Fish & Invertebrate Respiratory

Question 1

What are the different modes of respiration in terrestrial versus aquatic invertebrates?

Answer 1

Terrestrial arthropods – book lungs, tracheae.

Aquatic inverts – gills, cutaneous respiration.

Reference: Mitchell & Tully Chapter 3: Respiration

Question 2

What is the functional unit of respiration in arachnids and insects?

Answer 2

Book lungs.

Reference: M&T CTEPP Ch3 - Respiration

Question 3

Describe the anatomy of the respiratory system of arachnids & spiders.

Answer 3

Book lungs ventral in anterior opisthoma (abdomen).

Entrance to lungs communicates with outside by enveloped atrium through the lung slit (spiracle).

• Extends into many horizontal air sac pockets with hemolymph-filled lamellae.
• Series of flattened air-filled cuticular plates, where diffusive gas exchange occurs with hemolymph.

Tracheal system – network of branching tubes of decreasing size, directly contact tissues in their terminal stages by means of specialized epidermal cells (tracheoblasts).

• Insects – tracheae composed of epithelial cells, inward spiral cuticular layer (taenidia).
• Tracheae branch and taper, give rise to tracheoles lined by tracheoblasts that transfer O2 to mitochondria.
• Arachnids may have both tracheal system and book lungs.

Tracheoles – site of gas exchange, where oxygen is supplied faster vs book lungs.

• Gas enters tracheal system by way of spiracles on thorax and abdomen, may possess filters or muscular flaps for closing.
• Many insects retain tracheoles between moults.
• O2 transport by passive diffusion.
• Larger insects – pump mechanisms i.e. flight muscles, thoracic pumping, abdominal pumping, hemolymph engorgement ay assist with ventilation.

Reference: M&T CTEPP Ch 3 - Respiration

Question 4

What is the oxygen transport pigment of invertebrates?

How does is differ from the pigments of vertebrates?

Answer 4

Hemocyanin – most common O2-carrying pigment of hemolymph.

• Copper-based pigment.
• Higher O2 affinity vs hemoglobin.
• Functions more in O2 storage vs transportation.

Reference: M&T CTEPP Ch3 - Respiration

Question 5

What is the functional unit of respiration in molluscs?

Answer 5

Most have true gills also known as ctenidia

Others have lost these and rely on secondary derived gills or gas exchange across the mantle of body surface

Reference: M&T CTEPP Ch3 - Respiration

Question 6

What is the role of the mantle in mollusc respiration?

Answer 6

Mantle secondary constituent of respiration for O2 exchange.

• Also functions in shell deposition, particle collection, retention, sorting.
• In gravid bivalves, space occupation may affect O2 consumption and respiration.

In terrestrial species, mantle cavity functions as primitive lung.

• Modified into sac-like structure with increased vasculature and pneumostome (opening).
• Respiratory network of blood sinuses responsible for air exchange.

Question 7

What are the respiratory structures of crustaceans?

Answer 7

Gills in most species - vascularized lamellae for respiration and waste removal

Crabs, fewer gills with less gill surface area, especially in terrestrial spp.

• Some crab gills in branchial chamber, formed between thoracic body wall and inner surface of carapace.
• Resp exchange can occur secondarily within the chamber.
• If ventilation stops, there is a subsequent cessation of the heartbeat after which the gill filaments rapidly become deoxygenated, allowing O2 to diffuse out of the hemolymph into the environment.

Question 8

What is a primary cause of respiratory dissease in tarantulas?

Answer 8

Oral pangrolaimid nematodes can occluse book lungs

Reference: M&T CTEPP Ch. 3 - Respiration

Question 9

What flatworm species lays eggs exclusively on the gill lamellae of horseshoe crabs?

Answer 9

Bdelloura candida

Reference: M&T CTEPP Ch 3 - Respiration

Question 10

How does oxygen availibility differ in water than in air?

Answer 10

Lower oxygen concentrations - water is more dense and oxygen dissolves poorly. Even worse in tropical waters. Fish generally have lower oxygen requirements.

Reference: M&T CTEPP Ch 3 - Respiration

Question 11

What is the functional respiratory unit in fish?

How does it differ across taxa?

Answer 11

• All fish primarily use gills for gas exchange.
  
  • Variety of accessory respiratory organs i.e. skin, air-breathing organs.
  • Gills also for osmoregulation, acid-base balance, nitrogenous waste excretion.
  • Most fish larvae use passive diffusion and cutaneous respiration.
• Actinopterygii - Gill arches, two opercula over gills, buccal cavity.
• Chondropterygii – no opercula, gill slits (5-7 in elasmos).
  
  • Spiracle –hole caudal to eyes for entry of water, reduced in pelagic sharks.
• Agnatha – 7 gill slits.

Reference: M&T CTEPP Ch 3 Respiration

Question 12

Describe the structure of fish gills.

Answer 12

• Each gill arch composed of skeleton (hyoid bones) aka gill septum.
  
  • Comprised of connective tissue, gill rakers prevent food particles from entering opercular chamber.
  • Each gill septum supports two hemibranchs.
    
    • Series of filaments, together form a holobranch.
    • Space between gill septae – gill pouches.
    • Abductor and adductor muscle son gill arches regulate opening of gill pouches.
  • Hemibranchs fused in elasmobranchs.
    
    • Additional hemibranch is present on anterior side of the first branchial slit.
    • Number of filaments per hemibranch differs depending on spp.
  • Tips of hemibranchial filaments in close proximity in teleosts, maximizing area of water flow across their surface.
  • Cartilaginous rod provides mech support to filaments.
  • Secondary lemallae – site of gas exchange.
    
    • Afferent and efferent arteries adjacent to filament nerve.
    • Lamellae are plate-like, project at right angles from filaments.
    • Direction of lamellar blood flow is counter current to the direction of water – counter-current gas exchange system.

Reference: M&T CTEPP Ch 3 - Respiration

Question 13

What is the site of gas exchange in fish?

Answer 13

Secondary lemallae – site of gas exchange.

• Afferent and efferent arteries adjacent to filament nerve.
• Lamellae are plate-like, project at right angles from filaments.
• Direction of lamellar blood flow is counter current to the direction of water – counter-current gas exchange system.

Reference: M&T CTEPP Ch 3 - Respiration

Question 14

What epithelial cells are present on the lamellae of fish gills?

Answer 14

• 7 types of epithelial cells from lamellae.
  
  • Pavement cells (barrier).
  • Ionocytes (ion transporting cells aka chloride cells).
  • Goblet cells (mucus producing).
  • Neuroepithelial cells (chemoreceptor cells).
  • Taste cells (absent from filaments and lamellae).
  • Undifferentiated cells.
  • Interstitial cells.

