Fish & Invertebrate Parasitology

Question 1

Describe the effects of Ich infestation in fish.

What is the etiologic agent?

What is it’s lifecycle? How long does that take and how does it vary with temperature?

What species are commonly affected?

What are the clinical signs? What is the mortality rate like?

How is this diagnosed? What differentials should be considered?

How is it treated?

Answer 1

ICHTHYOPHTHIRIUS MULTIFILIIS

Etiology

• Phylum Ciliophora.
• Family Icthyophthiriidae.
• Species Ichthyophthirius multifiliis

Life Cycle & Transmission

• Trophont (burrowing feeding stage resistant to treatment) à leave host and become tomonts (encysted within the environment à tomonts rupture releasing tomites that differentiate into theronts (the stage sensitive to treatment)
• Time varies with temperature
  
  • 1.5–7 days at 20–25 °C (68–77 °F).
  • 10–14 days at 15 °C (59 °F).
  • 20–90 days at 5–10 °C (41–50 °F).

Distribution & Signalment

• All freshwater fish susceptible, distributed worldwide
  
  • Susceptible aquaculture species: rainbow trout, grass carp, common carp, channel catfish
  • No reports in elasmobranchs

Clinical Signs & Findings

• Usually seen 5-10 days after adding new fish
• Early signs – reduced feeding, increased hiding, skin darkening
• Later signs – white spots on skin, fins & gills; pruritus, dyspnea/tachypnea, keratitis, inappetence
• Mortalities start within days – can be as high as 100%

Diagnosis & Differentials

• SS/GC – trophonts are large, round, with classic C-shaped nucleus. Single organism is concerning.
• DDx – monogeneans, sessile ciliates, Flavobacterium, lymphocystis, herpesvirus

Medical Management

• Formalin immersion – 40-100 mg/L 5-7 doses q48h
• Copper sulfate – not tolerate by all species
• Increase salinity to reduce osmotic stress
• Chloroquine diphosphate is not effective

Question 2

What is the etiologic agent of crypt infection in fish?

What is the lifecycle? How does it compare to Ich?

What species are affected?

What are the typical clinical signs?

How is it diagnosed?

How is it treated?

Answer 2

CRYPTOCARYON IRRITANS

Etiology

• Phylum Ciliophora.
• Family Holophryidae.
• Species Cryptocaryon irritans

Life Cycle & Transmission

• Trophont (burrowing feeding stage resistant to treatment) à leave host and becometomonts (encysted within the environment à tomonts rupture releasing tomites that differentiate into theronts (the stage sensitive to treatment)
• Theronts don’t swim as well as Ich – likely acquired near the substrate
• Slower life cycle than ich – 7 days at 81F, 11-15 at 75F

Distribution & Signalment

• Tropical and subtropical saltwater habitats
• Sensitive aquaculture species – olive flounder, red seabream, obscure puffer fish
• No reports in elasmobranchs

Clinical Signs & Findings

• Usually seen 1-3 weeks after adding new fish
• Early signs – reduced feeding, increased hiding, skin darkening
• Later signs – white spots on skin, fins & gills; pruritus, dyspnea/tachypnea, keratitis, inappetence
• Mortalities start within days – can be as high as 100% - but can also become a chronic condition once established

Diagnosis & Differentials

• SS/GC - Trophonts are large, round, slowly rolling ciliates with lobulated nucleus. Single one concerning.
• Increase mucus and gill hyperplasia

Medical Management

• Copper sulfate – 0.16-0.21 mg/L for 5-7 days – monitor copper and alkalinity levels
• Formalin – 50 mg/L q24h until signs stop then q48h for 21 days
• Chloroquine diphosphate – 10-15 mg/L for 3-4 weeks (recurrence more common than with copper)
• Hyposalinity (18-20 g/L) – not tolerated by all species

Question 3

Describe the effects of Chilodonella infestations in fish.

What is the lifecycle like?

What fish are typically affected?

What are the typical clinical signs?

How are it diagnosed?

How is it treated?

Answer 3

CHILODONELLA SPP.

Etiology

• Phylum Ciliophora
• Family Chilodonellidae
• Chilodeonella Piscicola & C. hexasticha

Life Cycle & Transmission

• Direct life cycle, no encysted stages
• Transmitted horizontally

Distribution & Signalment

• Freshwater & brackish habitats worldwide
• Severely affected aquaculture species: channel catfish, Australian cod, carp, silver perch, freshwater salmonids, barramundi
• Severely affected aquarium fish – freshwater angelfish, discuss, platies, guppies
• Found on invertebrates, not on elasmobranchs

Clinical Signs & Findings

• Subtle – lethargy, hiding, hyporexia, skin color changes and ulcers, dyspnea/tachypnea
• Mortality is usually low but can be high with other stressors
• DDx – Ich, Cscuticociliates, trichodinids, sessile ciliates

Diagnosis & Differentials

• SS/GC – ciliates are oval or heart-shaped, dorsoventrally flattened and translucent with parallel rows of cilia
• Increase mucus and gill hyperplasia can be seen
• A single organism is concerning, but a high load is

Medical Management

• Formalin immersion – 25-50 mg/L once is typically effective

Question 4

Describe the effects of Brooklynella infestation in fish.

What species are typically affected?

What is the lifecycle of the parasite?

What are the typical clinical signs?

How is this diagnosed? What differentials should be considered?

What are some treatments?

Answer 4

BROOKLYNELLA SPP.

Etiology

• Phylum Ciliophora
• Family Hartmannulidae
• Brooklynella hostilis

Life Cycle & Transmission

• Direct life cycle, no encysted stages
• Transmitted horizontally

Distribution & Signalment

• Saltwater habitats, possibly worldwide
• Seahorses & pipefish (Sygnathids), marine angelfish (Pomacanthids), and clownfish (Amphiprioninae) particularly susceptible
• Does not infect inverts or elasmobranchs

Clinical Signs & Findings

• Initial signs are subtle – lethargy, hiding hyporexia, skin darkening or pallor
• Later signs – dsypnea/tachypnea, gray skin discoloration, opaque fins
• Mortalities can be high

Diagnosis & Differentials

• SS/GC – ciliates are oval or heart-shaped, dorsoventrally flattened, with a notched anterior end. Cilia more visible than Chilodenlla
• DDx – Crytocaryon, scuticociliates

Medical Management

• Formalin immersion – 25-100 mg/L once or repeated q2-3 days is usually effective
• Formalin dips in quarantine can help

Question 5

Describe the effects of scuticociliatosis in fish.

What parasites affect marine fish? Which affect freshwater fish?

What is the life cycle and transmission of these parasites?

What species of fish are particularly susceptible?

What are the typical clincial signs?

How are these parasites diagnosed? What differentials should be considered?

How are they treated?

Answer 5

SCUTICOCILIATES

• Etiology
  
  • Phylum Ciliophora
  • Subclass Scuticociliata
  • SW – Uronema marinum, U nigricans, Miamiensis avidus
  • FW – Tetrahymena corlissi, T. pyriformis
• Life Cycle & Transmission
  
  • Direct, no encysted stages
  • Facultative parasites that may be free-living
  • Crustaceans & mollusks may play a role in trasnsmission
• Distribution & Signalment
  
  • Marine scuticociliates (Uronema, Miamiensis) particularly affect Syngnathids, flatfish (turbot and olive flounder), European bass, southern bluefin tuna, zebra & horn sharks
  • Freshwater – livebearers (Poeciliids), tetras (characids), cichlids (cichlidae), carp, goldish and zebrafish (cyprinidae)
• Clinical Signs & Findings
  
  • Increased mucus, skin darkening with gray/white/brown lesions, petechiae & erythema around base of finds & mouth, muscle swelling, skin ulcers
  • Systemic disease – abnormal swimming (circling), enteritis with yellow mucoid feces, serosanginous coelomic effusion
  • Mortality can reach 100%
• Diagnosis & Differentials
  
  • SS/GC – small, tear droped shaped ciliates with fast, forward spinning movements
  • Intralesional ciliates may be perivascular; meningoencephalitis is common in tuna & elasmobranchs; systemic infections common in sygnathids
  • DDx – ich/crypto, Brooklyn-/Chilodonella, Trichodinids
• Medical Management
  
  • Formalin – 25mg/L x 6h, 250 mg/L x 1h
  • Metronidazole – 50 mg/L q24h x 10d

Scuticociliatosis - ZP

• Subclass Scuticociliata
  
  • Uronema marinum, U. nigricans, Miamiensis avidis aka Philasterides dicentrarchi.
  • Common in sygnathids, cultured black sea bass, sea bream, pleuronectids.
  • U. nigricans – severe CNS dz Bluefin tuna.
  • Ovoid, holotrichous ciliates, longitudinal rows of kineties and single long caudal cilium.
  • Anterior pole of U. marinum is flat, P. dicentrarchi si tapered.
  • Epidermal pallor, sloughing, ulceration, widespread systemic dz.
  • Inflammation often minimal.

Question 6

Describe trichodinid infestation in fish.

What species of fish are particularly suceptible?

What is the life cycle?

What are the typical clinical signs?

How is it diagnosed?

How is it treated?

Answer 6

Trichodinids

• Etiology
  
  • Phylum Ciliophora
  • Family Trichodinidae
• Life Cycle & Transmission
  
  • Direct, no encysted stages
  • Transmitted horizontally
• Distribution & Signalment
  
  • More common in freshwater, but all susceptible
  • Particulary carp, goldfish, Nile tilapia, & other cichlids
  • Older, rare reports of infection in skates
• Clinical Signs & Findings
  
  • Can be asymptomatic
  • Dyspnea/tachypnea, pruritus, endematous gills
  • Mortality is usually low
• Diagnosis & Differentials
  
  • SS/GC – round, radially symmetric, flat or domed shaped ciliated with steady gliding or erratic rotating movements
  • Can also be found in urogenital system
• Medical Management
  
  • Improving the environment is often enough to resolve signs
  • Formalin bath – 25-50 mg/L for 1-2 hours
  • Copper can also be used
  • Fresh/Saltwater baths

Trichodiniosis – Family Trichodinidae.

• Worldwide, FW and SW.
• Characteristic basal attachment disc possessing a ring of chitinoid denticles that mediates firm attachment to epidermal or gill epithelium.
• Feeds on organic matter and bacteria in the water column, sloughed cells and debris on skin surface.

Question 7

Describe sessile ciliate infestation in fish.

What are some of the more common parasites?

What species of fish are commonly affected?

What is the lifecycle like?

What are the typical clinical signs? What secondary infections may occur?

How are they diagnosed?

How are they treated?

Answer 7

SESSILE CILIATES

• Etiology
  
  • Phylum Ciliophora
  • Subclasses Peritrichia & suctoria
• Life Cycle & Transmission
  
  • Direct, no encysted stages
  • Transmission is horizontal
• Distribution & Signalment
  
  • More common in freshwater, but found in saltwater
  • Carp & Koi, goldfish, and catfish are particularly susceptible
• Clinical Signs & Findings
  
  • Early – hyporexia, pruritius, dyspnea/tachypena
  • Skin ulcers, white spots, white/gray/brown fluffy lesions particularly on the fin margins, around mouth
  • Secondary Aeromonas infections can occur
  • Mortality is usually low
• Diagnosis & Differentials
  
  • SS/GC – small parasites with an attachment stalk and oral rings or cilia
• Medical Management
  
  • Formalin immersion – 25-50 mg/L for 2 hours
  • Hypersalnity for FW fish or SW dips

Problem 32 – Solitary Ciliate Infestation – Apiosoma, Riboscyphidia, Amphiphyra, Capriniana

• Host/location: Freshwater fish, skin or gills
• Clinical Signs/Pathology: Superficial damage to skin or gills as they feed off bacteria and debris in the water
• Life Cycle: Reproduce by binary fission
• Diagnosis: Wet mounts of histology
• Treatment: Formalin or copper (for Capriniana), improve water quality at same time

Problem 33 – Colonial Ciliate Infestation – Epistylis

• Host/location: Freshwater fish, skin or gills, common in pond raised fish
• Clinical Signs/Pathology:
  
  • White or hemorrhagic lesions
  • Anchor to solid surfaces so skin is always ulcerated where they are attached
• Life Cycle:
  
  • Associated with mixed Gram-negative bacteria causing red-sore disease
  • Zooid from stalked colony transforms to a disc-shaped telotroch with cilia for locomotion to attach at a new site
• Diagnosis: Wet mount of histo, amorphous masses on skin, mouth or gill arches
• Treatment: Formalin, potassium permanganate, salt baths

Question 8

Describe cryptobia infestation in fish.

