo- been rare in cartilaginous fishes such as plasms of the brain and some endocrine and rays. organs that can be life threatening due to their location and deleterious physiologi- III. Clinical Signs cal effects on the host. Malignant tumors Neoplasms usually become apparent are often not well differentiated, may by gross observation of an external or grow rapidly, infiltrate normal tissues internal swelling, lump, or formation of and tend to metastasize. The names of an abnormal tissue growth. these neoplasms are often preceded by the word “malignant” or with the suf- IV. Transmission fixes “sarcoma” or “carcinoma”. Types Except for neoplasia caused by of cancer in fish include the following: infectious viruses, horizontal fish to fish

TISSUE TYPE BENIGN TUMORS MALIGNANT TUMORS epithelial papilloma epithelial carcinoma adenoma adenocarcinoma mesenchymal fibroma – connective tissue fibrosarcoma leiomyoma – smooth muscle leiomyosarcoma rhabdomyoma – striated muscle rhabdomyosarcoma lipoma – fat liposarcoma chondroma – cartilage chondrosarcoma osteoma – bone osteosarcoma hematopoietic lymphoma lymphosarcoma blood vessels hemangioma hemangiosarcoma neural – nerve cell schwannoma glioma, astrocytoma pigment erythrophoroma malignant melanoma embryonal nephroblastoma -

112 NON-INFECTIOUS DISEASES

VI. Prognosis for Host VII. Human Health Signifcance Prognosis for fish having neoplasms Although aesthetically disturb- depends on the type of tumor and ing, there are no direct human health whether the lesion is benign or malig- concerns associated with neoplasia in nant. Benign tumors are usually not fish. Neoplasia is generally a rare event life threatening. Malignant tumors can affecting one fish in several thousand. cause mortality if growth is rapid and Should tumors occur more frequently in interferes with normal organ functions. a population of fish, an indirect human health concern would be whether the cause is linked to environmental con- tamination.

Fibroma, on right dorsal anterior fank of a sockeye salmon.

Liposarcoma on the abdomen of a whitefsh.

113 NON-INFECTIOUS DISEASES 

Left: Cut surface of a liposarcoma on the back of a quillback rockfsh; Right: Thymic lymphosarcoma (arrow) in branchial cavity of a sockeye salmon.

Left: Fibrosarcoma (arrow) infltrating the muscle tissue from the body wall in a salmon; Right: Pedunculated papilloma on the back of a coho salmon.

Left: Rhabdomyosarcoma (green) in the musculature of a Pacifc halibut; Right: Black melanoma on the head of a chum salmon; Inset: Sockeye: when cut, melanomas can exude a black tarry fuid containing melanin pigment that stains surfaces, (photo: Scott Albert).

114

NON-INFECTIOUS DISEASES 

Left: Ameloblastoma from odontogenic epithelium of teeth in king salmon causing thickened maxillaries (arrow); Right: Fibrosarcoma in left posterior body wall of sockeye salmon.

Left: Multifocal dermal fbrosarcoma in skin of pink salmon; Right: Prickle cell carcinoma of the epidermis in a sablefsh.

Left: Fibrosarcoma of the skin in a sheefsh; Right: Unidentifed reddish neoplasm in anal area of a northern pike heavily infested with leeches.