Reference: M&T CTEPP Ch 3 - Respiration

Question 15

Describe the vasculature of fish gills.

Answer 15

• Two arteries on gill arches supply the filamental arterioles and lamellar capillary network.
  
  • Afferent branchial artery contains deoxygenated blood.
  • Efferent branchial artery contains oxygenated blood, passes across the lamellar cross-current exchange surface area.
  • These two integrate into systemic arterial circulation via dorsal arota.
• Two other vascular networks in gill filaments.
  
  • Nutrient and interlamellar vascular networks perfuse nonlamellar portion of the branchial filaments.
    
    • Branchial veins collect blood from nutrient arteries of nutrient vascular network, arises from branchial arteries.
    • Branchial veins flow into jugular or anterior cardinal veins.
    • Function of interlamellar vascular network unknown.

Reference: M&T CTEPP Ch 3 - Respiration

Question 16

Describe the phases and drivers of ventilation in fish.

Answer 16

• Pump action (buccal pump) and opercular cavity.
• Ventilation unidirectional, two phases.
  
  • First phase – increasing volume of buccal and opercular cavities draws water in.
  • Second phase – closing of mouth, opening opercular and contracting both cavities in order to direct water through gills and operculum.
• Water also flows completely or partially through spiracles in elasmobranchs.
  
  • Some pelagic spp i.e. tuna, sharks – ram ventilation.
    
    • Water flows through mouth and gills during swimming.
• Oxygen is main stimulus in triggering ventilator changes.
  
  • CO2, pH also effect ventilation.
  • Oxygen demands override acid-base disturbances in fish.

Reference: M&T CTEPP Ch 3 - Respiration

Question 17

Describe the various air breathing mechanisms in fish.

Give some species examples.

Answer 17

• Bettas, gouramis, plecos, etc.
• Air-breathing organs varied in form, function, effectiveness.
  
  • Three groups depending on body location – organs assoc with skin, structures located on head or along GIT, and lung and resp bladder structures.
• Skin – amphibious fish, catfish.
• Gills; simple but specialized resp epithelia in buccal, pharyngeal, branchial, opercular areas; specialized chambers in roof of pharynx, specialized structures derived from gills or operculum i.e. labyrinth; intestinal organs i.e. esophagus, pneumatic duct, stomach, intestines.
• Primitive lungs and swim bladder use.
  
  • Lungfish obligatory air breathers with modified swim bladders
    
    • Vascular system of most fish (except lungfish) organized with all organs in serial order.
      
      • Potential for loss of O2 obtained through air-breathing organs when partially oxygenated blood is draining through the gills in poorly oxygenated water.
    • Gill exchange surface area is reduced in most species possessing well-developed air-breathing organs.
• Ventilation in air-breathing fish usually achieved by buccal pump.
  
  • Air gulped from surface and forced into corresponding organ.
  • Inhalation and exhalation may be complex.
  • Ventilator control more complex than O2-driven system of exclusively water-breathing fish.

Reference: M&T CTEPP Ch 3 - Respiration, Smith FD

Question 18

What is the primary function of the swim bladder?

What species lack a swim bladder?

What is the air in the swim bladder composed of? Any species that don’t have air in there?

What are the two main types of swim bladder?

List four groups of fish for each type.

Answer 18

Buoyancy Organs

• Swim (gas) bladder - extensive spp. variations
• 1º function - buoyancy; but also sound production, pressure reception
• Absent in cartilaginous fish, some bottom-dwelling teleosts, weather loaches, some highly pelagic teleosts
• Filled w/ oil or fat in some bathypelagic spp. (laternfish, orange roughy)
• Volume to BW typically <5% in SW and <7% in FW
• Gas composed of CO₂, O₂, N - not in same %s as air
• Types of swim bladders -
  
  • Physostomous - pneumatic duct connect swim bladder to esophagus; gas maintained by swallowing air (FB or gavaged food can enter swim bladder); some have rete mirabile for some gas absorption
    
    • Salmon, trout, catfish, koi, goldfish, tetras
  • Physoclistous - lack connecting duct; inflation via blood gases diffusion along one or more rete mirabile (gas glands) or vessels (typ. cranial and ventral); some also have capillary plexus caudodorsally (oval or oval window) to help resorb gases
    
    • Most marine teleosts, cichlids, bass, sunfish
• Must know normal swim bladder appearance d/t species differences
  
  • Abnormalities - hyperinflation, hypoinflation, displacement, fluid, parasites
  • One lobe - most common - may be U-shaped (some pufferfish)
  • Two lobes in several spp. (goldfish, carp, koi - some goldfish breeds lost Cd. lobe)
  • Three lobes - cod, channel catfish, some pufferfish
  • Extension common - may connect to inner ear (herring, anchovies), extend into vertebrae (FW angelfish), extend down the tail (electric eel, arowana)
  • May be modified into lungs/lung-like tissues (garfish, tarpon, arapaima, lungfish)

Swim bladder.

• Phystostomous type – pneumatic duct connected to caudal end of esophagus
• Physoclistous type – no connection, other fish.
  
  • O2 secreted by gas gland into swim bladder, constitutes 80% swim bladder gas.
  • SB may also store oxygen in some spp.
• Transitional type - Eels have ductus pneumaticus and a gas gland
• Flatfish only have swim bladders during larval stages

Question 19

What fish species have physostomous swim bladders?

What fish species have physoclistous swim bladders?

Answer 19

• Found in most ganoid fish (gar, sturgeon, bowfin), lungfish (dipnoans), and early teleosts
  
  • Early Teleosts Include:
    
    • Clupeiformes (herring/anchovies)
    • Gonorynchiformes (milkfish)
    • Cypriniformes (carp, minnows, loaches)
    • Characiformes (characins – tetras, piranhas)
    • Gymnotiformes (knifefish)
    • Siluriformes (catfish)
    • Lepidogalaxiiformes (salamanderfish)
    • Esociformes (pike & mudminnows)
    • Salmoniformes (salmon, trout, chars, graylings, whitefish)

All teleosts evolutionarily beyond salmoniformes have physoclistous swim bladders

Question 20

What are the funcitons of the swim bladder?

Answer 20

• Adjustable float
• Maintains center of gravity
• Respiration
• Resonator through

Question 21

What causes low dissolved oxygen in water?

Are there any species of fish that are better at tolerating hypoxia?