Which species are hematozoic? Which are not?

What is the life cycle? How does it differ between the two groups?

What fish are commonly affected? Which demographic is most affected?

What are the typical clinical signs?

How is it diagnosed?

How are they treated?

What are the lesions associated with nonhemazoic cryptobia?

Answer 8

CRYPTOBIA SPP.

Etiology

• Phylum Euglenozoa
• Class Kinetoplastea
• Non-hematozoic – Cryptobia iubilans, C. branchialis
• Hematozoic – C. salmositica, C. bullock, C. borrelia – previously classified as Trypanoplasma

Life Cycle & Transmission

• Non-hematozoic species have direct life cycles
• Hematozoic species have indirect life cycles involving leeches
• Brook trout & sculpin can be carriers for C. salmositica

Distribution & Signalment

• Mostly freshwater, less common in SW, worldwide
• Non-hematozoic species – cichlids, particulary discus, Oscars, and tilapia
• Hematozoic species
  
  • Salmonids & sculpin – C. salmositica
  • Flatfish, hogchokers, croakers – C. bullocki
  • Cyprinids – C. borrleli
• Juvenile fish are more susceptible

Clinical Signs & Findings

• Exposure to leeches
• Lethargy, hiding, recumbency, skin darkening, increased mucus production, tachypnea/dyspnea
• Abnormal fecals
• Gill pallor, edema, exophthalmos, coelomic distension
• Mortality rate usually low but can reach 100%

Diagnosis & Differentials

• C. iubilans & C. branchialis – SS/GC – small teardrop to oval flagellates with anterior & posterior flagella with slow undulating movements
  
  • Can produce granulomas
• C. salmositica – identified on blood smears or coelomic effusion – two anterior flagella and one posterior
  
  • Microscopic hypochromic anemia & splenomegaly
  • Generalized hemorrhage with flagellates within capillaries
  • Examining the buffy coat increases sensitivity

Medical Management

• Increasing temp reduces C. salmonsicia mortalities
• Isometamidium chloride – 1mg/kg IM
• Dimetridazole immersion 80 mg/L q24h
• Ineffective tx – metronidazole, fenbendazole, chloroquine, primaquine, sulfonamides

Cryptobia spp - ZP

• Closely related to trypanosomes.
• Two flagella, undulant membrane. ‘Flowing’.
• Can parasitize GI tract.
• C. branchialis colonize skin and gill of FW and SW teleosts.
• C. iubilans affects GIT in cichlids. Also discus.
  
  • Variably severe granulomatous and necrotizing gastritis.
  • Hemorrhage and anemia.
  • Disseminated infections.
  • Not closely assoc with epithelium and round to oval vs Ichthyobody which is tightly attached and has a pyriform shape.

Question 9

Describe ichthyobodo infestations in fish.

What is the main pathogen species?

What is the life cycle?

What species of fish are commonly affected? What demographic is affected the worst?

What are the. typical clinical signs?

How is this diagnosed? What are some important differentials to consider?

How is it treated?

Answer 9

ICHTHYOBODO SPP.

Etiology

• Phylum Euglenozoa
• Class Kinetoplastea
• Icthyobodo necator (there are others as well)

Life Cycle & Transmission

• Direct life cycle – motile and sessile stages
• Both stages are susceptible to medications

Distribution & Signalment

• Freshwater habitats
• Rainbow trout commonly affected
• Juvenile fish are more susceptible

Clinical Signs & Findings

• Inappetence, hyporexia, lethargy, hiding, swimming at surface, pruritus, skin ulcers or dull grey-blue coloration, dyspnea/tachypnea, gill pallor
• Mortality is low but can be high with other stressors

Diagnosis & Differentials

• SS/GC – small flagellates, comma or tear-drop shaped, two pairs of flagella with characteristic flicking, tumbling motion
• MS-222 often causes parasites to detach
• DDx – Cryptobia, Sprionucleus/Hexamita

Medical Management

• Formalin – 25-80 mg/L x 2 h
• Copper sulfate

Problem 29 – Ichthyobodosis – Ichthyobodo necator

• Host/location:
  
  • All fish (aquarium, pond and marine fish), but likely different species for marine vs freshwater
  • Skin, gills
• Clinical Signs/Pathology:
  
  • Bluish/steel gray discoloration of skin with excess mucus (Blue Slime), lethargy, anorexia, flashing
  • Epithelial hyperplasia, spongiosis, sometimes little pathology
• Life Cycle: Direct life cycle
• Diagnosis: Flattened, small, pear-shaped organisms with 2 flagellae of different lengths
• Treatment: Salt (some strains may survive salt treatment), copper sulfate, potassium permanganate, formalin

Ichthyobodo

• I. necator aka Costia necatrix.
• Small flagellates, skin and gills of FW and SW teleosts.
• Characteristically pyriform, flagella. ‘Flickering’.
• Heavy infestations can result in high morbidity and rapid mortality with little lesion development.

Question 10

Describe hexamita and spironucleus infections in fish.

What species of fish are typically affected?

What is the life cycle of these parasites?

What are teh typically clinical signs in affected fish?

How are these diagnosed?

How are they treated?

Answer 10

Spironucelus & Hexamita spp

1. Etiology
   
   1. Phylum Metamonada
   2. Family Hexamitidae
   3. Spironucleus, Hexamita
2. Life Cycle & Transmission
   
   1. Direct with no encysted stages
   2. Transmission is horizontal
3. Distribution & Signalment
   
   1. Predominantly freshwater, also in cold marine
   2. Freshwater teleosts commonly affected particularly cichlids (angelfish and discus), cyprinids, salmonids, and Anabantids (bettas, gouramis)
4. Clinical Signs & Findings
   
   1. Inappetence, hyporexia, weight loss most common
   2. Lethargy, agitate swimming, coelomic effusion, exophthalmos, skin ulcers and darkening
   3. Stringy mucoid feces
   4. Lateral line depigmentation in cichlids
5. Diagnosis & Differentials
   
   1. Intestinal scrapes, fecal sample, or cloacal washes – small elongated, pear-shaped flagellates with paired nuclei & 6 anterior and 2 posterior flagella – fast jerky movements
   2. Fluid filled intestines & coelomic effusion on Nx with severe enteritis – systemic disease may produce granulomatous lesions
6. Medical Management
   
   1. Metronidazole 50-100 mg/kg PO q24h x 3-5d

Problem 73 – Diplomonad flagellate infection (spironucleosis, hexamitosis)

Method of Diagnosis

• Wet mount of skin, feces, or viscera with parasites
• Histopathology of lesion with parasites

History

• Anorexia, chronic mortalities
• Physical Examination
• Abdominal swelling, exophthalmos, cachexia

Treatment

• Metronidazole oral
• Metronidazole prolonged immersion
• Magnesium sulfate oral
• Raise temperature to 35 ° C (95 ° F) for 7 days

Epidemiology/pathogenesiss

• Diplomonad flagellates, comprised of various Spironucleus species, have long been associated with gastrointestinal disease in salmonids and aquarium fish.
• Predisposing stress appears to play an important role since these flagellates soften reside in the GI tract of clinically normal fish

Salmonid infections

• Spironucleus salmonis
• Infects debilitated or stressed freshwater salmonids and has also been reported from seawater-cultured salmon
• Primarily infects the anterior intestine and pyloric ceca, but can spread to gall bladder and other organs in advanced cases
• Fish may have abdominal distension caused by fluid accumulation in the gut or may have exophthalmos

Aquarium fish infections

• S. vortenss and S. eleganss infect primarily cichlids and anabantids, causing cachexia, gastroenteritis, and peritonitis
• Many cases of spironucleosis are mixed infections that involve other parasites or bacterial opportunists
• Amphibians may be vectors

Infections in other fish

• Usually incidental findings

Diagnosis

• Determining infection intensity is important for treatment and prognosis
• Fecal exam may reveal the presence of trophozoites, but necropsy will give a more accurate indication of degree of infection
• # organisms per field can help determine severity

Treatment

• Metronidazole is usually effective ass sa bath
• Magnesium sulfate has successfully treated freshwater salmonids
• Raising temperature has been suggested for aquarium fish tolerant of this treatment

Question 11

What are the etiologic agents of marine and freshwater velvet disease?

What is the typical life cycle like?

What species of fish are commonly affected?

What are the typical clincial signs? Which pathogen is more virulent?

How are they diagnosed?

How are they treated?

What are the typical lesions found on necropsy?

Answer 11

Amyloodinium & Piscinoodinium spp. -

Etiology

• Phylum Myxozoa
• Infraphylum Dinoflagellata
• Family Oodiniacea
• Amyloodinium, Piscinoodinium, Crepidoodinium

Life Cycle & Transmission

• Trophonts > tomonts > dinospores (most infective for first 24 hours, but can be up to 15 days; this is the susceptible form)
• Transmitted through water, fomites, aerosolization
• Life cycle takes 3-6 days at 20C (70F)

Distribution & Signalment

• Freshwater & saltwater habitats worldwide
• Amyloodinium ocellatum – marine & brackish fish
  
  • Red drum, gilthead seabream, striped bass, European bass, clownfish, bonnethead sharks
  • Piscinoodinium – freshwater teleosts

Clinical Signs & Findings

• Inappetence, hyporexia, lethargy, hiding, gray/golden/dark coloration of skin – can become granular or ulcerate, pruritus, dyspnea/tachypnea and gill edema may be seen
• Sudden death
• Mortality from Amyloodinium can reach 100% in days
• Mortality with Piscinoodinium is lower

Diagnosis & Differentials

• SS/GC – trophonts are golden-brown and round, oval, or hexagonal in shape; different size trophonts are often present
  
  • Increased mucus, bronchitis, dermatitis with hyperplasia, hemorrhage, necrosis
  • Lugol’s iodine can help visualize the parasites
• DDx – Cryptocaryon & Ich – but these move

Medical Management

• Clean fomites with quaternary ammonium compounds
• Copper sulfate – 0.10-0.15 mg/L for 10-21 days
• Chloroquine diphosphate – 5-10 mg/L for 10 days
• Long-term hypersalinity for FW fish (3-5 g/L)
• If unsuccessful, remove fish for at least 2 weeks

Problem 27 – Marine Velvet Disease - Amyloodinium

• Host/location: Warm water marine fish, may thrive in brackish environments - Gills, skin, eyes
• Clinical Signs/Pathology: Golden or brown dust-like sheen on skin
• Life Cycle:
  
  • Tissue phase is a photosynthetic, nonflagellated, nonmotile algae.
  • Trophont attaches by rhizoids to host -> trophont detaches from host, becomes a tomont -> tomont divides into infective dinospores -> dinospores attach to host and become trophonts
• Diagnosis: dinoflagellate, seen in wet mounts or biopsies
• Treatment: Copper sulfate, chloroquine, freshwater prolonged immersion, hydrogen peroxide bath q6 days x 2 (formalin, potassium permanganate, and altered salinity don’t seem to be as effective)

Problem 28 – Freshwater Velvet Disease - Piscinoodinium

• Host/location: Freshwater fish (common in anabantids, cyprinids, cyprinodontids), larval amphibians
• Clinical Signs/Pathology: Golden or brown dust-like sheen on skin, fish seem to withstand infection heavy infestations better
• Life Cycle: Tissue phase (trophont) detaches, becoming a tomont. Tomont divides into free-living dinospores, which invade fish and become (encysted) trophonts
• Diagnosis: Dinoflagellate, wet mounts or biopsies
• Treatment: Salt is the preferred treatment - copper sulfate, chloroquine also used

Algae (Zoo Path)

• Oodiniosis – cuased by 5 genera of dinoflagellates highly modified to a parasitic lifecycle.
• Amyloodinium ocellatum – amyloodiniosis and marine velvet disease (SW/brackish).
  
  • Mariculture. Affects hundreds of marine spp, elasmobranchs, public and home aquaria.
  • Trophozoites are pyriform to ovoid.
• Piscinoodinium spp – Velvet or rust dz (FW).
  
  • P. limnecticum – NA.
  • P. pillulare – Eu/Asia.
  • Less pathogenic, tropical and temperate FW fish, primarily in aquaria.
  • Trophozoites are pyriform to sac-like, ywllow-brown.
  • Peripheral cytoplasmic chloroplasts.
• Feed as sessile trophozoites (trophonts) on gill, skin, pharyngeal epithelia.
  
