Therapy and protozoan diseases

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Therapy of fish diseases

Therapeutic baths of eggs and fish

Baths

  • Water OFF, 15–30 min

  • Most effective

  • Best for hatcheries, low stocking density, high Oâ‚‚

  • Targets ecto-/endoparasites, fungal & bacterial skin/gill diseases

  • Substances: formalin, NaCl, antibiotics, metronidazole, praziquantel, mebendazole, anesthetics

  • Rules: starve 24 h, treat at lowest temperature, monitor fish, test one tank first, start with low dose

Flush treatments

  • Water ON

  • For large ponds/tanks

  • High stocking density, low oxygen

  • Easy but less effective

Dips

  • Short exposure

  • Small number of large fish

  • Effective for large parasites

  • ❌ Causes handling stress

Medicated feed

  • Pellets / granulated feed

  • Drugs: antibiotics, sulphonamides, anthelmintics

  • Best for intestinal/systemic diseases

Individual treatment

  • Probe (into GIT): few fish only

  • Injections: vaccines, precise dosing

  • Local treatment: focal lesions

Total Protection Strategy

  • Combination of immersion + injection + oral treatment

  • Includes Ergosan (immunomodulator feed)

  • Provides early, broad protection

  • Always performed in hatcheries

Exam memory tip

👉 Bath = off / Flush = on
👉 Dip = few big fish
👉 Feed = internal
👉 Injection = precise

2
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Piscioodiniosis:

Pathogen

Susceptible hosts

Localization

Life cycle

Clinical signs

Pathological changes

Prevention and therapy

Diagnosis

Freshwater Velvet Disease

Causative agent:
Piscinoodinium pillulare (ectoparasitic dinoflagellate protozoan)

Hosts:
Non-specific – aquarium fish; tropical & temperate species (e.g. common carp)

Localization:
Skin, fins, gills

Life cycle:
Trophont (on fish) → Tomont (encysted, off fish) → Dinospore (infective)
⏱ ~2 weeks, trophonts contain chloroplasts

Clinical signs:
Golden/yellow velvet sheen, excess mucus, dark skin, gill hyperplasia

Pathogenesis:
Most severe in young fish, rapid spread, possible mass mortality

Diagnosis:
Clinical signs ± skin/gill scraping

Prevention / Therapy:
↑ Temp 24–27 °C, remove fish for 2 weeks
NaCl, formalin, methylene blue

<p><strong>Freshwater Velvet Disease</strong></p><p><strong>Causative agent:</strong><br><strong><mark data-color="red" style="background-color: red; color: inherit;">Piscinoodinium pillulare</mark></strong> (ectoparasitic dinoflagellate protozoan)</p><p><strong>Hosts:</strong><br>Non-specific – aquarium fish; tropical &amp; temperate species (e.g. <strong>common carp</strong>)</p><p><strong>Localization:</strong><br>Skin, fins, gills</p><p><strong>Life cycle:</strong><br>Trophont (on fish) → Tomont (encysted, off fish) → <strong>Dinospore</strong> (infective)<br><span>⏱</span> ~2 weeks, trophonts contain <strong>chloroplasts</strong></p><p><strong>Clinical signs:</strong><br>Golden/yellow <strong>velvet sheen</strong>, excess mucus, dark skin, gill hyperplasia</p><p><strong>Pathogenesis:</strong><br>Most severe in <strong>young fish</strong>, rapid spread, possible mass mortality</p><p><strong>Diagnosis:</strong><br>Clinical signs ± skin/gill scraping</p><p><strong>Prevention / Therapy:</strong><br>↑ Temp <strong>24–27 °C</strong>, remove fish for 2 weeks<br><strong>NaCl, formalin, methylene blue</strong></p>
3
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Ichthyophthiriosis

Pathogen

Susceptible hosts

Localization

Life cycle

Clinical signs

Pathological changes

Prevention and therapy

Diagnosis

Freshwater White Spot Disease (Ich)

Causative agent:
Ichthyophthirius multifiliis (ciliate protozoan)

Hosts:
Virtually all freshwater fish
High risk: scaleless fish (e.g. catfish)
Outbreaks linked to stress

Localization:
Skin and gill epithelium

Life cycle:
Trophont (feeding stage inside nodules on skin/gills) → leaves host → Tomont (encysted, asexual division) → Tomites → motile Theronts (infective stage invading new host)

Clinical signs:
White/grey nodules ≤1 mm, fin & gill damage, respiratory distress, suffocation, rubbing the body against objects

Pathogenesis:
Heavy infections → up to 100% mortality

Diagnosis:
Typical white spots (± microscopy)

Prevention / Therapy:
Treat theronts
↑ Temp >30 °C for ~7 days, formalin, toltrazuril, UV
Daily vacuuming; cysts killed by drying