115 NON-INFECTIOUS DISEASES Organ and Tissue Anomalies

I. Causative Agent and Disease cartilage with displacement of angular Developmental anomalies that are bone from possible phosphorous imbal- not caused by infectious disease or ance resulting in a permanently fixed pollution are occasionally observed wide open mouth with flared opercula. in salmonids and other fish species. Gill respiration requires swimming These anomalies (coagulated yolk, blue continuously (ram ventilation); Fibrous sac disease and pigment aberrations osteodystrophy in Arctic char and discussed in other specific sections) may rainbow trout cultured at one hatchery in result from genetic or congenital defects Alaska results from incomplete morpho- and/or suboptimal environmental or genesis of dermal bones in the sensory water quality conditions during early life cranial canals and . This stages that cause abnormal development causes tissue separation and replace- of various organs and tissues. ment with fibrous connective tissue. The condition is associated with recirculation II. Host Species of well water and suspected imbalance All wild and cultured fish species are of calcium and phosphorous due to the susceptible to developmental anomalies chemistry of the water supply. Affected worldwide. These disorders are more fish show lower Ca:P serum concentra- easily observed in fish species that are tions, but further study is ongoing to cultured on a large scale such as salmon confirm the cause. and trout. IV. Transmission III. Clinical Signs These anomalies have no infec- Some of the more common defor- tious causes and cannot be transmitted. mities observed in Alaskan salmonid However, excluding those defects that aquaculture occur in fry and fingerlings are strictly congenital, some of the other including malformations such as: sia- conditions are likely caused by subopti- mese twinning; microphthalmia (small mal environmental and/or water quality eye) or anophthalmia (missing eye); variables during early development that spinal curvatures; vertebral compres- might be corrected in a hatchery facility sion and fusion (sunfish and humped to prevent deformity occurrence. back); pughead (hypoplasia of upper jaw); and shortened opercula (exposed V. Diagnosis gills). Three other deformities require Diagnosis is based on observation of further explanation: Double mouth the specific deformity and any other as- results from displacement of the lower sociated characteristics that may require end of the hyoid arch downwards and histological examination. backwards through the gap in the mouth floor. Trapped air from an obstructed VI. Prognosis for Host pneumatic duct and/or mechanical injury Some of these anomalies may be damages muscles in the jaw so that fatal and prevent fish from reaching the retractor muscles, left unopposed, maturity and/or predispose them to early pull the lower end of the arch into the de- death by predation. formed position; Mandibular ankylosis is an incomplete ossification of Meckel’s

116 NON-INFECTIOUS DISEASES

VII. Human Health Signifcance There are no human health concerns associated with these developmental anomalies in fish from unpolluted wa- ters.

Left: Eye deformity (sunken, darkened eyeball) in sockeye salmon; Inset: Eye dissected demonstrates concave center; Center: Siamese twins and curled spine in

juvenile sockeye salmon; Right: Sablefsh with spinal deformity (kyphosis and scoliosis). 

   Left: Double mouth deformity in juvenile coho salmon- displaced hyoid arch (arrow) below mouth (photo: SSRAA staf); Center: Mandibular ankylosis (fxed gaping mouth) in adult sockeye salmon; Right: Fibrous osteodystrophy in Arctic char; note the fbrous separation of the sensory canals in the cranium and lateral line (arrows).

117 NON-INFECTIOUS DISEASES Pigment Aberrations in Fish

I. Causative Agent and Disease III. Clinical Signs Pigment aberrations of flesh, oc- Aberrant external pigmentation in casionally observed in salmonids and fish is generally confined to the epider- other fish species, are not caused by any mis. Complete albinos have no melanin known infectious agents. In unpolluted pigment within any tissue. Marbled or waters, the abnormal pigmentation is completely white-fleshed Chinook or often due to genetic or congenital defects other salmon require observation of fil- resulting in abnormal overall body leted skeletal muscle. color or localized epidermal discolor- ation, most often yellow in salmonids. IV. Transmission Other abnormal pigmentation occurs Aberrant pigmentation has no infec- in Chinook salmon where the skeletal tious cause and cannot be transmitted. muscle is white rather than orange due Coloration is most likely due to pigments to a genetic inability to retain carotenoid obtained from food consumed, the pigments from consumed prey. Partial or natural environment or is hereditary complete albinism may also cause yel- allowing parent fish to pass the trait on low/green to white body color. Certain to some of their offspring, as is the case prey species and natural plant materials for some stocks of “white” king salmon. in the environment can influence body Albinism is caused by a genetic defect in color, as observed in the blue-green flesh tyrosinase that metabolizes tyrosine to of lingcod inhabiting kelp forests. Indus- the black pigment melanin. trial pollution also affected flesh color of Atlantic salmon in Scotland causing a V. Diagnosis yellow/orange to red pigmentation from Diagnosis is based on the observa- exposure to paper mill effluent. This tion of uncomplicated aberrant pigmen- caused hemolytic anemia and hyper- tation. Yellow pigmentation extending bilirubinemia resulting in jaundice, into the internal body fat suggests jaun- both externally and within the internal dice that is symptomatic of a systemic mesenteric fat. disease process that is not related to uncomplicated pigment aberration. II. Host Species In Alaska, albinism is common in VI. Prognosis for Host cultured chum salmon fry while adult Abnormal pigmentation from natural white king salmon occur occasionally food and plant materials or hereditary or frequently, depending on the fish defects causes no physical harm to stock. Varying degrees of white and red affected fish except that the unnatural skeletal muscle can produce a marbled coloration may be more conspicuous to appearance. White flesh also occurs in predators. sockeye and coho salmon while yellow pigmented epidermis occurs in cutthroat VII. Human Health Signifcance trout, Chinook salmon, pink salmon There are no human health concerns and most frequently in sockeye salmon. associated with uncomplicated aberrant Other aberrations include epidermal yel- pigmentation in fish from unpolluted low/green marbling in pink salmon, pink waters. flesh in halibut and pike, and blue-green pigmentation in lingcod.