  • Pedunculated attachment discs equipped with filiform feeding structures that embed in and damage host cells.
  • Trophozoites detach, become cyst-like tomonts, undergo asexual repro and release hundreds of biflagellated dinospores, attach to host and begin cycle again.
• Gills most important predilection site.
  
  • Skin, corneal involvement.
  • Heavy infestation appears as dusting with fine and grains and rusty hue.
  • Excessive mucus production.
  • Histo – variable degrees of epithelial hyperplasia, inflammation, hemorrhage, necrosis in assoc with trophozoites, attached by short stalk aka rhizoid.
    
    • Gill – hyperplastic clubbing of entire filaments.
    • Sac-like parasites between lamellae.
    • Abundant basophilic cytoplasm, numerous vacuoles and refractile granules.
      
      • Macronuclei centrally located with conspicuously condensed chromasomes.
  • Dx – wet mounts, ID parasite on scrapes or histo.
    
    • Trophozoites detach after death of host, stain dark brown with Lugol’s iodine.

Question 12

What is the etiologic agent of Amoebic Gill Disease? What is the FW equivalent pathogens?

What is the life cycle and transmission of these parasites?

What fish species are commonly affected?

What are the typical clinical signs? What is the morbidity and mortality like?

How is this diagnosed? What differentials should be considered?

How is it treated?

Answer 12

Amoebic Gill Disease

Etiology

• Phylum Amoebozoa
• Marine – Neoparamoeba perurans, N. pemauidensis, N. branchiphila
• FW – Acanthamoeba, Thecamoeba

Life Cycle & Transmission

• Horizontal through contact with infected fish or invertebrates
• Life cycle is unknown – we think the trophozoite is the ony stage
• Amoebae survive on the gills of dead fish for >30 hours

Distribution & Signalment

• Saltwater habitats around the world
• N. perurans – salmonids (esp rainbow trout), turbot, European bass, ayu

Clinical Signs & Findings

• Lethargy, dyspnea/tachypnea; Gills may have white or gray spots, focal pallor, edema, or increased mucus – lesions start at base of the gills
• Morbidity is high; Mortality low but can reach 50-70%

Diagnosis & Differentials

• GC – amoebae are abundant, spherical with some pseudopodia
• Gill hyperplasia, fusion of lamellae, and vesicles with trophozoites
• PCR, ISH, FA tests are available
• DDx – Piscirickettsia, Tenacibaculum, Ichythobodo

Medical Management

• Freshwater bath
• Routine gill exams for Atlantic salmon in sea pens

Problem 31 – Gill Amoebic Infestation – Neoparamoeba perurans

• Host/location:
  
  • Common in cold freshwater and cold marine (less common), common problem in salmonids and turbot
  • Gills
• Clinical Signs/Pathology:
  
  • Excess mucous and whitish grey swollen foci on the lamellae due to hyperplasia
  • Neutrophilic then monophilic infiltrate & mucous cell hyperplasia
• Life Cycle: Direct
• Diagnosis: Free floating amoeba in wet mount
• Treatment:
  
  • 2-6 hour freshwater bath – kills amoeba & reduces osmotic stress from gill damage
  • Formalin bath

Gill amoeba in salmonids (ZP)

• Neoparamoeba spp – Atl salmon, other SW salmonids; economic importance.
  
  • Amoebic gill dz.
• Family Cochliopodidae - Nodular gill dz in RBT.
• Multifocal to coalescing, grey-white, flattened nodular areas.

Question 13

Describe lamprey infestation in fish.

What lesions may be present on affected fish?

How is this treated?

Answer 13

Problem 12 – Lamprey Infestation

• Prevalence: Only in wild fish
• Diagnosis: They’re right there on the fish
• History: Wild caught fish from lamprey-endemic area
• Physical Examination: anemia, circular skin lesions
• Treatment: TFM (3-trifluoro-methy-4-nitrophenol)

Question 14

What are the two subclasses of monogeneans? What part of their anatomy distinguishes them?

What is their lifecycle like?

What are some of the general clinical findings of monogenean infestation?

How are they diagnosed?

How are they treated?

Answer 14

MONOGENEANS IN GENERAL

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea
• Subclasses Monopisthocotylea (prominent hooks – most of the fish parasites) & Polyopisthocotylea (multiple suckers with small hooks)

Life Cycle & Transmission

• All are direct
• All are hermaphroditic and capable of self-fertilization
• Most are oviparous – except for gyrodactylids
  
  • Eggs are produced singly but continuously
• Transmission is horizontal – some vectors exist
• Oncomiricidium (infective larvae) moves by cilia > migrates to perfered tissue site then matures (may take weeks to months)

Distribution & Signalment

• Found worldwide in both salt and freshwater
• Host ranges tend to be narrow but are generally wider in fish under human care
• Some have wide host ranges (Neobenedenia)
• Juvenile fish are more susceptible

Clinical Signs & Findings

• Some may be asymptomatic
• Lethargy, hiding, inappetence, hyporexia, pruritus, dyspnea/tachypnea, yawning & piping
• Erythema, ulcers, fin erosions, small plaques, trailing lines on the skin
• Corneal opacity due to ulcerative keratitis common with Neobenedenia spp
• Secondary infections are common
• Morbidity is high, mortality can be high too

Diagnosis & Differentials

• SS, GC, Corneal scrapes – also often found on other epithelial surfaces – oral cavity, nares, urinary bladder, anus or cloaca
• Flatworms – anterior end is used for feeding, posterior end (haptor) has prominent hooks or multiple suckers to attach to the host
• Fix in ethanol or AFA (ethanol, formalin, acetic acid) for further identification
• Egg assessment
  
  • Following tips – you can collect the sediment and evaluate it with a McMasters slide
  • A fine mesh filter sock on the skipper or on a siphon can be used to count trapped eggs

Medical Management

• Once introduced into a system, eggs that did not hatch during treatment and adults that were not killed will reinfect fish
• An effective strategy is to dose and move the fish to a new system
• Treatment is largely the same for each group, generally consisting of praziquantel immersion, praziquantel orally, trichlorfon immersion, salinity changes, supportive care, and treatment of secondary infections
• All-in-all-out management of breeding groups – keeping systems fallow for 4-6 weeks before a new group is brought in
• Immune stimulant like beta glucans and allicin can decrease severity of clinical signs

Problem 17 – Monogenean Infestation

• Prevalence: WF - 1, WM - 1, CF - 1, CM - 1
• Epidemiology/Pathogenesis:
• Diagnosis: Wet mount or histo of skin or gills with parasite
• History/PE: Grey-white cloudiness to skin, eroded fins, focal hemorrhages on skin, pruritus, dyspnea
• Treatment:
  
  • Formalin
  • Organophosphates
  • Acetic acid, potassium permanganate – freshwater only
  • Praziquantel – marine only
  • Copper
  • Mebendazole, fenbendazole
  • Hydrogen peroxide bath

Question 15

What are some of the important capsalid monogenean parasites of fish?

What is their lifecycle like?

What are some of the host specific capsalids? What are some with wide host ranges?

What are the typical clinical signs like?

How are they diagnosed?

What are some ways to treat and control these parasites?

Answer 15

CAPSALID MONOGENEANS

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea, Subclass Monopisthocotylea
• Family Capsalidae
• Important Genera: Benedenia, Benedeniella, Capsala, Encotyllabe, Entobdella, Neobenedenia, Neoentobdella, Nitzchia, Trilobiodiscus
• Pseudonitzchia

Life Cycle & Transmission

• Direct life cycle, oviparous
• A single Neobenedenia can produce 3300 eggs in 17 days
• Oncomiracidia hatch, attach, and migrate to preferred feeding site

Distribution & Signalment

• Saltwater habitats, probably worldwide
• Many have single host species & strict tissue specificity
  
  • Benedeniella posterocolpa on skin of cownose rays
  • Entobdella bumpusii on the gills of southern stingrays
• Some have wide host ranges
  
  • Benedeniella seriolae – amberjacks in aquaculture
  • Nitazchia species on turgeons
  • Neobenedenia – surgeonfish, spadefish, puffers, butterflyfish, marine angelfish, groupers, barramundi, seabream, olive flounder, obia, amberjacks, tilapia

Clinical Signs & Findings

• Lethargy, hiding, inappetence, hyporexia
• Pruritus, skin darkening, vague white foci on skin, white-to-brown plaques or strands on skin, gills, around teeth, petechiae or skin ulcers
• Ocular opacities from keratitis – Neobenedenia
• Recurrence following stressors is common
• Mortality can be high – disruption of osmoregulation & secondary infections

Diagnosis & Differentials

• Large (2-12 mm), oval, unsegmented flatworms that move by stretching and jerking
  
  • Capsalids are larger than dactylogyrids and gyrodactylids and usually rounder
  • White, gray, translucent
  • Four large black eye spots at anterior end
  • Larvae are smaller, thinner
  • Eggs can be found on gill biopsies and are brown & tetrahedral
• DDx
  
  • Marine teleosts – gyrodactylid, or polyopisthocotyle monogeneans, leeches
  • Marine Rays – monocotylid monogeneans or leeches

Husbandry & Medical Management

• Cleaner fish & inverts – Neon, barber, or cleaner gobies; cleaner wrasse, pacific cleaner or Pederson shrimp
• Reduce brightness & contrast – reduces Neobenedenia hatching
• Praziquantel immersion – 2-10 mg/L
• Praziquantel 120-150 mg/kg PO q24h x 3d, 50-75 mg/kg PO q24h x 3-6 days
• Freshwater dips or long-term hyposalinity - < 18 g/L

Question 16

What are some of Dacylogyrid monogenean genera of concern?

What is their lifecycle like?

What fish do they affect?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 16

DACTYLOGYRID MONOGENEANS

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea, Subclass Monopisthocotylea
• Order Dactylogyridea
• Important genera – Dactylogyrus, Ancylodiscoides, Euryhaliotrema, Euryhaliotrematoides, Haliotrema, Haliotremtoides, Pseudodactylogyrus

Life Cycle & Transmission

• Direct, oviparous
• Ectoparasitic species shed eggs in water; endoparasitic species are found in kidneys and shedd eggs in urine
• Life cycle is temp dependent (6-13d at 80F, 5-6 months at 36F)

Distribution & Signalment

• Predominantly freshwater, but has been found in SW
• Dactylogyrus sp – cyprinids (carp, koi, goldfish, grass carp) and cichlids (discus, freshwater angelfish)
• Pseudodactylogyurs – Eels; Haliotrema – butterflyfish, surgeonfish, groups; Acolpenteron - bass

Clinical Signs & Findings

• Lethargy, hyporexia, weight loss; dark coloration, gray sheen, vague gray or white foci, hyperemia on skin; dyspnea/tachypnea, gill pallor or edema
• Compare to other monogeneans, this is a slow course over months
• Mortality is low but can reach 50%

Diagnosis & Differentials

• SS/GC – loads higher on gills
  
  • Adults are 0.2-2.0 mm in length, 4 small eye spots, one pair large anchor hooks, a small pair of hooks and then marginal hooklets; scalloped head
  • Eggs are tetrahedral
• DDx – Gyrodacylid monogeneans or leeches for FW

Medical Management

• Praziquantel 10 mg/L q2-7d

Question 17

What are some of the gyrodactylid monogeneans of concern to fish?

What is their life cycle like? How does it differ from other monogeneans?

What fish are affected by these monogeneans?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 17

GYRODACYTYLID MONOGENEANS

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea, Subclass Monopisthocotylea
• Order Gyrodactylidea, Family Gyrodactylidae
• High pathogenicity – G. anguillae, G. derjavinoides, G. salaris

Life Cycle & Transmission

• Direct, viviparous (up to 3 generations in a single worm)
• Fast lifecycle (24-60 hours)
• Survives off host a few days

Distribution & Signalment

• Freshwater and saltwater, worldwide
• G. salaris – Atlantic salmon, rainbow trout, Arctic charr
• Pipefish – G shorti, G. syngnathi, G. pisculentus
• European eels – G. anguillae
• Guppies – G. turnbulli, G. bullatarudis

Clinical Signs & Findings

• Lethargy, hiding, hyporexia, weight loss; dark coloration or pallor, vague white or gray foci, pruritus, dsypnea/tachypnea
• Mortality is generally low – but can be up to 30-45% in systems; up to 100% in salmon w/ G. salaris

Diagnosis & Differentials

• SC/GC – less common on gills
  
  • Adults are 0.3-1mm in length, no eye spots, two pairs large central hooks, v shaped head
• PCR is available for G. salaris (OIE guidelines)
• DDx FW – Dactylogyrid monogeneans or leeches
• DDx SW – capsalid or gyrodactylid monogeneans, polypoisthocotyles, leeches

Medical Management

• Virkon, freezing or heating for disinfection
• Prazi – 2-10 mg/L, repeat in 7days (morbidity can be high if parasite loads are high
• Formalin 250 mg/L for 1 hour q7d x 3 treatments – can result in morbidity and mortality
• Hyrdogen peroxide – 50-100 mg/L for 30-60 min q48h x 3 doses – no withdrawal
• Hyperslainity can also be used

Question 18

What are some of the monocotylid monogeneans that are of concern to fish?