<p><strong>Freshwater White Spot Disease (Ich)</strong></p><p><strong>Causative agent:</strong><br><strong><mark data-color="red" style="background-color: red; color: inherit;">Ichthyophthirius multifiliis</mark></strong><mark data-color="red" style="background-color: red; color: inherit;"> </mark>(ciliate protozoan)</p><p><strong>Hosts:</strong><br>Virtually <strong>all freshwater fish</strong><br>High risk: <strong>scaleless fish</strong> (e.g. catfish)<br>Outbreaks linked to <strong>stress</strong></p><p><strong>Localization:</strong><br>Skin and gill epithelium</p><p><strong>Life cycle:</strong><br><strong>Trophont</strong><span> (feeding stage inside nodules on skin/gills) → leaves host → </span><strong>Tomont</strong><span> (encysted, asexual division) → </span><strong>Tomites</strong><span> → motile </span><strong>Theronts</strong><span> (infective stage invading new host)</span></p><p><strong>Clinical signs:</strong><br>White/grey <strong>nodules ≤1 mm</strong>, fin &amp; gill damage, respiratory distress,<span>&nbsp;suffocation, rubbing the body against objects</span></p><p><strong>Pathogenesis:</strong><br>Heavy infections → <strong>up to 100% mortality</strong></p><p><strong>Diagnosis:</strong><br>Typical white spots (± microscopy)</p><p><strong>Prevention / Therapy:</strong><br>Treat <strong>theronts</strong><br>↑ Temp <strong>&gt;30 °C for ~7 days</strong>, <strong>formalin</strong>, <strong>toltrazuril</strong>, <strong>UV</strong><br>Daily vacuuming; cysts <strong>killed by drying</strong></p>
4
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Chilodonellosis; Trichodinosis

Pathogen

Susceptible hosts

Localization

Life cycle

Clinical signs

Pathological changes

Prevention and therapy

Diagnosis

Chilodonellosis

Causative agents:
Chilodonella piscicola
Chilodonella hexasticha (less common; mainly older fish, higher temperatures)

Hosts:
All freshwater fish (especially fingerlings); also brackish water fish

Localization:
Skin and gills

Life cycle:
Trophont (feeding on epithelium) → Tomont (asexual division in environment) → Theront (infective)

Clinical signs:
Excess mucus, whitish/blueish sheen, gill necrosis, dyspnea, skin ulcers

Pathogenesis:
Direct epithelial feeding → tissue damage
Heavy infections → secondary bacterial disease, high mortality

Diagnosis:
Microscopy of skin and gill

Prevention / Therapy:
Formalin bath and immersion, acetic acid bath, salt baths, potassium permanganate immersion, copper immersion

Trichodinosis

Causative agents:
Trichodina jadranica (+++)

Trichodinella, Tripartiella, Dipartiella

Hosts:
Low host specificity; freshwater and marine fish

Localization:
Skin and gills
Some species: urinary bladder, oviducts, GIT, kidneys

Life cycle:
Trophont → Tomont → Theront

Clinical signs:
Grey/blue coating, frayed fins, epithelial erosion, suffocation

Pathogenesis:
Usually mild–chronic disease
↑ losses in young fish, secondary bacterial infections

Diagnosis:
Microscopy of skin and gill scrapings

Prevention / Therapy:
Formalin bath. Acetic acid, salt baths (FW only)
Freshwater baths (marine fish)
Copper, potassium permanganate

extra comparing:

Both are ciliate ectoparasites of skin and gills with similar life cycles and treatment, but Chilodonella feeds directly on epithelium and is more pathogenic, while Trichodina mainly causes mechanical irritation and is usually chronic