Answer 21

• O2 solubility decreases with salinity and in warmer water (summer ponds).
• Low surface exchange with insufficient circulation, limited photosynthetic organisms, high stocking densities, inadequate water quality all contribute.
• Formalin also reduces Do.
• Tolerance to hypoxia spp specific; goldfish are more resistant

Reference: M&T CTEPP Ch 3 - Respiratory, Smith FD - Respiratory

Question 22

What changes to the gills result from ammonia toxicity?

Answer 22

Hyperplasia and hypertrophy

Reference: M&T CTEPP Ch3, Smith FD - Respiratory

Question 23

What is the appearance of the gills in fish with nitrite toxicity?

Answer 23

Gills appear brown due to methemoglobinemia

Reference: M&T CTEPP, Smith FD - Respiratory

Question 24

What is the etiologic agent of Columnaris disease?

Describe the clinical signs, diagnosis, and management of this disease.

Answer 24

Flavobacterium columnare

• Affects gills, skin, fins or systemic in FW fish, especially warm water species.
• Gram neg, yellow-pigmented bacterial.
• Wide range of wild and cultured FW fish.
• Horizontal transmission, typically opportunistic.
• CS – saddle-back on skin, gills and skin lesions.
  
  • Gills – distal tips of lamellae and progressing toward the base, chronically infected tissues become necrotic.
    
    • Usually yellowish mucoid mass consisting of mostly F. columnare colonies.
• Histo – lamellar epithelium becomes dissociated from the capillary bed due to the edematous accumulation of fluids, congestion, scattered masses of gram neg bacteria throughout epithelium.
• Ddx – F. columnare and F. branchiophilium differentiated based on spp affected i.e. warm-water (columnare) vs cold-water (branchiophilum) fish. Also presence of yellow material and necrotic gills.
• Dx – long slender, flexing bacteria in typical haystack on wet mounts.
  
  • Isolation on Cytophaga, Hsu-Shotts, or TYES (tryptone yeast extract salts) agar followed by standard biochemical, serological or molecular assays.
• Management/control:
  
  • Optimize water quality, reduce stress.
  • Aquaflor is approved for tx.
  • Oxidizing agents and quaternary ammonias for disinfection.

Question 25

The gill lesions from this Channel Catfish are most consistent with infection with which etiologic agent?

Answer 25

Columnaris Disease - Flavobacterium columnaris

Question 26

What is the etiologic agent of Bacterial Gill Disease?

Describe the pathogenesis, diagnosis, and treatment of this condition.

Answer 26

Flavobacterium branchiophilum

• Cultured salmonids. Worldwide.
• Flavobacterium branchiophilium.
  
  • Yellow-pigmented, gram negative, nonmotile rod.
• Highly contagious, readily adheres to gill tissues. Ubiquitous in water and sediment.
  
  • Typically associated with stressors.
  • Overgrowding, overfeeding, low dissolved O2, inadequate water flow, elevated ammonia levels, increased organic matter, increased turbidity of water.
• CS – lethargy, loss of appetite, signs of resp distress.
  
  • Primarily colonizes external surface of gill tissue with gill filaments appearing pale and swollen.
  • Not generally assoc with the yellow mucoid exudate typical of columnaris in warm-water fish.
• Pathology:
  
  • Hyperplasia, hypertrophy of gill epithelium, fusion of lamellae, clubbing. Mucus cell hyperplasia. Necrosis.
• Dx:
  
  • Gram neg filamentous rod-shaped bacteria.
  • Definitive based on isolation on Cytophaga agar, serology and PCR also available but mostly for research.
• Management/control:
  
  • Based on good management principles of optimizing water quality and reducing stresses.

Question 27

What etiologic agent is most consistent with the gill lesions of this fingerling trout?

Answer 27

Bacterial Gill Disease - Flavobacterium branchiophilum

Question 28

Describe the pathogenesis, diagnosis, and management of Epitheliocystis in fish.

Answer 28

• Chlamydia-like organism.
  
  • Typically chronic, benign infectious dz characterized by cysts in gill epithelium of wild or farmed fish.
  • Gram neg, intracellular chlamydia-like bacteria, order Chlamydiales.
    
    • Other organisms also cause epitheliocystis-like lesions in gills.
  • Horizontal transmission through water assumed following cyst rupture and release of bacteria into water.
  • FW, marine, and anadromous fish, warm and cold.
  • CS – lethargy, flared opercula, increased gill mucus and increased RR.
    
    • Cysts may appear as transparent to white elongated nodules along gill filaments.
    • Gill, skin, pseudobranch, esophagus may also be affected.
  • Pathology:
    
    • Cysts in branchial epithelia of host.
      
      • Cysts are hypertrophic host cells – mucus, chloride, epithelial, filled with the organisms.
      • Usually little to no mortality, cysts may also be incidental without clinical signs.
  • Ddx: Viral dz, opisthokonts i.e. Dermocystidium, protozoans i.e. Ichthyophthirius, Loma spp, or bacterial pathogens.
  • Dx – squash of gill tissue showing cyst with thick capsule and homogenous basophilic granular contents. No serology available. EM for specific diagnosis where intracellular forms can be distinguished.
  • Management/control: Reduce stress.

Question 29

What bacterial disease is the cause of these gray mucoid plaques in the gills of this Atlantic salmon (Salmo salar)?

Answer 29

Epitheliocystis

Question 30

What is the etiologic agent of Koi Herpesvirus?

Describe the pathogenesis, clinical signs, diagnosis, and management of this disease.

Answer 30

Koi Herpesvirus (Cyprinid Herpesvirus 3):

• Highly contagious viral disease, feral and cultivated carp. High morbidity and mortality.

Cyprinid herpesvirus-3

• Alloherpesviridae, enveloped.
• Also known as carp interstitial nephritis, gill necrosis virus.

Pathogenesis

• Younger fish up to 1 year most susceptible to clinical dz.
• Transmission horizontal – feces, urine, sloughed gill and skin mucus.
• Inverts, other fish, birds, mammals may be involved in transmission.
• Goldfish and grass carp may harbor the virus without clinical signs.
• Temp dependent between 16-25 deg C.

Clinical Signs

• Gill lesions with hemorrhage, inflammation, sloughing, necrosis. Excessive mucus.
• Endophthalmia, pale areas to ulcerations of skin and hemorrhage of fins.

Pathology

• Enters through epithelium of skin and gill.
• Inflammation and necrosis in gill, kidney, spleen, liver, pancreas.
• Loss of osmoregulatory function of gill, kidney, intestine.
• Survivors have chronic infection, intermittent shedding.

Differentials

• Spring viremia of carp, other bacterial and parasitic gill infections.

Diagnosis

• PCR, ELISA, immunofluorescence testing.
• Cell culture not as sensitive but possible.