What species of fish are affected by these monogeneans?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 18

MONOCOTYLID MONOGENEANS

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea, Subclass Monopisthocotylea
• Order Monocotylidea, Family Monocotylidae
• Several genera of concern

Life Cycle & Transmission

• Direct, oviparous
• Eggs drop to substrate, produce oncomiracidia within weeks
• Wide temperature tolerance

Distribution & Signalment

• Saltwater habitats
• Marine rays, skates, and guitarfish
• Dendomonocotyle – bat rays, whipray, bluespotted stingrays, yellow stingrays, dasyatid stingrays, black blotch stingray, whitespotted eagle rays

Clinical Signs & Findings

• Lethargy, pruritus, hyporexia
• White, translucent, or dark flatworms, particularly on dorsal skin for Dendromonocotyle; other genera tend to be in gills or nasal tissue
• Mortality is generally low

Diagnosis & Differentials

• SS/GC, Grossly Removed
• Adults are large unsegmented worms (1-6 mm); opisthaptor is large relative to body size (looks like a wagon wheel)
• DDx – Capsalid monogeneans or leeches

Husbandry & Medical Management

• Cleaner fish – bluehead and bluestreak cleaner wrasse
• Praziquantel 10 mg/L x 2 hours – good for skin, gill/nasal ones need longer; repeat q2d-2w
• Praziquantel 100-150 mg/kg PO
• Long-term hyposalinity <15 g/L prevented hatching

Question 19

What are some of the pathogenic microbothriid monogeneans?

What species do they affect?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 19

MICROBOTHRIID MONOGENEANS

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea, Subclass Monopisthocotylea
• Order Monocotylidea, Family Microbothriidae
• Several genera of concern

Life Cycle & Transmission

• Direct, oviparous, suspected similar to monocotylids

Distribution & Signalment

• Elasmobranchs, particularly requiem sharks (Carcharhinidae) – host ranges don’t widen under managed care
• Dermophthirius – smalltooth sawfish, Galapagos sharks, bignose sharks, dusky sharks, blacktip reef ,
• Leptocotle - smallspotted catsharks
• Neodermophthirius - lemon sharks

Clinical Signs & Findings

• Pruritus is common; white or gray skin plaques or ulcers – partciulaly on the head and trailing edges of dorsal and caudal fins
• Mortality is low

Diagnosis & Differentials

• Large (2-5 mm) worms with lanceolate to ovoid/round shape. Haptor without hooks or suckers
• Eggs are brown and triangular with short filaments

Medical Management

• Because of narrow host range, its best to remove susceptible species and treat them
• Praziquantel 10 mg/L q2w-2months

Question 20

What are some of the polyopisthocotyle monogeneans that affect fish?

What is different about these monogeneans from the other groups?

What are the typical clinical signs?

How are they diagnosed and managed?

Answer 20

POLYOPISTHOCOTYLE MONOGENEANS

Etiology

• Phylum Platyhelminthes
• Class Monogenoidea, Subclass Polyopithocotylea

Life Cycle & Transmission

• Direct, oviparous, eggs drop off host, oncomiracidia swim or creep till they find a host

Distribution & Signalment

• Predominantly saltwater
• Narrow host ranges
  
  • Erpocotyle – bonnethead sharks
  • Heterobothrium – tiger buffers
  • Microcotyle sebastis – rockfish
  • Neoheterobothrium – olive flounders
  • Zeuxapta - amberjacks

Clinical Signs & Findings

• Lethargy, inappetence, weight loss, pruritus, flounder may stop burrowing, gill pallor, dyspnea/tachypnea
• Mortality is low but can increase with stressor

Diagnosis & Differentials

• SS/GC – up to 0.5 mm with several pairs of clamps or suckers on posterior end
• Eggs are spindle shaped and form long strings or tangled bunches

Husbandry & Medical Management

• Remove egg strings/tangles
• Praziquantel – 100 mg/L x 4 minutes
• Praziquantel 50-400 mg/kg PO q24-48h x 30 days – adding cimetidine allows lower doses
• Long term hyposalinity (18-20 g/L) can help, but some species can tolerate it

Question 21

What is the general life cycle of digenean flukes?

What digeneans have fish as their direct host? What are some of the ones where fish are the indirect host?

What are two important flukes of food fish?

What are the typical clinical signs?

How are these diagnosed?

How are they treated?

Answer 21

DIGENES (EXCLUDING BLOOD FLUKES)

Etiology

• Phylum Platyhelminthes
• Class Trematoda, Subclass Digenea
• Fish as IH – Bolbophorus, Clinostomum, Cryptocotyle, Diplostomum, Nanophyetus, Neasucs, Posthodiplostomum
• Fish as DH – Crepidostomum, Hemiurus

Life Cycle & Transmission

• All indirect with two intermediate hosts – first is typically mollusks, second is fish or amphibians, DH is fish or piscivorous birds
• Some have been elucidated – Bolbophorus damnificus – 1IH is rams-horn snail, 2 IH is channel catfish, DH is the American white pelican
• Sexual reproduction occurs within DH > operculate eggs produce ciliate miracidia that penetrate first IH > miracidia become sporoocysts that develop into cercariae which leave and find the second IH where they develop into metacercariae which then invade the GI tract of the DH when the 2 IH is consumed

Distribution & Signalment

• FW & SW, worldwide
• All bony fish are susceptible, some reports of elasmobranchs
• Some have narrow ranges – B. damnificus in channel catfish; N. salmonicola in Chinook salmon
• Others have wider ranges

Clinical Signs & Findings

• Fish as IH – usually asymptomatic, hyporexia, poor growth, black, white or yellow foci on the skin; corneal opacities or cataracts; abnormal behavior or swimming – increased predation
• Fish as DH – signs are more common; inappetence, poor growth, weight loss, abnormal buoyancy, dark coloration; mortalities

Diagnosis & Differentials

• Adults – found in GI – two suckers (anterior and ventral) no hooks, move in a jerking motion
• Encysted metacercariae can be found in any tissues – generally produce white, yellow, or black cysts

Husbandry & Medical Management

• Reduce contact with snails & birds – cover enclosures, consider mulluscicides or fish that will control snails
• Praziquantel immersion – 1-10 mg/L x 1-9 hours
• Praziquantel 35-330 mg/kg PO

Problem 58: Digenean Trematode Infection

• Diagnosis: wet mount of GI contents or tissue, histopathology
  
  • Distinguished from monogeneans by lack of chitinous hooks and suckers
• History: wild-caught, pond-raised
• Treatment:
  
  • Medical: Praziquantel, surgical removal of cysts
  • Environmental: molluscicide (copper, lime)
• Epidemiology: typically asymptomatic, typically freshwater fish
• Life cycle: egg hatches, infects mollusk, cercaria released by snail, penetrates fish and forms metacercaria
• Pathogenesis:
  
  • Adults: infect GI, rarely swim bladder, ovary, bladder, circulation
  • Cercaria: migration cause hemorrhage, necrosis, inflammation, can be fatal
  • Metacercaria: typically innocuous, will encysts (white/yellow grub, black spot disease), eye flukes can blind fish
• Zoonotic potential: some can infect humans if infected fish ingested

Question 22

What is the life cycle of digene blood flukes?

What are the typical clinical signs?

How are these diagnosed?

How are they treated?

Answer 22

DIGENE BLOOD FLUKES

Etiology

• Phylum Platyhelminthes
• Class Trematoda, Subclass Digenea
• Superfamily Schistosomatoidea, Family Aporocotylidae

Life Cycle & Transmission

• Direct, 1 IH (mollusk or polychaete)
• Worms are dioecious (separate sexes) adults live in major blood vessels or heart; eggs released into vascular system and rupture capillaries in the gills > miracidia develop in IH until they become cercariae and leave to find the DH
• PP 1-3 months

Distribution & Signalment

• Fresh, brackish, and marine fish susceptible including elasmobranchs
• Host range is narrow
• Young fish are more susceptible

Clinical Signs & Findings

• Hyporexia, weight loss, dyspnea/tachypnea; gill pallor may be severe
• Mortalities are possible – occur after increased activity such as feeding or handling

Diagnosis & Differentials

• Finding eggs in vasculature; histology may show significant bronchitis with necrosis, thrombi, and epithelial hyperplasia
• Adults are less commonly identified but can be in large blood vessels or heart chambers – up to 20 mm in length

Medical Management

• Praziquantel 7.5-15 mg/kg PO q24h x 3d – recurrence was reported after treatment

Problem 59: Digenean Gill Infection (Centrocestus infection)

• Diagnosis: gill clip, histopathology
• History: wild-caught, pond-raised, dyspnea
• Physical exam: dyspnea, flared opercula, deformed gill lamella
• Treatment:
  
  • Environmental: molluscicide (snail has operculum and can protect itself from noxious agents)
• Epidemiology: can cause significant morbidity/mortality
• Life cycle: aquatic snail (red rim melania) is intermediate host, adults reside in piscivorous birds and mammals
• Pathogenesis: reactive chondroplasia of gills, capsule forms around parasite, gill inflammation
• Zoonotic potential: snail is intermediate host for human liver fluke, oriental lung fluke

Question 23

What is the life cycle of turbellaria?

What species do they affect?

What is their general life ccyle like?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 23

TURBELLARIA

Etiology

• Phylum Platyhelminthes, Subphylum Rhabditophora
• Parasites: Paravortex, Piscinquilinus, Micropharynx

Life Cycle & Transmission

• Viviparous, direct life cycle completed within 10 days

Distribution & Signalment

• Tropical marine teleosts & elasmobranchs
  
  • Paravortex – butterflyfish, surgeonfish (esp Yellow Tangs), carangids (esp Lookdowns and Florida pompano)
  • Micropharynx – skates and rays

Clinical Signs & Findings

• Black or white foci or linear masses on skin; lethargy, inappetence also reported

Diagnosis & Differentials

• SS/GC – ciliated flatworms (may be within a thin-walled cyst that ruptures with gentle pressure) – typically <0.5 mm but can be up to 3 mm
• DDx – digenes, and Huffmanela spp

Medical Management

• Formalin >50 mg/L
• Prazi immersion 10-20 mg/L or IM 20—40 mg/kg q30d

Problem 18 – Turbellarian Infection

• Prevalence: WM - 3
• Epidemiology/Pathogenesis:
  
  • Species: Ichthyophaga, Paravortex (most studied – affects tangs)
  • Life cycle: has a proliferative phase off the host
• Diagnosis: Wet mount or histo of skin or gills with parasite
• History/PE: Black (rarely white) skin lesions up to 1 mm; larger white lesion that coalesce
• Treatment: Freswhater bath, formalin bath, organophosphate

Question 24

What are some of the cestodes that affect fish?

What is their general life cycle?

How are fish typically affected?

How are these diagnosed?

How are they treated?

Answer 24

CESTODES

Etiology

• Phylum Platyhelminthes
• Class Cestoda, Subclass Eucestoda
• Genera of concern: Schyzocotyle, Diphyllobothrium, Eubothrium, Khawia, Proteocephalus

Life Cycle & Transmission

• Indirect with 1 or 2 IH (inverts or fish)
• DH can be fish or other vertebrates
• Adults are within GI tract of DH > eggs passed in feces > coracidiae eaten by IH > Pleurocercoids encyst in IH which is ingested by DH

Distribution & Signalment

• FW & SW worldwide
• Often narrow host specificities, but some have large ones

Clinical Signs & Findings

• Usually asymptomatic; may see hyporexia, abnormal fecal output, gill pallor, coelomic distension

Diagnosis & Differentials

• Adult segmented worms in GI tract; larvae may be found encysted in gills, muscle, coelom, or viscera
• Tissue cyst DDx – digenes, cestodes, nematodes, leeches, pentastomids, acanthocephalans

Medical Management

• Rarely reported
• But Prazi IM or PO and albendazole PO have been used

Problem 61: Cestode infection

• Diagnosis: wet mounts, histopathology
• History: wild/pond-raised, feeding live copepods or other intermediate hosts
• Physical exam: Worms in intestine, larvae in peritoneal cavity/liver/muscle, emaciation, usually asymptomatic
• Treatment: no proven treatment for larvae
  
  • Medical: praziquantel (oral or bath)
  • Environmental: do not feed potential intermediate hosts
• Epidemiology: fish can be intermediate and/or definitive host
• Pathogenesis: larval cestodes can be damaging to freshwater fish, Asian tapeworm can cause obstruction
• Zoonotic potential:

Question 25

What are some of the leeches that commonly affect fish?