118 NON-INFECTIOUS DISEASES

Left: Marbled white fesh of sockeye salmon; Center: Marbled white-feshed coho salmon compared to normal red on right; Right: Blue-green pigmented lingcod.

Left: Yellow pigmented sockeye salmon; Center: Yellow pigmented ventral foci on cutthroat trout; Right: Yellow pigmented area in the epidermis of a Chinook salmon.

Left: Pink feshed halibut; Center: Pink feshed northern pike; Right: Yellow-green marbled epidermis of pink salmon likely due to partial albinism.

119 NON-INFECTIOUS DISEASES Sunburn (Back-Peel)

I. Causative Agent and Disease V. Diagnosis Sunburn is a non-infectious disease Sunburn is diagnosed by the obser- in cultured fish caused by overexposure vation of typical lesions with a history of to ultraviolet radiation (UV) from sun- lengthy exposure to sunlight. light. Certain diet ingredients causing photosensitization can be predisposing VI. Prognosis for Host factors. Sunburn is most commonly ob- When the lesions are uncomplicated served during the summer months in the by secondary infections of bacteria or northern latitudes when hatchery fish are fungi, the mortality is generally quite moved from an indoor rearing container low. If shade is provided, healing of the to shallow outside units with very clear lesions is rapid with complete recovery. water. Wild fish in shallow lakes and rivers could be potentially susceptible VII. Human Health Signifcance except they rarely remain in direct sun- There are no human health concerns light long enough for overexposure. associated with sunburn in fish.

II. Host Species Sunburn is observed almost exclu- sively in cultured salmonids exposed for long periods to direct sunlight. Other fish species with small delicate scales, partial scaling or no scales at all would also be particularly susceptible.

III. Clinical Signs Lesions from sunburn are first recognized by a darkening of the skin between the head and the . The epidermal layer turns white and eventually sloughs off. The underlying dermal layer of skin becomes exposed and eventually a white, craterous lesion forms. This lesion can begin with the dorsal fin that first becomes whitened and then erodes to the body surface. Any lesion from sunburn is very likely to become infected with opportunistic bacteria, water molds or fungi.

IV. Transmission Since sunburn is an environmentally mediated disease, transmission between fish does not occur.

120 NON-INFECTIOUS DISEASES

Sunburn lesion on dorsal surface of coho salmon with secondary infection by Saprolegnia water mold.

Sunburn lesion (arrow) eroding dorsal fn of a juvenile cultured Chinook salmon.

121 REFERENCE Glossary of Terms

Acanthocephalans – a phylum of spiny the base of the caudal fin. headed worms, these parasites require two hosts for completion of the life cycle Cercariae – infectious larvae of digene- and are most commonly found in the in- ans usually released from the gastropod testines of fish. first intermediate host.

Acid-fast – a physical property of some Cestode – a tapeworm with a modified bacteria that are resistant to decoloriza- head segment or scolex used for attach- tion by acids during the staining proce- ment, usually in the gut. Tapeworms dure. generally require three hosts for develop- ment. Alevin – a newly hatched fish still with yolk sac attached. Copepod – small planktonic crustaceans which are an important part of the aquatic Anadromous – relating to fish, such as food chain. Some are parasitic. salmon, that migrate up rivers from the sea to in freshwater. Coracidium – the ciliated first stage of an aquatic cestode hatched from an egg that, Anemia – deficiency of red blood cells when ingested, infects the first intermedi- and/or hemoglobin. ate host, typically a crustacean.

Arthropod – belonging to the phylum CPE (Cytopathic Efect) – damage to cul- Arthropoda, an insect or crustacean that tured cells caused by virus infection. has a cuticle made of chitin forming an exoskeleton with segments and jointed Crustacean – an having a appendages. segmented body and jointed appendages with two pairs of antennae at some stage Ascites – the presence of fluid in the ab- in their life cycle. dominal cavity. Cyprinid – a fish of the Cyprinidae family Bacteria – any of a large group of uni- consisting of , shiners and minnows. cellular prokaryotic organisms that lack a cell nucleus, reproduce by fission or by Cyst – a capsule of connective tissue forming spores, and in some cases cause formed by the host around a foreign body, disease. such as a parasite, that acts as an irritant.