Management/Control

• No effective tx or vaccine.
• Avoid exposure, good biosecurity and quarantine important.
• Raising water temp may decrease mortalities.
• Depopulation should be considered.

Question 31

What is the etiologic agent for these lesions in this Cyprinus rubrofuscus?

What is the most common signalment of affected animals?

How is it transmitted?

Answer 31

Cyrpinid herpesvirus 3

Fish younger than 1 year

Transmission horizontal – feces, urine, sloughed gill and skin mucus.

Inverts, other fish, birds, mammals may be involved in transmission.

Goldfish and grass carp may harbor the virus without clinical signs.

Question 32

What is the most common superficial fungal pathogen of the gills of fish?

Describe it’s diagnosis and treatment.

Where else may you see infection?

Answer 32

• Hyphae of saprolegnia spp rarely penetrate deeper tissues, unlike Aphanomyces invadans or Branchiomyes spp that typically penetrate the deeper tissues of the gill.
  
  • Epithelial hyperplasia of gill results in impaired osmoregulation and resp difficulties.
• Tx – formalin, hydrogen peroxide, sodium chloride, potassium permanganate, and iodophores have been used to control the free-swimming infectious zoospores, generally not effective vs vegetative mycelial growth on the fish.
  
  • Ozone and UV irradiation have been used to limit spread.
  • Prevention, treatment of primary infections.
• Often also on fins and wounds of fish

Reference: Smith & CTEPP Respiration

Question 33

What is the most likely diagnosis for this gill lesion?

How would you treat it?

Answer 33

Formalin, hydrogen peroxide, sodium chloride, potassium permanganate, and iodophores have been used to control the free-swimming infectious zoospores, generally not effective vs vegetative mycelial growth on the fish.

Question 34

What is the etiologic agent of gill rot in freshwater fish?

Describe its transmission, clinical signs, pathology, and management.

Answer 34

• Branchiomyes sanguinis, Branchiomyes demigrans.
  
  • Both produce branched, non-septate hyphae.
• Horizontal transmission of fungal spores.
  
  • Adhere to gill tissue, germinate, produce hyphae that penetrate epithelium and blood vessels of gill.
  • Most FW fish, esp those cultured in intense production systems i.e. tilapia, carp, channel catfish, eels.
• CS – lethargy, anorexia, resp distress.
  
  • Pale gills, swollen gill filaments, hemorrhage and necrosis.
• Pathology:
  
  • Focal areas of infarctive necrosis of gills.
  • Fungal hyphae in lamellar epithelium or penetration of blood vessels causing obstruction, thrombosis, necrosis of gill tissues.
  • Channel gatfish – primarily confined to gill arches and base of primary amlennae.
• Dx: Microscopic evaluation of gill tissue. Fungus can be cultured on Sabouraud dextrose agar 25-32 deg C followed by speciation based on morphological or molecular ID.
• Management/control: Reducing stress, removal of moribund or dead fish.

Question 35

What is the most likely etiologic agent causing these lesions in these freshwater fish?

Answer 35

Branchiomycosis

Branchiomyes sanguinis, Branchiomyes demigrans

Question 36

Identify 5 top differentials for parasitic gill disease of fish.

Answer 36

1. Ichthyophthirius multifilis or Cryptocaryon irritans.
2. Trichodinids.
3. Ichthyobodo necator.
4. Parasitic dinoflagellates – Amyloodinium ocellatum, Piscinoodinium spp, Oodinium spp.
5. Dactylogyridae, Gyrodactylidae.
   
   • Monogenean trematodes mainly direct LC. Typically external.
   • Digenean trematodes IM hosts. Typically internal.
6. Copepods – Ergasilus, Salmonicola.
   
   • Aka gill lice.
   • Only mature females are parasitic.
     
     • Juveniles and mature males free-living in water.
     • Females result in localized swelling, epithelial hyperplasia, hemorrhage, inflammation, occlusion of gill filament vessels and atrophy of tips of filaments.
7. Henneguya ictaluri
8. Neoparamoeba perurans, pemaquidensis, branchiphilia

Question 37

What is the etiologic agent of proliferative or hamburger gill disease?

What species does it commonly affect?

Describe its lifecycle, associated clinical signs, diagnosis, and management.

Answer 37

• Parasitic gill disease of channel catfish
• Caused by Henneguya ictaluri.
  
  • Myxosporian parasite, required oligocaete IM host i.e. Dero digitate in which the infectious actinospore develops.
  • Oligochaete worm releases actinospore stage into water, attaches to skin of fish.
  • Sporoplasm from actinospore penetrates fish, migrates to gills and other organs.
  • Develops into multicellular spores in gills, released into water.
  • Optimal temp range 16-25 deg C.
  • Channel catfish only host spp in which H. icataluri can complete LC.
  • Hybrids are partially refractive.
• CS – lethargy, reduced appetite, congregation near aerators or incoming water.
  
  • Swollen gills, areas of hemorrhage adjacent to necrotic areas.
  • Young fish stocking into ponds recently most severe infection.
• Pathology – Extensive gill hyperplasia, hypertrophy with focal areas of collagen loss leading to chrondrolysis and dyschondroplasia accompanied by extensive inflammatory response in acute and subacute stages of disease.
  
  • Other organs may harbor developing parasite, not usually assoc with inflammation or significant pathology.
• Ddx – protozoan parasites, monogeneans, branchiomycosis.
• Dx – hx of recently stocked young fish with resp distress, histo of gill tissues.
  
  • Myxospores cannot be differentiated from other Henneguya spp, PCR and qPCR for tissue and pond water is available.
• Management/control:
  
  • No effective therapy.
  • Applying hydrated lime to dry ponds prior to filling with water can significantly reduce the number of Dero spp in the pond.
  • Biological control for organisms that feed on Dero spp have not been effective.
  • Using qPCR to estimate number of Dero spp in pond may help determine which ponds are suitable for stocking young naïve fish.

Question 38

What is the most likley etiologic agent of these lesions in this Ictalurus punctatus?

Answer 38

Henneguya ictaluri

Question 39

What is the etiologic agent of amoebic gill disease in marine enrivonments?

What are the agents in freshwater environments?

What species are typically affected?

How are they transmitted, what clinical signs are observed, how can this be diagnosed and treated?

Answer 39

• Primarily cultured salmonids. SW and FW.
  
  • Neoparamoeba (formerly paramoeba) with Neoparamoeba perurans, N. pemaquidensis, and N. branchiphilia bring the primary species causing AGD in the marine environment.
  • FW – genera Thecamoeba, Protacanthamoeba, and Acanthamoeba cause similar CS and pathology in freshwater cultured salmonids.
• Horizontal through water.
• CS – lethargy, increased RR, flared operculum, congregation near water surface.
  