What are the typical clincial signs?

What are some important pathogens that can be transmitted by leeches?

How are they treated?

Answer 25

LEECHES

Etiology

• Phylum Annelida
• Class Clitellata, Subclass Hirudinea

Life Cycle & Transmission

• Direct
• Some stay on host for life of parasite – eggs within cocoons are shed, hatch in substrate and attach to any fish within range
• Other species leave host after a meal (less pathogenic)

Distribution & Signalment

• FW & SW worldwide
• Most fish are susceptible
  
  • Myzobdella in clupeids, drums, and catfish
  • Piscicola in FW pacific salmonids
  • Brachellon in whitespotted eage rays, cownose rays, yellow rays, porcupine rays, and zebra sharks

Clinical Signs & Findings

• Leeches visible on skin, fins, mouth, eyes
• Lethargy, gill pallor (can be severe)
• Pruritus, skin ulcers
• Secondary disease – vectors of infectious hematopoietic necrosis virus, viral hemorrhagic septicemia, infectious pancreatic necrosis virus, Cryptobia spp, hemogregarines, & piroplasms

Diagnosis & Differentials

• Adult leeches – up to 5 cm in length, segmented appearance, anterior and posterior suckers
• Hematology may show anemia & hypoproteinemia

Medical Management

• Coccoons are resistant to treatment – recurrence is common; may be more effective to dose and move to a clean system
• Trichlorfon – 0.25-0.50 mg/L x 1-24h q10-14d
• Individual animals may need fluids, transfusion, iron, or erythropoietin

Problem 13 – Leech Infestation

• Prevalence: WF - 4, WM - 4, CF - 4, CM - 4
• Epidemiology/Pathogenesis:
  
  • Rare in cultured fish, seen in wild-caught or pond-raised fish.
  • Direct life cycle
  • Adults and larvae are both hematophagous
• Diagnosis:
  
  • Larger than monogeneans, segmented (they are annelids with posterior and anterior suckers)
• History: Wild-caught or pond raised fish
• Physical Examination: Anemia, red or white lesions on skin, leeches themselves
• Treatment: Organophosphates

Question 26

What are some of the ascarid nematodes that affect fish?

What are their life cycles like?

What species of fish are affected?

What are some of the typical clinical signs?

How are they diagnosed and treated?

What is the zoonotic potential of this group?

Answer 26

ASCARID NEMATODES

Etiology

• Phylum Nematoda
• Order Rhabditida
• Families Anisakidae & Raphidascaridae

Life Cycle & Transmission

• Indirect, fish are usually the IH or paratenic host
• Gravid females in DH lay eggs that are passed in feces > larvae develop and are ingested by IH where they become encapsulated
• Anisakis simplex – DH are cetaceans and pinnipeds, IH are planktonic crustaceans, 2^nd IH are marine teleosts
• Contracaecum – DH are piscivorous birds or pinnipeds, IH are fish or planktonic crustaceans
• Terranova – DH are elasmobranchs, IH include bony fish

Distribution & Signalment

• Mostly saltwater
• A. simplex – Atlantic cod, hake, mackerel, herring, capelin, monkfish, sardines, salmon

Clinical Signs & Findings

• Usually asymptomatic
• Hyporexia, coelomic distension
• Hemorrhage at vent in salmon (red vent syndrome)

Diagnosis & Differentials

• Found in GI at necropsy or encysted in filets, larvae can also be on serosal surfaces
• DDx – ascarids, cammalanids, capillarids, eustrongylids, philometrids. Leeches, pentastomids, and acanthocephalsn can resemble roundworms.

Medical Management

• Morbidity & mortality has been reported from inflammatory response to deworming
• Reported treatments – albendazole, enamectin, fenbendazole, ivermectin, mebendazole – all PO
• ZOONOTIC POTENTIAL
  
  • A. simplex and Pseudoterranova are the most common food-borne pathogens in this group
  • Gastroenteritis with nodules in intestinal wall
  • Allergic reactions also reported
  • Prevent by cooking or freezing

Question 27

What are some of the important camallanid nematodes of fish?

What is their life cycle like?

What fish species are commonly affected?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 27

CAMALLANID NEMATODES

Etiology

• Phylum Nematoda
• Family Cammalanidae
• Camallanus cotti – most common reported

Life Cycle & Transmission

• Indirect – fish are DH, copepods are IH
• C. cotti is ovoviviparous

Distribution & Signalment

• Freshwater habitats
• Cichlids, livebearers (Poeciliids), Gouramis (Anabantiformes), and Redfin perch are susceptible

Clinical Signs & Findings

• Can be asymptomatic
• Inappetence, weight loss, coelomic distension, red worms can be passing through anus, cloaca or body wall
• Mortalities are rare

Diagnosis & Differentials

• Found in GI at necropsy – up to 1 CM long, usually red
• DDx – ascarids, cammalanids, capillarids, eustrongylids, philometrids. Leeches, pentastomids, and acanthocephalsn can resemble roundworms.

Medical Management

• Morbidity & mortality has been reported from inflammatory response to deworming
• Reported treatments – enamectin PO, fenbendazole immersion, levamisole immersion, pyrantel PO

Question 28

What species of philometrid nematodes most commonly affects fish?

What is the general life cycle of these nematodes?

What species are particularly affected?

What are the typical clinical signs?

How is this diagnosed?

What treatments are effective? Which are not?

Answer 28

PHILOMETRID NEMATODES

Etiology

• Phylum Nematoda
• Order Rhabdita
• Superfamily Dracunculoidea, Family Philometridae
• Philometra is the most commonly reported

Life Cycle & Transmission

• Likely indirect
• IH – copepods, DH are fish
• Males die after mating, so usually only females seen
• Most are viviparous

Distribution & Signalment

• Freshwater, brackish, and saltwater worldwide.
• Philometra – multiple teleosts – particularly centrarchid (bass, sunfish)
• Also reported in several shark species

Clinical Signs & Findings

• Can be asymptomatic
• Lethargy, hyporexia, abnormal swimming
• Exophthlamos with a red appearance to conjunctiva is common if nematodes are retrobulbar

Diagnosis & Differentials

• Found at necropsy – retrobulbar, SC tissues, gills, teeth, oral cavity, GI tract – adult females are up to 35 mm long
• DDx – ascarids, cammalanids, capillarids, eustrongylids, philometrids. Leeches, pentastomids, and acanthocephalsn can resemble roundworms.

Medical Management

• Morbidity & mortality has been reported from inflammatory response to deworming
• Enamectin – 0.05 mg/kg q24h x 7d.
• Fenbendazole & levamisole are ineffective
• Surgical removal also successful

Question 29

What fish are susceptible to anguillicolid nematodes? Which species have greater pathogenicity?

What is the life cycle of these parasites?

What are the typical clinical signs?

How is this diagnosed?

How is this treated?

Answer 29

ANGUILLICOLID NEMATODES

Etiology

• Phylum Nematoda
• Order Rhabditida
• Superfamily Dracunculoidea, Family Anguillicolidae
• Anguillicoloides crassus is biggest pathogen

Life Cycle & Transmission

• Indirect
• Anguillid eels are DH, copepods and ostracods are IH, teleosts are parentenic hosts

Distribution & Signalment

• FW & SW worldwide
• All anguillid eels are susceptible – Japanese, American, European eels – pathogenicity is higher in the American and European eels

Clinical Signs & Findings

• Can be asymptomatic
• Hyporexia, negative buoyancy, coelomic distension, gill pallor, decreased swimming speed or migration
• Mortality rate correlates with tissue damage and dissolved oxygen more than parasite load – can reach 10-20 %

Diagnosis & Differentials

• Eels are large and found in the swim bladder on necropsy – can be seen on radiography, coeliotomy, or endoscopy
• Nematodes in swim bladder of affected species are pathognomonic

Medical Management

• Levamisole immersion 20 mg/L x 6days

Question 30

What species of fish are susceptible to Trichosomoidid Nematodes?

What is the life cycle of these parasites?

What are the typical lesions in affected animals?

How is this diagnosed?

How is this treated?

Answer 30

TRICHOSOMOIDID NEMATODES

Etiology

• Phylum Nematoda
• Order Trichinellida
• Family Trichosomoididae
• Huffmanela spp are the pathogens of concern

Life Cycle & Transmission

• Indirect, IH is crustacean or amphipod, may be prolonged
• Epidermal sloughing may release eggs

Distribution & Signalment

• Saltwater & San Marcos River in Texas
• Many FW & SW species are susceptible
  
  • Carcharhinid sharks are the most commonly reported (Sandbars, Grey Reef, Atlantic sharpnose)
  • Pouting, rockfish, and swordfish also reported
  • FW centrarchid species also reported

Clinical Signs & Findings

• Gray or black, sinuous linear tracts or spots on the skin, similar or nothing in teleosts

Diagnosis & Differentials

• Diagnosed based on eggs found in direct microsopy of lesions
• Eggs are darkly pigmented (golden, brown, or black) and ellipsoid and have bipolar plugs and larvae within them.
• Adults are rarely seen as they are filariform

Medical Management

• Levamisol 10 mg/kg IM repeated q2w for 2 more doses
• Potentially zoonotic – no lesions identified, but eggs have been found in human fecals from consuming infected fish

Question 31

What fish species are commonly affected by pentastomids?

What is the lifecycle of these parasites?

What are the typical clinical signs?

How are they diagnosed?

How are they treated?

Answer 31

PENTOSTOMIDS

Etiology

• Phylum Arthropoda, Subphylum Crustacea
• Subclass Pentastomida
• Agema, Alofia, Diesingia, Leiperis, Sebekia, Subtriqetra

Life Cycle & Transmission

• Indirect – fish are usually the IH, with crocodilians or piscivorous turtles (soft-shell, snapping, mud turtles) as DH
• In DH adults are found within the trachea or lungs; eggs with mite-like larvae are coughed up and passed in feces > larvae become encysted in IH tissue after ingestion or attachment > travel to lungs when IH is ingested

Distribution & Signalment

• Freshwater
• Tilapia, Flagfish, Danios, Poeciliids commonly affected

Clinical Signs & Findings

• Fish are usually asymptomatic, but skin nodules, negative buoyancy, or coelomic distension may be seen

Diagnosis & Differentials

• Pentastomid larvae are usually found on direct microscopy of skin, muscle, swim bladder, serosal surfaces or viscera
• Larvae are multicellular, round-bodies, short, and coiled with small hooks at the anterior end.

Medical Management

• No effective treatment has been reported

Question 32

What fish are particularly susceptible to ancanthocephalans?

What is the life cycle of these parasites?

What are the typical clinical signs of affected fish?

How are they diagnosed?

How are they treated?

Answer 32

ACANTHOCEPHALANS

Etiology

• Phylum Acanthocephala
• Genera of concern – Acanthocephalus, Corynosoma, Ecinorhynchus, Pomphorhyncus, Sclerocollum

Life Cycle & Transmission

• Indirect – one or two IH are typically crustaceans or fish
• Fish can be DHs or paratenic hosts
• Gravid females lay bipolar eggs that are passed in the feces and eaten by first AH > acanthellae hatch and migrates to body cavity and become infective cystacanth stage > IH is ingested and parasite excysts and anchors its proboscis to the intestinal wall

Distribution & Signalment

• FW & SW fish – cyprinids, sea breams, salmonids, suckers and elasmobranchs (spiny dogfish) reported

Clinical Signs & Findings

• Usually asymptomatic; parasites may be seen dangling from anus or cloaca, coelomic distension
• Some mortalities may occur

Diagnosis & Differentials

• Adults are found in intestines – about 1 cm in length but can be much longer, with eversible spiny proboscis anchored in intestinal wall
• Encysted larvae can be anywhere but usually are in mesentery or coelomic wall

Medical Management

• Treatments are not commonly reported
• Benzimidazoles may be affected, but there will likely be inflammatory sequelae as their heads are embedded within the intestinal walls

Problem 62: Acanthocephalan Infection

• Diagnosis: wet mount of GI tract, hooked proboscis
• History: wild-caught fish
• Physical exam: adult worms in intestine, larvae in mesentery or liver
• Treatment: none reported
• Epidemiology: rare in cultured fish
• Life cycle: egg ingested by intermediate host, forms cystacanth, host consumed and cystacanth matures into adult or encysts
• Pathogenesis: minimal clinical signs, heavy burden would presumably cause GI damage

Question 33

What fish are susceptible to copepod parasites?