Basophilic – tissue components having Cytoplasm – the fluid-like substance that an affinity for dye under basic pH condi- fills the cell, consisting of cytosol and or- tions that stain blue (as in histology). ganelles excluding the nucleus.

Buccal cavity – cavity inside the mouth Diplobacilli – paired rod-shaped bacte- anterior to the gill arches. rial cells.

Caudal peduncle – the region of the fish DNA – deoxyribonucleic acid containing body between the end of the anal fin and the genetic information for the reproduc-

122 REFERENCE

tion, development and function of living Exophthalmia (popeye) – abnormal pro- organisms including some viruses. trusion of the eyeball, often from fluid imbalance. Electron microscopy – use of an electron microscope that generates an electron Explant culture – tissue that is placed in beam focused through a series of mag- a culture medium for either growth of the netic lenses to create an enlarged image tissue cells or growth of an organism con- of ultrastructural details at thousands of tained in the tissues. times higher magnification than a stan- dard light microscope. Extracellular – outside the cell.

ELISA – enzyme-linked immunosorbent Fibrotic nodules – focal areas of excess assay is an antigen/antibody reaction fibrous tissue formed as a reparative pro- coupled with an enzyme substrate that cess or as a reaction to a foreign body. produces a color change measured in a spectrophotometer. The test is used to Final host (defnitive host) – the host in detect the presence of a target organism which a parasite develops into an adult antigen or an antibody directed towards a form to reproduce. target organism. Fluorescent antibody test (FAT) – a test Encyst – to enclose in a cyst. using antibody against a specific patho- gen or primary antibody that is conjugat- Endoparasitic – a parasite that lives ed with a fluorescein dye. The conjugated within the body of another organism rath- antibody sticks to the target organism er than on the surface. causing fluorescence when viewed with a fluorescent microscope. Eosinophilic – a red color of cells or tis- sues in histological sections or smears Fungi – heterotrophic organisms (with that have been stained with eosin dye. chitinous cell walls) that form spores pro- ducing hyphae which penetrate dead or Epibiont – an organism that uses the living material to obtain nutrients. body surface of another as a substrate but takes no nourishment or other benefit. Furuncle – boil like lesion in the muscu- lature. Epithelium – one or more layers of spe- cialized cells forming the covering of Gill Lamellae – gill filaments bear many most internal and external surfaces of the branches known as lamellae covered by body and its organs. a single layer of epithelium and each containing a blood capillary. Lamellae Epizootics – an outbreak of a disease increase the surface area of the gill fila- in an animal population or an unusually ments to enhance respiration and gas ex- large increase in prevalence and/or inten- change from ambient water. sity of a parasite. Gram-negative rod – a rod-shaped bac- Erythema – an abnormal red color of the terium that does not retain the crystal vio- skin or other tissues caused by capillary let in the Gram stain, but is stained by the congestion. pink safranin counter stain.

Erythrocyte – red blood cell. Gram-positive rod – a rod-shaped bac-

123 REFERENCE

terium that retains the crystal violet in the Lethargy – a state of sluggishness or in- Gram stain and is dark purple in color. activity.

Granuloma – a chronic focal inflamma- Macrophage – a large host white blood tory lesion that walls off a foreign body cell occurring in tissues and in peripheral and usually consists of different types of blood that ingests foreign particles and host inflammatory cells and fibroblastic infectious microorganisms by phagocy- connective tissue. tosis.

Hemagglutinate – the clumping together Melanocytes – an epidermal cell of neu- of red blood cells. ral crest origin capable of synthesizing the black pigment melanin. Hemorrhage – occurrence of blood with- in the tissues outside the normal vascular Metacercariae – a developmental stage channels. from encysted cercariae of digenean trematodes generally occurring in a sec- Hemostasis – the ability of an organism ond intermediate host. or cell to maintain internal equilibrium by adjusting its physiological processes. Micropyle – the tiny opening in an egg through which a spermatozoon can enter Hemotocrits – the packed cell volume of for fertilization. erythrocytes in whole blood expressed as a percentage. Miracidium – the ciliated larval stage of a digenean trematode hatching from the Histological (histology) – the micro- egg which infests the first intermediate scopic anatomy of cells and tissues as host, usually a snail. viewed in thin stained sections on glass slides. Mycosis – fungal infection.