  • Increased mucus on gills, multifocal patches of swollen, pale tissue.
  • Clinical disease is most commonly observed at temps > 16 deg C, salinity above 32%.
    
    • Mort 10-20%, losses as high as 70% reported.
• Pathology – Prominent epithelial hyperplasia resulting in lamellar fusion with significant leucocyte infiltration.
  
  • Parasite most commonly found palisading along the surface of the lamellae.
• Ddx: Other viral, bacterial, parasitic, fungal diseases that cause increased mucus on the gills and respiratory distress.
• Dx: Macroscopic exam of gills, smears and histo. PCR – conventional and TaqMan PCR.
• Management/control: FW baths and hydrogen peroxide tx for marine infestations, formalin for FW amoebic infections.

Question 40

What is the likely etiologic agents of the lesions of the salmon on the left?

What about those on the trout on the right?

Answer 40

SW - Neoparamoeba (formerly paramoeba) with Neoparamoeba perurans, N. pemaquidensis, and N. branchiphilia bring the primary species causing AGD in the marine environment.

FW – genera Thecamoeba, Protacanthamoeba, and Acanthamoeba cause similar CS and pathology in freshwater cultured salmonids.

Question 41

What are the most common neoplasms of the fish gill?

Describe their clinical significance.

Answer 41

• Branchioblastoma and tumors of the pseudobranch.
  
  • Neoplasia of gill tissues are rare.
    
    • Majority is spontaneous with no known cause.
      
      • Chemical contamination and viral etiologies should always be considered.
      • Assume all spp susceptible.
  • Reports – Branchioblastomas or branchial lamellar neoplasm in wild salmonids, branchial chondroma in Atlantic salmon, adenoma brown trout, branchioblastomas koi, branchioblastomas, lymphosarcoma in bass, osteochondroma in sea bream, osteoblastic osteosarcoma barbels.
  • Chemically induced neoplasia in medaka, zebrafish, platyfish x swordtails.
  • Rarely interfere with respiration.
  • Ddx: Granulomatous responses to bacteria, encysted parasites, foreign bodies.
    
    • Distinguish from thyroid hyperplasia (i.e. goiter), commonly occurs in branchial cavity.
  • Dx: Histo.
  • Management/control: Cause for neoplasia not known.

Question 42

Name 5 substances toxic to gills.

Answer 42

• Copper
• chlorine
• cyanine
• manganese
• rotenone
• detergents
• algal biotoxins
• mycotoxins.

Question 43

What causes gas bubble disease and what are its effects?

How can it be managed?

Answer 43

• Gas Bubble Disease:
  
  • Supersaturation of dissolved gases i.e. nitrogen or oxygen causing bubbles in capillaries of gills.
    
    • Numerous etiologies – water leaks in plumbing, sudden extreme temp changes, heavy algal blooms, use of ground water that has not been sufficiently degassed.
  • CS – loss of equilibrium, abnormal buoyancy, aimless swimming, spasmodic convulsions prior to death.
  • Pathology – Overt lesions include air emboli in capillaries of gills with or without petechial hemorrhages. Other tissues with air bubbles.
    
    • Air bubbles in caps of secondary lamellae prevent normal circulation of blood through the gills.
      
      • Reduces efficiency of gas transfer across gill, hypoxia.
  • Dx: Visual observation, gas emboli.
  • Management/control: Lesions generally regress once the elevated gas levels are eliminated.
    
    • Monitor culture water for elevated dissolved gas levels with saturometer.

Question 44

What is the etiologic agent of Phomamycosis or Coelomycosis?

What clinical signs and pathology occur with this disease?

Answer 44

• Phomamycosis.
  
  • Chinook salmon, coho salmon, RBT.
  • Aka coelomycosis, SB dz, air bladder dz, swollen vent dz.
  • Etiology – Phoma herbarum – coelomycete fungus.
    
    • Aspiration of fungal spores through pneumatic duct.
    • Generally impacts only fry and fingerlings < 100 days old.
  • CS – abnormal swimming, loss of sq, exophthalmia, focal body wall discolorations, protrusion of vent and red discoloration.
  • Pathology – May have evidence of local and visceral spread.
    
    • Numerous small white foci at anterior pole of SB near pneumatic duct.
    • May lead to gelatinous caseous white mass filling the SB.
    • Gastric distention with adhesions between SB and GIT may be present.
  • Dx – Aspiration of SB, culture and cytology.
  • Management/control – No therapeutic control measures, some fish may recover.

Question 45

What is the etiologic agent and pathology associated wtih Phomamycosis?

Answer 45

• Paecilomycosis aka Isariamycosis.
  
  • Ascomycete fungal infection of SB.
  • Atl farmed salmon, low mortality.
  • Etiology – Isaria farinose aka Paecilomyces farinosus.
  • Has been used as biologic control in insects.
  • CS – generalized hyperpigmentation, abnormal buoyancy, coelomic distention, low levels of mortality.
  • Path – distended SB, mural and local hemorrhage, lumen with white branching, septate, hyaline hyphae infiltrating and effacing the wall.
  • Dx – Fungal culture.

Question 46

What metazoan parasite causes coelomic distension in eels?

What is its lifecycle?

What other pathology is present?

How is it diagnosed and treated?

Answer 46

• Anguillicolidae infection.
  
  • Nematodes of SB of eels.
    
    • Anguillicoloides australensis.
      
      • Dracunculoid nematodes.
      • LC involves eel definitive host, crustacean IM host or small fish or invert paretenic host.
      • Transmission through direct oral exposure.
      • Sexual repro in SB lumen with embryonated eggs.
      • Larvae leave SB through pneumatic duct, enter GIT, released into water with feces.
    • Series of molts when in definitive eel host GIT and migrate to SB, become adults.
  • CS – Pathogenic in Eu and American eels; not usually pathogenic in Pacific eels.
    
    • Hyporexia, decreased swimming speed, coelomic distention, skin ulcers along posterior abdomen.
    • Predisposed to SB rupture.
  • Path – consume blood from host via wall of SB.
  • Luminal hemorrhage, inflammation, thickening.
  • Lumen filled with degenerate eggs, larvae, blood and debris.
  • Dx – radiology and gross necropsy.
    
    • A Length Ratio Indix (LRI) described to use rads for disease severity.
      
      • Scoring based on alterations in length and regularity of SB silhouette, dilation and gas distension of pneumatic duct, and worm contours within SB lumen.
  • Tx – no treatment in wild.
    