What is the general lifecycle of these parasites?

What are the typical clinical signs?

What secondary infections are associated with copepod infestation?

How are they diagnosed?

How are they treated?

What is sea lice? What species does it affect? What carrier species exist?

What is the anchor worm?

What are ergasilids?

Answer 33

COPEPODS

Etiology

• Phylum Arthropoda, Subphylum Crustacea
• Subclass Copepoda
• Orders Siphonostomaoida (most), Poecilostomatoida (Ergasilus), and Cyclopoida (Lernaea sp)

Life Cycle & Transmission

• Most are direct - single host and multiple life stages
• Dioecious – males are temporary parasite, females stay attaches and produce egg sacs > free living nauplii hatch and develop into infectious copepodids
• Duration varies with temps
• Important asymptomatic carriers – three-spined sticklebacks for Lepeophtheirus salmonis

Distribution & Signalment

• FW & SW – L. salmonis just in northern hemisphere
• All fish are susceptible
• Alebion – carcharinid sharks, Caligus – silverisdes, Lepeophthiris – zebra, reef, shovenose sharks & mantas; L. salmonis – salmonids; L. cycyprinacea – cyprinids

Clinical Signs & Findings

• Grossly visible white to gray foci or trailing lines
• Lethargy, inappetence, petechia, skin ulcers at attachment sites; ulcerative keratitis, gill pallor, dypnes/tachypnea
• Coinfections with Aeromonas, Pseudomonas, Vibrio, Tenacibaculum, infectious salmon anemia virus, infectious hematopoietic necrosis virus

Diagnosis & Differentials

• Adults are 1-30 mm with several compartment and four pairs of jointed swimming appendaged
• Lernea sp have long thin bodies with reduced limbs for burrowing
• Free living species are sometimes found on scrapes – they don’t have the big grasping arms

Husbandry & Medical Management

• Cleaner fish – goldsinny, rock-cook, corkwing, ballan, scale-rayed wrasse; cunner fish, goldfish, lumpfish
• Permanently attached adults resistant to treatment
• Trichlorfon immersion - 0.2-1.0 mg/L for 1-24 h repeated 1-2 times q5-10 days
• Diflubenzuron immersion – 0.01-0.05 mg/L for 8-24 hours repeated a few times
• Lufuneron immersion – 0.01 mg/L q24h x 7d
• Enamectin PO – 50 mcg/kg q24h x 7d for L. salmonis

Problem 14 – Copepod Infestation

• Prevalence: WF - 2, WM - 4, CF - 3, CM - 1
• Epidemiology/Pathogenesis:
• Diagnosis: Wet mount or histo of gills, skin, or mouth with parasite
• History: Wild-caught, pond-raised, cage-cultured fish, skin sores
• Physical Examination:
  
  • Copepods attached to gill arches, oral cavity, or skin
  • Erosions, ulcerations, or raised red areas on the skin
• Treatment:
  
  • Organophosphates
  • Diflubenzuron
  • Salt v Freshwater Bath
  • Enamectin, Ivermectin

Ergasilids

• Freshwater fish, attaches to gills and skin
• Resembles free-living copepods, may crawl on skin of fish
• Often incidental findings

Sea Lice – Lepeophtherius salmonis & Caligus spp

• Pen-reared salmonids, most common in Europe
• Heavy feeding causes skin ulcers, petechial hemorrhage at feeding site
• Life cycle: Free-living nauplius-> copepodid->chalimus->pre-adult->adult, temperature dependent
• L. salmonis frequently transmits aeromonas and infectious salmon anemia virus

Anchor Worms – Laernea spp

• Aquarium and pond reared fish, tadpoles
• Attach to skin, gills
• Possess specialized anchors
• Life Cycle: Temperature important, undergoes several stages off the host. Adults on host release eggs, which hatch as Nauplius larvae, mature into infective copepodid larvae. Male dies after mating, female penetrates skin and differentiates into adult
• Manual removal, treat with organophosphates

Question 34

What fish are susceptible to isopods?

How do cymothoid versus gnathiid isopods differ?

What are the typical clinical signs of affected fish?

How are these diagnosed?

What species is found in the pericardium of carcharhinid sharks?

How are these treated?

Answer 34

ISOPODS

Etiology

• Phylum Arthropoda, Subphylum Crustacea
• Class Malacostraca, Order Isopoda
• Cymothoids – adults are parasitic
• Gnathiids – larvae are parasitic

Life Cycle & Transmission

• Direct, one host, multiple larval stages
• Larger female typically seen with marsupium filled with larvae
• Gnathiidae – larvae feed on blood and tissue fluids (skin and gills mostly); adults are free-living

Distribution & Signalment

• Saltwater habitats
• Ceratothoa – Atlantic Salmon
• Gnathia trimulata – triplefins, many elasmobranchs: G. maxillaris – seabream and European bass

Clinical Signs & Findings

• Isopods grossly visible on skin or oral cavity
• Dyspnea/tachypnea; unilateral distension of a gill operculum; gill pallor
• Gnathiid isopods are much smaller and in higher numbers

Diagnosis & Differentials

• Adults can be up to 6 cm in length, have segmentation and needle-like mouthparts for feeding
• Larvae are up to 6 mm, with segmentation around body but not in mid-abdominal area
• Nataolana borealis – found in pericardium of carcharhinid sharks

Medical Management

• Manual removal or crushing adults
• Trichlorfon immersion – 0.3-0.5 mg/L for 48h q7d x 3 tx for gnathiid larvae

Problem 16 – Isopod Infestation

• Prevalence: WF - 4, WM - 4, CM - 4
• Epidemiology/Pathogenesis:
• Diagnosis: Observation of parasite in gill chamber, mouth, or skin
• History/PE: Isopod visible grossly
• Life Cycle: Most are parasitic as both juveniles and adults
• Treatment: Remove with forceps, organophosphate baths

Question 35

What fish are susceptible to branchiurans?

What is the typical life cycle of these parasites?

What are the typical clinical signs?

How are they diagnosed?

How are they controlled?

Answer 35

BRANCHIURANS

Etiology

• Phylum Arthropoda, Subphylum Crustacea
• Subclass Branchiura, Family Argulidae
• Argulus most well known

Life Cycle & Transmission

• Direct, adults are dioecious, mating occurs on the host, females leave to lay eggs in dark areas – larvae are immediately infective – takes 30-100 days

Distribution & Signalment

• Mostly freshwater fish (parasite seen in SW too)
• Argulus – salmonids (rainbow trout), cyprinids (goldfish, carp, koi); FW stingrays (Potamotrygon)

Clinical Signs & Findings

• Pruritus, inappetence
• Grossly visible on skin, fins, or oropharynx – resemble white or dark plaques which move slowly; skin ulcers
• Argulus may be vectors for infectious disease

Diagnosis & Differentials

• Adults are 3-20 mm in length, with small jointed appendages –they’ll leave when fish is disturbed

Husbandry & Medical Management

• Cleaners – mosquitofish, white crappies, longear sunfish
• Diflubenzuron, Lufenuron, Trichlorfon immersions
• Hypersalinity & formalin not effective

Problem 15 – Branchiuran Infestation (Fish Lice – Argulus sp)

• Prevalence: WF - 3, WM - 4, CF - 3, CM - 3
• Life Cycle: Eggs hatch in vegetation, juveniles have no suckers
• Diagnosis: wet mount of skin or buccal cavity
• History: Pruritius, red sores, wild-caught or pond-raised fish
• Physical Examination: Focal red lesions on skin, focal darkening of skin
• Treatment: Organophosphates, formalin, potassium permanganate

Question 36

What type of parasite are myxozoans?

What is their general life cycle? What are the two stages?

What are some general clinical signs? Are there any specific signs to certain species?

How are they diagnosed?

How are they treated?

Answer 36

MYXOZOANS IN GENERAL

Etiology

• Phylum Cnidaria, Subphylum Myxozoa
• Classes Myxozoa & Malacosporea

Life Cycle & Transmission

• Indirect
• Typically, vertebrates are the DH and invertebrates are the IH
• Myxospore stage occurs in vertebrate hosts
• Actinospore stage occurs in invertebrate hosts and are released when host dies or is ingested

Distribution & Signalment

• FW & SW
• Host ranges are typically narrow
  
  • Sinuolinea – Weedy sea dragons
  • Kudoa & Chloromyxum in elasmobranchs
• Juvenile fish show more severe signs

Clinical Signs & Findings

• Can take weeks to months or years for signs to develop
• Inappetence, weight loss (can be severe), gill pallor
• Most are histozoic and produce white nodules known as pseudocysts
  
  • Gill infections – dyspnea/tachypnea – Henneguya, Myxobolus
  • Renal infections – coelomic distension – Hoferellus
  • Neural & cartilaginous infections – Myxobolus
• Mortality is low but can reach 100% with severe or chronic stressors

Diagnosis & Differentials

• White pseudocyst
• Spores – most have two polar capsules
• PCR is available for some organisms

Medical Management

• Salinomycin, amprolium, fumagillin PO

Problem 63: Myxozoan Infection

• Diagnosis: wet mount, stained smear, histopathology
• History: wild-caught, pond-raised, nodules that enlarge slowly
• Physical exam: white/yellow nodules (pseudocysts)
• Treatment:
  
  • Medical: fumagillin PO
  • Environmental: disinfection difficult
• Epidemiology: obligate parasites of tissues (intracellular space, vessels) or organ cavities (gall, swim, urinary bladder), most intracellular
• Life cycle: undetermined, suspect indirect cycle with asexual reproduction in fish and sexual reproduction in invertebrate. Multicellular spore released from fish and ingested by invertebrate. Infective stage released from invertebrate and penetrates epithelium/gill of fish
• Pathogenesis: most innocuous, heavy burdens can cause tissue damage and necrosis

Myxozoa - ZP

• Characterized by multicellular spores that form when constituent cells come together to form 1-7 outer spore shell valves that enclose one to many amoeboid germ cells (sporoplasms) and one to multiple nematocyst-like polar capsules.
  
  • Polar capsule has extrudible filament for host cells.
• Myxobolus cerebralis – Whirling dz of salmonids.
• LC involves alternation between vertebrate and invertebrate host with sporogony ine ach.
• Two classes:
  
  • Malacosporea.
  • Myxosporea.
    
    • Myxospore phase in fish, rarely amphibians or reptiles are vertebrate host, produces myxospore infective to the invert host.
      
      • Invert host is an annelid.
• Most cause little or no inflammation. May incite chronic inflammation, granulomas.

Question 37

What fish species are susceptible to enteromyxum?

What is different about this myxozoans transmission?

What are typical clinical signs?

How is this diagnosed?

How is it treated?

Answer 37

ENTEROMYXUM SPP

Etiology

• Phylum Cnidaria, Class Myxozoa
• Family Myxidiidae
• Enteromyxum spp.

Life Cycle & Transmission

• Indirect, invertebrate IH, fish DH
• E. scophthalmi can transmit between fish which is unusual

Distribution & Signalment

• Tropical marine teleosts
  
  • Aquaculture – seabream, tiger puffer, red drum, knifejaw, turbot, European bass, flounder
  • Aquarium – blennies, wrasses, yellow and powder blue tangs, emperor angelfish

Clinical Signs & Findings

• May take months to show following infection
• Inappetence, coelomic distension is common, cloacal or anal prolapse, skin discoloration, enopthalmos, gill pallor
• Mortalities are chronic and intermittent, can reach 100%

Diagnosis & Differentials

• Finding spores on cytology, histology or fecal
• Spores have two polar capsules and are thin walled
• Necropsy usually shows severe emaciation, catarrhal enteritis, and an enlarged gallbladder
• PCR is available for E. leei

Medical Management

• Salinomycin & amprolium PO together

Question 38

What is the etiologic agent of hamburger (proliferative) gill disease?

What fish species are susceptible?

What is the life cycle like?

What are the typical clinical signs?

How is this diagnosed? What are the classic lesions on necropsy?

How are these cases treated?