Hyperplasia – an increase in the growth Myopathy – a degenerative disease of of cell numbers of a tissue or organ that muscle. may or may not increase its overall size; usually stimulated by an irritant. Necropsy – a postmortem examination of an animal. Hyphae – long branching vegetative fila- ments of a fungus or certain molds. Nematode – unsegmented worm of the phylum Nematoda, having an elongated, Infammation – a host response to tissue cylindrical body; a roundworm. damage or irritation comprised of swell- ing, redness, heat (in warm blooded ani- Neoplasms/neoplasia – cancer caused mals), pain, sometimes causing dysfunc- by uncontrolled abnormal growth of tis- tion of the tissues and organs involved. sue cells.

Intermediate host – a host in which there Operculum – the flap on either side cov- is development of the asexual or imma- ering the gill chamber in bony fishes. ture stage of a parasite. Opisthaptor – a posterior attachment or- Intracellular – inside the cell. gan in monogenean flukes.

124 REFERENCE

Organogenesis – the process where the ond intermediate fish host. embryonal ectoderm, mesoderm and en- doderm differentiate and develop into the Poikilothermic – animals with internal internal organs of the juvenile and adult body temperatures that cannot be self- fish. regulated, often determined by the ambi- ent temperature of the environment; cold- Parasite – an organism that lives on or blooded. within another organism at whose ex- pense it obtains some advantage. Proboscis – any of various elongate feed- ing, defensive, attachment or sensory or- Paratenic host – an additional or option- gans of the oral region, found in certain al intermediate host in which no develop- leeches and worms. ment of the parasite occurs but is a host which may serve as an essential link in Procercoid – the solid first parasitic larva the completion of the parasite’s life cycle. of some tapeworms that develops usually in the body cavity of a copepod. Pathogen – an infectious agent that can cause disease. Prognosis – a prediction of how a disease will progress, and the chance for recov- PCR (Polymerase Chain Reaction) – ery. amplification of targeted lengths of RNA or DNA by repeated thermal cycling reac- Protozoan – any of a large group of sin- tions using polymerase enzyme. gle-celled, usually microscopic, eukary- otic organisms, such as , ciliates, Pericardium – the membrane surround- , and some molds. ing the heart. Pycnidia – an asexual structure contain- Peritonitis – inflammation of the lining ing conidia, found in certain fungi. of the abdominal cavity (peritoneum). RNA – ribonucleic acid; the nucleic acid Petechial hemorrhage – a small focal or that is used in key metabolic processes for pinpoint hemorrhage. all steps of synthesis in all living cells and carries the genetic information Pinheading – young fish that exhibit an for many viruses. emaciated body from poor feeding re- sponse producing the appearance of an Salmonid – belonging or pertaining to enlarged head. the family including salmon, trout, char, and whitefishes. Piscivorous – fish eating. Scolex – the head segment of a cestode Plaque Forming Unit (PFU) – number of that attaches to its host. infectious virus particles per unit volume based on the number of holes or plaques Scoliosis – lateral deviation in the nor- in the monolayer of the infected cell cul- mally straight line of the spine. ture. Septate – divided by crosswalls or septa. Plerocercoid – the third larval stage of cestodes parasitizing fish that have an ob- Septicemia – presence of bacteria in the vious scolex. Generally found in the sec- blood.

125 REFERENCE

Sequencing – techniques used to deter- Trematodes – worms with a characteris- mine the nucleotide sequence of RNA or tic flattened oval to elongated shape hav- DNA in the of an organism or ing oral and ventral suckers and a com- virus to help obtain a taxonomic identi- plex (digenetic) life cycle involving two or fication. three hosts.

Serotype – a unique antigenic property of Virulence – the pathogenicity or ability a bacterial cell or virus identified by sero- of an infectious agent to produce disease. logical methods. Virus – a very small infectious agent Sporangia – a single or many celled composed of a nucleic acid core (RNA or structure from which spores or zoospores DNA) surrounded by a protein coat that are produced in a fungus or mold. replicates only within living host cells.

Spore – a reproductive structure that is Viscera – internal organs of an animal. adapted for dispersion and survival for extended periods of time in unfavorable Vitelline – relating to or associated with conditions. the yolk of an egg.

Teleost –the group of fishes with a bony skeleton.

126 REFERENCE Fish Disease References

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