    • Aquaculture – levamisole, metrifonate, enamectin benzoate efficacious.
    • Control in ponds – Not practical.

Question 47

What is the most likely parasite causing the infestation of this eel’s swim bladder?

Which eels are affected and which are not?

Answer 47

Anguillicoloides australensis

Pathogenic in european and American eels - not usually in Pacific eels

Question 48

Which parasitic infestation is pictured here?

What groups of fish are affected?

Answer 48

• Cystidicola infection.
  
  • Spiurid nematodes.
  • Genus Cystidicola – parasites of SB of physosomous fishes.
  • C. cristivomeri and C. faronis.
  • Direct oral exposure.
    
    • C. cristivomeri IM host opossum shrimp.
    • C. farionis IM host FW amphipod.
    • Larvae migrate through pneumatic duct via retrograde migration from stomach to esophagus.
  • CC infects arctic char and lake trout in NA.
  • CF infects NA, Asian, and Eurasian salmonids.
  • Mortality is low despite heavy worm burdens.
  • Path – RBT with CF have raised ulcers, central plaque of ochre-colored material overlying a central crater.
    
    • Lake trout with CC – ulceration only with massive worm burdens.
    • Raised ulcers along ventrolateral surface of SB.
  • Dx – gross necropsy, parasite ID.
  • Tx – No control measures.

Question 49

What is the etiologic agent of swim bladder inflammation of carp?

What speces are affected?

Describe its pathology, diagnosis, and treatment?

Answer 49

• Sphaerosporosis.
  
  • Swim bladder inflammation of carp (SBI) aka cyprinid swim-bladder inflammation.
    
    • Commercial carp.
    • Etiology – IM stage of renal myxosporean – Sphaerospora renicola.
  • Transmission undetermined.
  • Common carp throughout Asia, NA, Eu.
  • Prevalence of dz peaks in July.
  • CS – chronic dz, abnormal buoyancy, swimming on back or side with head pointed down.
    
    • Difficulty diving.
  • Path – Aerocystitis.
    
    • Early – loss of transparency of the inner wall of the SB, petechiae.
    • Later – thickening of SB wall and accumulation of red-brown exudate.
    • Rarely involves the posterior sac of the SB.
    • One differentiating feature from other causes of aerocystitis is the development of marked multifocal hemorrhage and layers of fibrin on the outer surface of the SB in severe cases.
    • Cysts may form in final stages of disease.
      
      • Organisms within fibrous tissue of tunica interna, most often extravascular at border between hemorrhagic and healthy tissues.
      • Pansporoblasts and spores in renal tubules.
  • Dx – cytology and histology. Impression smears of anterior SB will contain Giemsa-positive, multicellular stages of parasite.
  • Tx – none.
    
    • Fumagillin reported effective experimentally for prevention of sphaerosporosis.
    • Drying and disinfecting ponds will destroy spores.

Question 50

What is the most likely etiologic agent causing the lesions in this Micropterus salmoides?

Describe the pathogenesis, clinical signs, and diagnosis of this disease.

Answer 50

• Largemouth bass virus.
  
  • FL, adult, trophy-size fish, summer > 30 deg C.
  • Iridovirus, can be isolated from clinically normal fish.
  • Transmission waterborne or consumption of infected prey.
    
    • Retains infectivity in water after 2 days, can still be detected after 7 daus.
    • SMB can also be infected.
    • Predominantly dz of wild fish.
  • CS – floating at surface.
  • Path – red discoloration/distension of SB with yellow or brown exudate in lumen.
  • Inflammation and necrosis of exocrine pancreas, stomach, intestine, intestinal ceca.
  • Dx – Virus isolation, PCR.
  • Tx – No tx. Risk of transmission between fish shedding virus and naïve fish during catch and release tournaments suggested as a link.

Question 51

Discuss neoplasia of the swim bladder.

Are there any associations with infectious disease?

Answer 51

• Swim bladder sarcoma.
  
  • Atl salmon, NA.
  • Swim bladder sarcoma virus SSSV – rerovirus, fam Epsilonretroviridae.
  • Route of transmission unknown.
  • Cultured and wild Atl salmon between 1-4 years of age.
  • CS – chronic morbidity, mortality.
    
    • Lethargy, poor BCS, buoyancy problems.
  • Path – Multifocal to coalescing, firm tan masses wall of SB.
  • IHC consistent with leiomyosarcoma.
  • Dx – rads, US, gross necropsy. Histo.

Question 52

Compare and contrast mechanical disease of the swim bladder.

Answer 52

• Barotrauma/catastrophic decompression disease.
  
  • Rapid surfacing due to angling or scientific sampling.
  • Changes as little as 10-20 ft can impact some spp.
  • Increase in partial pressure of dissolved gas within blood and tissues (Boyle’s law) as fish surfaced.
    
    • Blood and tissues upersaturate, gas leave solution and form emboli.
  • Physoclists may be more vulnerable due to inability to rapidly adjust gas volume.
  • CS – Acute – abdominal distention, exophthalmia, respiratory distress, abnormal buoyancy, external hemorrhage, gastric eversion, intestinal herniation.
    
    • May sink if SB is ruptured.
    • Chronic impacts of SB rupture – inefficient swimming, inability to control volume, increased energy expenditure, higher O2 consumption.
  • Path – many different injuries assoc with overexpansion of SB.
    
    • Additionally – alterations in coagulation proteins, erythrocyte lysis, increased conc of tissue-damaging enzymes.
  • Tx – puncture of SB i.e. venting.
    
    • Allows for contamination of lumen, controversial.
      
      • Does not improve survival.
      • Discouraged in fishery practice.
      • Alternatives – lowering fish to a depth in a basket using weights.
      • Low cost hyerbaric chambers. Decompress over days.
• Overinflation.
  
  • Ornamental fish and goldfish.
  • Etiology – Acid-base abnormalities.
    
    • Pneumatic duct obstruction due to infection, metaplasia, mucus.
    • Altered body conformation through selective breeding may be a factor.
  • CS – abnormal buoyancy.
  • Dx – rads, aspiration of SB.
  • Tx – Return to neutral buoyancy. Peas may be fed.
    
    • Sx removal or reduction of SB have been used for chronic overinflation.
• Swim bladder torsion.
  
  • Rare – ornamental fish and farmed RBT.
  • Torsion midviscus causing caudal distention of the coelom and dilation of SB.
  • Dx – radiographs.
  • Tx – aspiration. May spontaneously resolve. Coeliotomy with either pneumocystoplasty or surgical correctin of torsion.