Answer 38

HENNEGUYA SPP. AKA HAMBURGER GILL DISEASE

Etiology

• Phylum Cnidaria
• Class Myxozoa
• Family Myxobolidae

Life Cycle & Transmission

• Channel catfish are vertebrate host (DH)
• Benthic oligochaetes are the invertebrate host

Distribution & Signalment

• FW & SW
• Large problem in southeastern US aquaculture
• H. ictalurid – channel catfish
• H. koi – carp
• H. salminicola & H. zschokkei – Chinook & coho salmon

Clinical Signs & Findings

• Inappetence, weight loss
• Dyspnea/tachypnea despite adequate DO
• Gills look mottled, mashed, edematous, and bleed easier (looks like hamburger meat)
• Mortality can exceed 50%

Diagnosis & Differentials

• Suspect based on signs, confirmed with cytology, histology, or molecular testing
• Mature spores are slender with two polar capsules, each spore has two caudal processes or tails
• Histology – severe bronchitis with epithelial hyperplasia, fusion, gill cartilage lysis (pathognomonic in catfish)
• PCR & qPCR tests available

Medical Management

• Fish can recover if removed from source of infection and stressors are minimized
• Medical treatment is rarely effective

Problem 64: Proliferative Gill Disease (Henneguya ictalurid)

• Diagnosis: wet mount, histopathology
• History: pond-raised channel catfish
• Physical exam: pale, thickened, broken gill lamellae, dyspnea
• Treatment:
  
  • Medical: supplemental oxygen, avoid stress
• Epidemiology: variable mortality in channel catfish in SE US and CA, 61-68F
• Life cycle: worms release actinospore A ictalurid which then infects fish orally or dermally
• Pathogenesis: epithelial hyperplasia, granulomatous bronchitis, cartilage necrosis

Question 39

What is the etiologic agent of whirling disease?

What species are affected? Are there any reservoir species?

What is the life cycle like?

What are the typical clinical signs?

How is it diagnosed?

How is it treated?

Describe the pathophysiology of disease.

Answer 39

MYXOBOLUS SPP. AKA WHIRLING DISEASE

Etiology

• Phylum Cnidaria
• Class Myxozoa
• Family Myxobolidae

Life Cycle & Transmission

• Salmonids are the vertebrate host (DH)
• Oligochaetes (Tubifex) are the invertebrate host
• Actinospores are viable for 3-4 days

Distribution & Signalment

• M. cerebralis is native to Eurasian continent but is now many locations
• M. cerebralis – farmed and wild FW salmonids (rainbow trout esp, sockeye salmon, cutthroat trout, gila salmon, brook trout, Danube salmon, grayling). Brown trout and lake trout rarely show signs
• M. albi common in gobies & lungfish
• Disease is more severe in young fish before it becomes ossified

Clinical Signs & Findings

• M. cerebralis affects cartilage and nerves
  
  • Rapid spiraling swimming, dark tails common in 3-6 MO juveniles
  • Skeletal abnormalities – short opercula & rostrums, jaw & spinal deformities
• M. koi affects gill cartilage
• M. albi affect gill, skull, pectoral cartilage

Diagnosis & Differentials

• Tentative off signs, confirmed by molecular testing
• Mature spores within pseudocyst
• Histology shows granulomatous inflammation and spores at tissue site (in salmonids in the cartilage)
• PCR & qPCR available for M. cerebralis

Medical Management

• Treatment rarely effective – salinomycin and amprolium PO 110 mg/kg q24h x30d has been most effective at reducing severity of disease

Problem 68 – Whirling Disease (Black tail)

• Method of Diagnosis
  
  • Wet mount of cartilage digest having typical spores
  • Histology of cartilage having typical spores
• History
  
  • Whirling or tail - chasing behavior in young salmonids fish raised on mud bottom
• Physical Examination
  
  • Scoliosis, kyphosis, other axial skeletal deformities; postural defi cits; regional pigment abnormalities
• Treatment
  
  • Disinfect and quarantine
  • Raise stock in parasite - free water for first 6 months of life
  • Disinfect water source
• Epidemiology
  
  • Caused by Myxobolus cerebralis
  • Previously only in culture fish, now there are outbreaks in wild salmonid populations
  • All salmonids in the genus Oncorhynchus (esp rainbow trout) are susceptible
    
    • Brown trout are more resistant and is considered a reservoir
  • Severity inversely proportionate to age (100% mortality in newly hatched fry, little to no clinical signs in fish over 6 months)
  • After 1 year there is little cartilage available in the skeleton for infection, but even fish that are several years old can be infected via the gill cartilage and thus become carriers.
  • Depending on temperature (takes longer in low temps) the entire life cycle may require over 1 year, making it an insidious problem that may go undetected for a long time.
  • Most myxospores remain trapped in the skeletal tissues until the fish dies but some
  • can be released by live fish.
  • Myxospores can be spread in the feces of piscivorous birds.
  • Myxopores must be ingested by an oligochaetefi nal host, the sludge worm ( Tubifex tubifex)
  • The myxopore releases the sporoplasm, which differentiates into an actinosporean.
  • After completion of both asexual and sexual stages in tubifex the actinosporean directly penetrates a new host via the skin, gill, or buccal epithelium.
  • It then migrates from the epithelium to the peripheral nerves and then the central nervous system, finally reaching the cartilage.
• Pathogenesis
  
  • The parasite feeds on cartilage of the axial skeleton and clinical signs are related to this damage
  • First signs is usually a black tail caused by vertebral instability and damage to the spinal cord
  • Predilection for cartilage causes impaired balance and a frenzied, tail-chasing behavior (whirling)
  • Heavy infections may cause mortality without clinical signs
  • The parasites lyse cartilage and feed on chondrocytes; histologically there is a reactive chondrosteal proliferation
• Diagnosis
  
  • Hard to make a wet mount of fresh tissues since spores are in the cartilage
  • Usually diagnosis by hisstopath
• Treatment
  
  • Whirling disease can be eliminated in culture facilities only by thorough disinfection and quarantine and repopulation with specific - pathogen - free stock.
  • Raising fish in concrete raceways to avoid exposure to mud is also useful
  • Whirling disease is reportable in the US
  • Spores can survive in fresh and frozen fillets for over 3 months and can survive drying
  • All spores are killed by unslaked lime and chlorine

Question 40

What fish are susceptible to Ceratonova and Ceratomyxa infestations?

What is the life cycle of these parasites?

What are the typical clinical signs?

How are these diagnosed?

How are they treated?

Answer 40

CERATONOVA & CERATOMYXA SPP.

Etiology

• Phylum Cnidaria
• Class myxozoa
• Family Ceratomyxidae
• Ceratonova shasta is the main organism of concern

Life Cycle & Transmission

• Salmonids are vertebrate host (DH)
• Freshwater polychaetes (Manayunkia) are the IH
• Mature actinospores are viable for days to weeks

Distribution & Signalment

• C. shasta - Restricted to Oregon & California river systems
• Ceratonova shasta – rainbow trout, Chinook salmon
• C. gasterostea – three-spined stickleback
• Ceratomyxa spp – marine teleosts & elasmobranchs

Clinical Signs & Findings

• Lethargy, inappetence, weight loss
• Coelomic distension due to ascites and granulomatous inflammation is common; Vent swelling and hyperemia is common; Skin darkening common in rainbow trout; Gill pallor may be seen
• Mortality in juvenile salmonids ~ 40%, can reach 100%

Diagnosis & Differentials

• Finding spores on impression smears, histology of GIT, GB, kidney or coelom
• Spores are arcuate (kidney-bean shaped) with two polar capsules
• Coelomic effusion and hemorrhage/necrosis or caudal intestines and vent are common
• PCR available for C. shasta

Medical Management

• Not reported

Problem 65: Ceratomyxa shasta infection

• Diagnosis: west mounts, histopathology
• History: salmonids exposed to parasite-endemic waters
• Physical exam: swollen coelom, necrotic muscle lesions
• Treatment:
  
  • Medical: no known treatment
  • Environmental: can slow progression with saltwater, disinfection of water
• Epidemiology: Western US/Canada, can be infected at 39-43F but grows fastest at 64F
• Life cycle: infection acquired from actinospores released by freshwater polychaete Manayunkia speciosa
• Pathogenesis: diffuse granulomatosis in GI then spreads to liver, kidney, spleen, gonads, muscle

Question 41

What is the etiologic agent of polycystic kidney disease in goldfish?

What is the lifecycle of this parasite?

What are the typical clinical signs?

How is this diagnosed?

How is this treated and controlled?

Answer 41

HOFERELLUS SPP. – POLYCYSTIC KIDNEY DISEASE IN GOLDFISH

Etiology

• Phylum Cnidaria
• Class Myxozoa
• Family Myxobilatidae
• Hoferellus carasii is the most important organism

Life Cycle & Transmission

• Fish are vertebrate host
• Freshwater oligochaetes (Branchiuriua, Nais spp) - IH

Distribution & Signalment

• Originally in European & Japan FW, now worldwide
• H. carassii – goldfish & Prussian carp, not koi
• H. cyprinid – koi, but not goldfish
• H. gilsoni – European eels
• H. gnathonemia – elephantnose fish

Clinical Signs & Findings

• Coelomic distension from severe renomegaly and coelomic effusion
• Inappetence, abnormal swimming/buoyancy, or gill pallor may also be seen
• Mortality is generally low
• DDx – obesity, egg retention, neoplasia, infection

Diagnosis & Differentials

• US to find cysts; confirm with cytology of kidney, urinary bladder, cystic or coelomic fluid
• Spores are shaped like bishops hat with pointed anterior end and two symmetrical polar capsules

Medical Management

• Supportive care may help, but euthanasia should be considered if clinical signs are severe

Problem 66: Hoferellus carassii infection (kidney enlargement disease)

• Diagnosis: wet mounts, histopathology
• History: pond-raised goldfish
• Physical exam: coelomic swelling, often asymmetrical
• Treatment:
  
  • Environmental: disinfect and restock with uninfected goldfish
• Epidemiology: Europe, NA, Asia, infected in summer and show signs in fall, spores produced in spring with signs are severe and most mortality occurs.
• Life cycle: Oligochaete worms are final host
• Pathogenesis: kidney is cystic and hypertrophied, can displace swim bladder

Question 42

What fish species are affected by Kudoa?

What are the effects of this infection?

How is this diagnosed?

What are the effects of eating contaminated meat?

Answer 42

KUDOA SPP.

Etiology

• Phylum Cnidaria, Class Myxozoa
• Order Multivalvulida, Family Kudoidae
• Kudoa thyrsites is the most important organism

Life Cycle & Transmission

• Poorly understood, likely involves marine invertebrates as IH

Distribution & Signalment

• SW & brackish habitats worldwide
• Usually marine teleosts, but has a wide host range
• K. thyrsites – Atlantic salmon mostly, but reported in >18 fish families
• K. clupeidae – Atlantic menhaden
• K. Lutjanus – crimson snapper

Clinical Signs & Findings

• Fish are generally asymptomatic, reduced. Feeding or abnormal swimming may be seen
• Signs of infection occur after processing due to proteolytic damage as the spores release causing post-harvest myoliquefaction in cultured fish

Diagnosis & Differentials

• Impression smears or histology of affected muscle
• Spores are radially symmetrical with four (up to 7) polar capsules

Medical Management

• Little effect & not reported
• Potential as foodborne pathogens following consumption of undercooked meat – self-limiting vomiting and diarrhea

Question 43

What is the etiologic agent of proliferative kidney disease?

What fish species are commonly affected? Are any asymptomatic carriers?

What is the life cycle of this parasite?

What are the typical clinical signs of affected fish?

How is it diagnosed?

What treatments are used?

Answer 43

TETRACAPSULOIDES BRYOSALMONAE

Etiology

• Phylum Cnidaria, Subphylum Myxozoa
• Class Malacosporea
• Tetracapsuloides bryosalmonae being most important

Life Cycle & Transmission

• Salmonids are vertebrate hosts (DH)
• Freshwater bryozoans are IH
• Spores are released through urine, remain infectious for 12-24 hours

Distribution & Signalment

• FW salmonid habitats, particularly NA & Europe
• T. bryosalmonae – rainbow trout, pike; brown trout may be asymptomatic carriers

Clinical Signs & Findings

• Lethargy, inappetence, exophthalmos is common, coelomic distension (dorsocaudal coelom) is common, skin darkening, gill pallor
• Morbidity and mortality generally low, but can reach 90%

Diagnosis & Differentials

• Spores found on cytology or histo or kidneys (may also be on gills, liver, or spleen)
• Spores are ovoid with two spherical polar capsules
• Necropsy shows renomegaly, splenomegaly, serosanguinous coelomic effusion, pale viscera. Kidneys may be gray and mottled

Medical Management

• Treatment is rarely effective
• Hypersalinity immersion 8-12 g/L for 14-21 days may reduce morbidity and mortality

Problem 67: Proliferative kidney disease (Tetracapsuloides bryosalmonae)

• Diagnosis: histopathology, impression smear
• History: chronic morbidity/mortality in salmonids
• Physical exam: hypertrophic kidney, anemia, swollen coelom, splenomegaly
• Treatment:
  
  • Medical: malachite green bath (not in food fish), salt bath 8-12ppt can decrease morbidity/mortality
  • Environmental:
• Epidemiology: Pacific NW, primarily in summer, 10-95% mortality,
• Pathogenesis: interstitial nephritis then spleen, GI, gill, liver, pancreas, muscle

Question 44

Describe the eimeria that affect fish.

What is the general life cycle?

What Eimeria species affect weedy sea dragons? What about rays?

What are the typical clinical signs?

How are these diagnosed?

How are they treated?

Answer 44

Eimeria spp.

Etiology

• Phylum Myzozoa, Subphylum Apicomplexa
• Subclass Coccidiasina, Family Eimeriidae

Life Cycle & Transmission

• Direct & indirect cycles
• Oocysts sporulate, release sporocysts with sporozoites within. Sporozoites develop into schizonts that asexually produce merozoites to generate more schizonts. Micro- (male) and macro- (female) gametes are then produced to develop into oocysts.
• Oocysts can survive more than 2 years in SW at 70F

Distribution & Signalment

• Host ranges are narrow
  
  • E. fundulid – killifish
  • E. phyllopterycis – weedy sea dragons
  • E. southwelli – myliobatid rays (cownose, spotted eagle, and bullnose eagle rays most reported)
  • E. syngnathi – blackline pipefish
  • Juvenile fish may be more susceptible

Clinical Signs & Findings

• Weight loss and poor body condition are common
• Regurgitation and mucoid or white fecals and lethargy may be seen
• Coelomic distension due to effusion is common
• In cownose rays, blotchy skin discoloration & distended cutaneous lymphatics are reported
• Mortality is generally low, but may reach 100% in cownose rays once clinical signs are seen

Diagnosis & Differentials

• Finding oocysts on fecal, intestinal scrapings, coelomic fluid or impression smears
• Coelomic aspirates and flushes are most diagnostic for myliobatid rays
• E. southwelli oocysts are elongated (pea-pod shaped) with four sporocysts each with two sporozoites
• E. phylopterycis – spherical with thin wall

Medical Management

• Toltrazuril 10 mg/kg q24 x 3-5 days, repeat in 10 days (q48 dosing has been ineffective)
• Ponazuril 50 mg/kg PO q7d x 4w reduced oocyst #s
• Copper wire particles (37-2000 mg/kg) have improved signs

Problem 74 – Tissue coccidiosis

• Method of Diagnosis
  
  • Wet mount of affected tissue having oocysts
  • Histological section of affected tissue with parasite life stages
• History
  
  • Varies with organs affected; may be acute or chronic
• Physical Examination
  
  • Varies with organs affected (Table II - 74 )
• Treatment
  
  • Monensin oral
  • Epidemiology
  • Some coccidia are hemoparasites, but the most important fish pathogens affect solid tissues
  • Almost all tissue coccidia that infect fish belong to family Eimeriidae (**see pg 259 for list of species)
  • Cryptosporidium also reported but rare
  • All are intracellular parasites
  • They are uncommon problems in most cultured fish but have caused serious disease in some (ie common arp)
  • Piscine coccidia ten to be less species-specific than mammalian coccidia
  • The infective stage (sporozoite) is formed within an oocyst
  • After ingestion by the host the sporozite penetrates the intestinal wall to reach the final site of infection
  • In the host cell, the parasite forms a schizont, which produces many merozoites by asexual reproduction
  • Merozoites produce flagellated microgametes and oocyte - like macrogametes, which mate, producing a zygote
  • Zygote then forms an oocyst containing sprocysts
  • Unlike those of mammals, oocysts of fish - parasitic intestinal species that are shed in the gut are very short - lived and lose infectivity in several days.
  • Life cycle is usually direct, but a few species are indirect
• Pathogenesis
  
  • Intestinal infections are often asymptomatic but can cause enteritis
  • Extraintestinal parasites can cause lesions with characteristic destruction of target cells followed by inflammation
    
    • Common infection sites are repro organs, liver, spleen and swim bladder
• Diagnosis
  
  • Diagnosis is based on identification of oocysts
  • In contrast to coccidia infecting mammals, oocysts of fish parasites are thin walled, the walls are of host origin, and they are usually sporulated (i.e., sporozoites are present) when shed
  • The fragile oocyst wall prevents the use of concentration procedures that are used for mammalian coccidia, requiring use of fresh smears or histopathology.
• Treatment
  
  • Monensin significantly reduces infection burdens of some species
  • Toltrazuril has also shown experimental efficacy, amprolium has as well

Question 45

Describe cryptosporidiosis in fish.

What is the general life cycle of these parasites?

What fish species are susceptible?

What are the typical clinical signs?

How is it diagnosed?

How is it treated?

Answer 45

Cryptosporidium spp.

Etiology

• Phylum Myzozoa, Subphylum Apicomplexa
• Subclass Coccidiasina, Family Cryptosporidiidae
• C. molnari & scophthalmi

Life Cycle & Transmission

• Oocysts ingested by host, sporozoites released which parasitize GI & respiratory epithelium. Sporozoites develop into schizonts that produce merozoites and eventually micro- and macro- gametes to produce more oocysts.

Distribution & Signalment

• FW & SW
• FW Aquarium – koi, goldfish, Oscars, guppies, FW angelfish, tetras, gouramis
• SW Aquarium – orange spined unicornfish, seahorses & sea dragons
• Aquaculture – gilthead sea bream, European bass, turbot, sea mullet, barramundi
• Juveniles are more susceptible

Clinical Signs & Findings

• Weight loss, poor body condition are most common
• Regurgitation, mucoid or white feces can be seen
• Mortality is generally low

Diagnosis & Differentials

• Finding parasites on cytology or histology of GI mucosa
• Oocysts are spherical with indistinct sporozoites and are acid-fast positive
• Histology may show granulomatous gastritis or enteritis
• PCR should be followed by sequencing
• DDx – Mycobacterium, Nocardia

Medical Management

• Treatment may improve signs, but recurrence is common
• Supportive care
• Ponazuril or metronidazole may reduce clinical signs
• Fish species are not zoonotic, but C. parvum has been isolated from a variety of fish

Question 46

Describe some of the challenges in addressing parasites in large saltwater aquariums.

How are capsalid monogeneans managed?

What about leeches?

Spotted eagle rays are affected by what type of monogeneans? How are they managed?

How is Eimeria southwellii managed in cownose rays?

What advancements in scuticociliatosis have been made in sygnathid and elasmobranch species?

Answer 46

Fowler’s 9th: Ch 47 Techniques for addressing parasites in saltwater aquariums

• · It’s important to:
• o Establish a thorough quarantine protocol
• o Implement a thorough routine preventative medicine protocol
• o Examples of both are provided in ch for referral if needed
• o The ch contains an extensive chart of reported treatment protocols
• · Diagnostics
• o Water quality
• o Visual observation
• o Wet mount (skin scrape, fin clip, gill clip)
• o Necropsy
• · Clinical signs
• o abnormal/ erratic swimming, flashing (rubbing body across surfaces), clamped fins (holding fins close to body), increased respiratory rate/ effort, piping (gulping at the surface), color change to skin/ gills, excessive mucus, raised nodules, ulcerative/ erosive lesions, scale/ fin loss, exophthalmia/ cloudy eyes, coelomic distention, emaciation, gross large external parasites
• · Treatment
• o Water quality is key
• o Factors affecting treatment plan: target parasite, fish species, temperature, salinity, DO, pH
• o Formalin decreases dissolved oxygen and is toxic to invertebrates
• o Oviparous parasites are harder to treat/ usually require longer and repeat treatments vs viviparous parasites
• o Treating entire system vs individual
• § When possible, treatment of entire aquarium environment is recommended
• § Must consider effect on filtration, microbe community, plants, and other animals if treating entire system
• o Once a parasite is introduced to a complex, established system -> treatment is often problematic
• o Environmental manipulations can be beneficial for treatment
• § Changes to temp or salinity
• § Addition of biological control (ie cleaner fish) or manual removal of parasites
• o Oral medication dictated by animal appetite and food (gel diet, tablets hidden in food items)
• § For individual anorectic fish, parenteral or gastric lavage treatments may be indicated
• · Challenges and novel treatment considerations
• o Degradation of praziquantel and formalin in recirculating system
• o Research has shown significant degradation of both praziquantel and formalin in marine systems at standard published doses and frequencies
• o Praziquantel 2mg/L and formalin 25mg/L degraded to less than detectable limits in 9 days and 14 hours respectively in naive recirculating systems
• o Removal rate was faster for repeat doses
• o Removing fish from an experienced system into a naive system can help minimize rapid degradation
• · Capsalid management in a large mixed species saltwater aquarium
• o Capsalids are large, oviparous monopisthocotylean flatworms (TSF) -> extremely difficult to eliminate from a system
• o Fresh water dips often used to reduce parasite load
• o Chronic to indefinite hyposalinity has been successful at preventing recurrent outbreaks in large mixed-species exhibits -> when salinity was increased, outbreaks recurred
• § No reported negative effects from hyposalinity in the telostats, elasmobranchs, turtles, or other species in the exhibits
• o Cleaner fish are also a viable option for large exhibits
• · Leech infestation in large mixed-species salt-water aquarium
• o Branchellion tropedinis are marine leeches that exclusively parasitize elasmobranchs
• o Treatments include:
• § Manual removal -> time consuming
• § Trichlorfon (organophosphate) 5-6 hr bath -> premedicate with atropine
• · Repeat treatment in 30 days for leech coccon hatching
• § Supportive care including topical or systemic antibiotics and blood transfusions
• · Monogeneans in spotted eagle rays (aetobatus narinari)
• o Decacotyle floridana and Clemacotyle australis are monogeneans associated with morbidity and mortality in spotted eagle rays
• o Praziquantel immersion reduces parasite loads but does not eradicate
• § Requires repeat and frequent handling
• o Praziquantel administration via gastric lavage to anesthetized rays have dramatically decreased load
• o On facility has reported management with praziquantel immersion in naive tank for 30 hr followed by chloroquine and praziquantel immersion for 405 months has been used successfully -> no effects on eagle or atlantic stingrays but cownose rays demonstrated abnormal swimming behavior
• · Eimeria southwelli in cownose rays
• o Eimeria southwelli are apicomplexa coccidia parasites, reported to cause morbidity and mortality in cownose rays
• o The current, most successful treatment includes copper wire particles administered orally once
• § No negative effects have been documented to date and no copper excretion has been detected in the environment
• o Other reported treatments with inconsistent or inconclusive results include toltrazuril, ponazuril, clindamycin, and sulfadimethoxine
• · Copper immersion in cownose rays
• o Copper immersion typically avoided in elasmobranchs due to intolerance and mortalities
• o It has been used safely for prolonged immersion in cownose rays for 3-4 months in conjunction with praziquantel prolonged immersion weekly for 4-5 treatments to treat capsalid parasite infestations
• § Close monitoring of copper and praziquantel concentrations essential
• o Negative effects reported in atlantic stingrays
• · Scuticociliatosis in Sygnathid and elasmobranch species
• o Scuticociliatia are ciliated protozoa that cause disease in marine teleost fish including seahorses and sea dragons
• § Treatment with prolonged immersion of metronidazole for 10 days successfully treated systemic disease in Australian pot-bellied seahorses
• o Philasterides dicentrarchi cause rapid lethal systemic infections in zebra sharks, port jackson sharks, and japanese horn sharks and similar ciliate infections have been identified in additional elasmobranch species
• § Thought to be an emerging or previously unrecognized disease in elasmobranchs
• § Systemic invasion has a poor prognosis with no reported effective treatment protocols
• · Oral metronidazole followed a month later with oral ponazuril may have been helpful in reducing parasitic load in a zebra shark with subcutaneous scuticociliatosis
• · Summary
• o it is better to prevent parasite introduction to your systems because once its there is a huge pain