Question 53

What is the honeybee tracheal mite?

What disease does it cause?

Answer 53

Acarapis woodi

Lives in trachea, sucks hemolymph, reduces host life span.

Question 54

What differentials shoudl be considered with fish presenting with dyspnea & tachypnea?

What clinical findings might you appreciate that would suggest difficulty breathing?

What diagnostics should be performed with these fish?

How should the systems be managed?

Answer 54

B2 Respiratory and Cardiovascular Signs

Dyspnea and Tachypnea

• · True emergency, typically associated with environmental problem, ectoparasite or infectious disease
• · Common presentation associated with mortality
• · Stressed fish more susceptible; air breathing fish less susceptible
• · Clinical findings
• o One or more fish
• o Dyspnea - opercular or gill slits have increased flaring, gaping of the mouth, head or body movements associated with ventilation, gasping at surface (piping)
• o Tachypnea - assessed with previous normal values and/or normal conspecifics
• o Fish gather in areas of highest oxygen (surface, inflowing water)
• o May have rigid posture or reduced responsiveness to food
• o May have oral or gill pathology visible
• o Mortalities - opercular flaring, mouth gaping
• · Etiologies
• o Most common: low DO, ammonia toxicity, contaminants, columnar, ciliates, monogeneans
• o Neoplasia/hyperplasia - goiter, oral, pharyngeal, branchial
• o Vascular - anemia, cardiovascular disease
• o Infectious/inflammatory
• § KHV, herpesviral hematopoietic necrosis, carp edema virus, ISA, Atlantic salmon paramyxovirus
• § Bacteria ( Flavobacterium spp.)
• § Branchiomyces spp., oomycetes, some Microsporidia.
• § Protozoa
• § Metazoa - monogeneans, blood flukes, leeches, copepods, isopods
• § Myxozoa (Henneguya spp., Myxobolus koi)
• o Toxic
• o Trauma
• o LSS/environmental - low DO, supersaturation, high temperature, excessive turbidity, rapid change in pH, ammonia, nitrites, nitrates

Diagnostic Approach

• Assess animals and identify if signs are acute (erythema, flashing) vs chronic/acute-on-chronic (weight loss, poor coloration)
• Assess habitat, LSS, and water quality
• Review history - when animals first added, recent additions, quarantine, feeding response, water source, changes in LSS or recent water changes, meds, recent or known causes of prior mortalities, weather
• Necropsy (and skin/fin/gill) mortalities - fresh euthanized sick fish prefer
• Live fish exam - oral cavity (masses), gills, gill biopsy, skin scrape, blood collection

Management

• Remove dead asap
• Increase aeration to 95-100% (if no signs of gas supersaturation)
• 20-50% water change if source is not contaminated
• Remove dead plants and organic debris
• Treat or manage problem
• Supplement FW with 2-3 g/L salt
• Reduce feeding short term if fish in adequate condition
• Reduce light/visual stress
• Consider short steroid course (dexamethasone SP 0.5-1 mg/kg IM 2-3 doses)
• Monitor for secondary disease

Question 55

What differentials should be considered in fish with gill pallor?

What are the most common etiologies of gill pallor?

What should the diagnostic approach be? What samples should be taken?

How do you determine if the anemia is acute or chronic?

How should these fish be managed?

Answer 55

Gill Pallor

• Typically due to anemia
• · Group - infectious, toxin, nutritional deficiency
• · Gills become pale and then tan colored after death due to autolysis and should not be over interpreted
• · Clinical findings
• o Normal: dark red gill
• o Abnormal: pale red, pink, brown, gray, yellow, white (focal, multifocal, generalized)
• o Parasites on skin or gills
• o Lethargy, dyspnea, tachypnea
• · Etiologies (infectious, toxic most common)
• o Artifact - post mortem, autolysis
• o Nutritional
• § Vitamin C, E, K, B deficiency
• § Iron deficiency
• § Suboptimal fatty acid or carbohydrate diet composition
• o Neoplasia (kidney, spleen)
• o Infectious - hemorrhage, hemolysis, chronic disease
• o Inflammatory - vasculitis, transfusion reaction
• o Chronic liver or kidney disease
• o Toxic - nitrites, nitrates, chlorines, metals, hydrogen sulfide, anticoagulants, mycotoxins
• o Trauma

Diagnostic approach

• · Review history - recent editions, food eaten (food storage and prep), prior causes of morbidity or mortality, chronicity
• · Assess animals - dyspnea, tachypnea, systemic inflammation (erythema, hyperemia, ulcers), bloody discharge, parasites, signs of trauma
• · Water quality (nitrite, copper, chlorine, zinc)
• · Necropsy mortalities
• o Skin/fin/gill, cultures, wet mounts, histology
• o PCR if KHV or ISA suspected and archive frozen samples
• o Fecal smears
• · Peripheral blood smears
• · If fish asymptomatic with PCV <8%, chronic
• · Live fish exam with imaging (coelomic effusions, foreign bodies)

Management

• · Increase aeration - DO 95-100%
• · Treat/manage problems
• · 20-50% water change
• · Improve diet/food handling
• · Supportive care - fluids, blood transfusion, erythropoietin, darbepoetin, nutritional support, analgesia

Question 56

Describe the causes and management of positive buoyancy in fish.

What species are prone to positive buoyancy issues?

What additional clinical signs may be seen?

What are some of th epotential etiologies? What nutritional issues? What infectious issues? What traumatic issues? What life support or environmental issues can cause this?

How do you differentiate a positive buoyancy issue from a neurological fish?

What diagnostics should be considered in these cases?

How can these caes be managed?

Answer 56

Positive buoyancy

• Usually due to abnormal gas accumulation in swim bladder, GI, coelom, subcutis, or pouch
• Abnormal gas accumulations can be removed with centesis, recurrence is common

Signalment

• Fancy goldfish: orandas, moors, lionheads, bubble-eyes, ryukins, ranchus
• Seahorses due to swim bladder or pouch inflation or SQ gas emboli
• Deep water species: red-banded rockfish

Clinical signs

• Exophthalmos or buphthalmos may be seen

Etiologies: most common causes are swim bladder disease and barotrauma

• Developmental: selective breeding for characteristic deformities (fancy goldfish)
• Anomalous
  
  • Swallowing air during restraint or transfer
  • Lack of access to breeding females in male seahorses with gas in the pouch
• Metabolic: acidosis (theoretically)
• Neoplasia: swim bladder, kidney, tissues near pneumatic duct, nervous system
• Nutritional
  
  • Floating foods allowing swallowing of air
  • Dry foods that can expand in the GI tract
  • Foreign body obstruction of the pneumatic duct
• Normal behavior: several species perch in vertical or ventrodorsal orientation (rockfish, upside-down catfish)
• Infectious/inflammatory: any systemic, swim bladder, renal, GI, or neuro inflammation and pouch inflammation in seahorses
  
  • Viral: spring viremia of carp, largemouth bass virus
  • Bacterial: vibriosis, Aeromonas, Streptococcus, Mycobacterium
  • Fungi/fungi-like: Exophiala, Phoma spp.
  • Metazoa: anguillicolid nematodes, encysted pentastomids
  • Myxozoa: Hoferellus, Sphaerospora spp.
  • Apicomplexa: Goussia spp.
• Trauma
  
  • Barotrauma (recent catch from depth)
  • Physical to the spine, swim bladder, or pneumatic duct
  • Electrical stunning
• Life support system/environmental
  
  • Gas supersaturation
  • Low pH (theoretically)
  • Stray voltage and poor electrical grounding
  • Lightning strike

Diagnostic highlights

• Gas emboli may be grossly visible (in or around eyes or under skin)
  
  • Gill or fin biopsies under direct microscopy to look for gas emboli
  • Radiographs: resting (vertical beam) and standing (horizontal beam) lateral views

§ Compare to normal conspecific

• Differentiate from neurologic or respiratory disorder or displacement
  
  • Neuro: fish often show no effort to correct abnormal posture or position
  • Resp: fish may gather at the surface but commonly show dyspnea and tachypnea
  • Displaced fish may resolve if the social group is changed
• Check water quality including gas pressures over 24-48 hours
  
  • If a total gas pressure meter is not available, dissolved O2 can be used to detect O2 supersaturation but is less useful
• Check life support system for visible cracks, check water for microbubbles suggesting supersaturation
• Necropsy
  
  • Normal swim bladder wall is thin and translucent or thick, white, and opaque but there may be pigmented areas
  • Abnormal findings in swim bladder: serosanguinous fluid, purulent exudate, soft tissue, petechiae or ecchymoses, adhesions, tears
  • Swabs or tissues for PCR testing for spring viremia of carp or largemouth bass virus
• Swim bladder volume is often reported as 4-7% of body volume, freshwater spp at higher end of range, clinically normal fish can have larger swim bladders
• Consider rigid endoscopy of coelom or swim bladder for diagnosis and treatment

Management highlights

• Keep exposed skin or fins wet
• Recompression is usually preferred treatment for excess gas accumulation: weight crates sunk to specific depths or chambers that can be pressurized
  
  • Smiley JE, Drawbridge MA. Techniques for live capture of deepwater fishes with special emphasis on the design and application of a low‐cost hyperbaric chamber. Journal of Fish Biology. 2007 Mar;70(3):867-78.
• Remove swim bladder gas (pneumocentesis) or free gas to provide temporary relief, lateral approach, under rad or U/S guidance, recurrence over several days is common
• Remove SQ gas by percutaneous aspiration or pouch gas by catheter in seahorses
• Consider acetazolamide (carbonic anhydrase inhibitor): reduces concentration of CO2 in the eyes and plasma, may reduce oxygen secretion
  
  • Typical dose 2.5-5 mg/kg IM every 3-7 days for up to 3 treatments
  • High dose can be associated with negative buoyancy, neurologic signs, mortalities
• Consider surgical correction of swim bladder pathology: pneumocystoplasty, pneumocystectomy
• In marine fish: consider reducing salinity slightly to help maintain buoyancy
• Can inject fluid (eg hetastarch) into swim bladder to reduce buoyancy and gas secretion
• Idiopathic cases in fancy goldfish: anecdotal reports of improvement with feeding fresh, crushed or cooked peas, fasting 2-3 days, using magnesium sulfate to reduce constipation, and managing buoyancy with small weights attached to the fish

Question 57

Describe the causes and management of negative buoyancy in fish.

What fish are particularly susceptible?

What additional clinical signs may be present?

What are some of the causes? What deveopmental issues? What nutritional issues? What infectious issues?

How should these cases be managed?

Answer 57

Negative buoyancy

• Fish maintain neutral buoyancy with a variety of methods: gas-filled swim bladder, fat deposition in the liver, body shape and movement
• Ddx neurologic, musculoskeletal, GI, swim bladder pathology, and loss of body condition
• Prognosis is usually guarded

Signalment: larval bony fish in aquaculture are particularly susceptible

Clinical findings

• fish is on the substrate, lower in the water column than normal, or swimming with tail-down posture
• Edematous or ulcerative skin or eye lesions may develop in dependent areas (leading edge of anal fin)

Etiologies: most commonly swim bladder disease in bony fish with swim bladders or loss of fat reserves in cartilagenous fish

• Developmental
  
  • Failure to inflate swim bladder as fry
  • Selective breeding for characteristic deformities (fancy goldfish)
  • Genetic
  • Methylene blue exposure during development
• Neoplasia: swim bladder (swim bladder sarcoma virus), kidney, tissue near pneumatic duct, nervous system
• Nutritional
  
  • Loss of fat reserves, particularly in the liver
  • Inability to swallow air
  • Foreign body obstruction of the pneumatic duct
  • Myopathy (particularly seahorses)
• Infectious/inflammatory
  
  • Viral: spring viremia of carp, Atlantic salmon swim bladder sarcoma
  • Bacterial: vibriosis, Aeromonas, Mycobacterium
  • Fungi/fungi-like: Exophiala, Phoma spp.
  • Metazoa: anguillicolid nematodes, encysted pentastomids, encysted digenes
  • Myxozoa: Hoferellus, Sphaerospora spp.
  • Apicomplexa: Goussia spp.
• Toxic: drug toxicity (acetazolamide, idiosyncratic)
• Trauma: esp spine, swim bladder, or pneumatic duct

Diagnostic highlights

• Fish may be displaced into abnormal locations, may resolve if the social group is changed
• Collect aspirates of fluid or soft tissue abnormalities in swim bladder for cytology and culture
• Consider U/S to evaluate liver size and echogenicity and any coelomic abnormalities
• Consider rigid endoscopy of coelom or swim bladder

Management highlights

• Nutritional support is particularly important for elasmos showing negative buoyancy to restore fat reserves in the liver
• Provide smooth and clean substrate (round gravel or smooth fiberglass)
• Consider increasing salinity slightly to help maintain buoyancy if tolerated
• Consider injecting sterile air (such as from the inside of a fluid bag) into small swim bladders, recurrence is common
• For idiopathic cases in fancy goldfish: anecdotal reports of temporary management with floats attached to the fish