<p><strong>Chilodonellosis</strong></p><p><strong>Causative agents:</strong><br><strong><mark data-color="red" style="background-color: red; color: inherit;">Chilodonella piscicola</mark></strong><mark data-color="red" style="background-color: red; color: inherit;"><br></mark><strong><mark data-color="red" style="background-color: red; color: inherit;">Chilodonella hexasticha</mark></strong><mark data-color="red" style="background-color: red; color: inherit;"> </mark>(less common; mainly older fish, higher temperatures)</p><p><strong>Hosts:</strong><br>All <strong>freshwater fish</strong> (especially <strong>fingerlings</strong>); also <strong>brackish water fish</strong></p><p><strong>Localization:</strong><br>Skin and gills</p><p><strong>Life cycle:</strong><br><strong>Trophont</strong> (feeding on epithelium) → <strong>Tomont</strong> (asexual division in environment) → <strong>Theront</strong> (infective)</p><p><strong>Clinical signs:</strong><br>Excess mucus, <strong>whitish/blueish sheen</strong>, gill necrosis, dyspnea, skin ulcers</p><p><strong>Pathogenesis:</strong><br>Direct epithelial feeding → tissue damage<br>Heavy infections → <strong>secondary bacterial disease</strong>, high mortality</p><p><strong>Diagnosis:</strong><br>Microscopy of <strong>skin and gill</strong></p><p><strong>Prevention / Therapy:</strong><br>Formalin bath and immersion, acetic acid bath, salt baths, potassium permanganate immersion, copper immersion</p><p></p><p><strong>Trichodinosis</strong></p><p><strong>Causative agents:</strong><br><strong><mark data-color="red" style="background-color: red; color: inherit;">Trichodina jadranica</mark></strong><mark data-color="red" style="background-color: red; color: inherit;"> (+++)</mark></p><p><strong><mark data-color="red" style="background-color: red; color: inherit;">Trichodinella</mark></strong><mark data-color="red" style="background-color: red; color: inherit;">, </mark><strong><mark data-color="red" style="background-color: red; color: inherit;">Tripartiella</mark></strong><mark data-color="red" style="background-color: red; color: inherit;">, </mark><strong><mark data-color="red" style="background-color: red; color: inherit;">Dipartiella</mark></strong></p><p><strong>Hosts:</strong><br>Low host specificity; <strong>freshwater and marine fish</strong></p><p><strong>Localization:</strong><br>Skin and gills<br>Some species: <strong>urinary bladder, oviducts, GIT, kidneys</strong></p><p><strong>Life cycle:</strong><br><strong>Trophont</strong> → <strong>Tomont</strong> → <strong>Theront</strong></p><p><strong>Clinical signs:</strong><br>Grey/blue coating, frayed fins, epithelial erosion, suffocation</p><p><strong>Pathogenesis:</strong><br>Usually <strong>mild–chronic</strong> disease<br>↑ losses in <strong>young fish</strong>, secondary bacterial infections</p><p><strong>Diagnosis:</strong><br>Microscopy of <strong>skin and gill scrapings</strong></p><p><strong>Prevention / Therapy:</strong><br><strong>Formalin</strong> bath. <strong>Acetic acid</strong>, <strong>salt baths</strong> (FW only)<br><strong>Freshwater baths</strong> (marine fish)<br><strong>Copper</strong>, <strong>potassium permanganate</strong></p><p></p><p><strong>extra comparing:</strong></p><p><span><span>Both are ciliate ectoparasites of skin and gills with similar life cycles and treatment, but </span></span><strong>Chilodonella feeds directly on epithelium and is more pathogenic</strong><span><span>, while </span></span><strong>Trichodina mainly causes mechanical irritation and is usually chronic</strong></p>
5
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Ichthyobodosis

Pathogen

Susceptible hosts

Localization

Life cycle

Clinical signs

Pathological changes

Prevention and therapy

Diagnosis

Causative agent:
Ichthyobodo necator complex(flagellate protozoan)

Hosts:
Freshwater and saltwater fish
Mostly young or stressed adults

Localization:
Skin and gills

Life cycle:

  • Motile stage – free-living, off the fish

  • Pyriform stage – feeding stage attached to epithelium

  • Binary fission for reproduction

Clinical signs:

  • Grey/blueish or whitish film on body

  • Epithelial hyperplasia, increased mucus

  • Respiratory distress in severe cases

Pathogenesis:

  • Feeds and penetrates the epithelium → disrupts osmoregulation

  • Dangerous for young or stressed fish

Diagnosis:
Microscopic examination of skin and gills

Prevention / Therapy:

  • Formalin baths, potassium permanganate

  • Raise temperature to shorten parasite cycle

  • Oral metronidazole in severe cases

<p><strong>Causative agent:</strong><br><strong><mark data-color="red" style="background-color: red; color: inherit;">Ichthyobodo necator complex</mark></strong>(flagellate protozoan)</p><p><strong>Hosts:</strong><br>Freshwater and saltwater fish<br>Mostly <strong>young or stressed adults</strong></p><p><strong>Localization:</strong><br>Skin and gills</p><p><strong>Life cycle:</strong></p><ul><li><p><strong>Motile stage</strong> – free-living, off the fish</p></li><li><p><strong>Pyriform stage</strong> – feeding stage attached to epithelium</p></li><li><p>Binary fission for reproduction</p></li></ul><p><strong>Clinical signs:</strong></p><ul><li><p>Grey/blueish or whitish <strong>film on body</strong></p></li><li><p><strong>Epithelial hyperplasia</strong>, increased mucus</p></li><li><p>Respiratory distress in severe cases</p></li></ul><p><strong>Pathogenesis:</strong></p><ul><li><p>Feeds and penetrates the epithelium → disrupts <strong>osmoregulation</strong></p></li><li><p>Dangerous for <strong>young or stressed fish</strong></p></li></ul><p><strong>Diagnosis:</strong><br>Microscopic examination of <strong>skin and gills</strong></p><p><strong>Prevention / Therapy:</strong></p><ul><li><p><strong>Formalin baths</strong>, potassium permanganate</p></li><li><p><strong>Raise temperature</strong> to shorten parasite cycle</p></li><li><p><strong>Oral metronidazole</strong> in severe cases</p></li></ul><p></p>
6
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Spironucleosis

Pathogen

Susceptible hosts

Localization

Life cycle

Clinical signs

Pathological changes

Prevention and therapy

Diagnosis

Causative agents:
Spironucleus salmonicida, S. salmonis, S. barkhanus, S. torosa, S. vortens (flagellated protozoans)

Hosts:

  • Salmonids (freshwater, seawater, cage-cultured)

  • Aquarium fish

Localization:

  • Intestine (primary)

  • Gall bladder, stomach

  • Some species: internal organs, muscle, skin

Life cycle:

  1. Trophont – reproduces by binary fission in intestinal mucosa

  2. Encysted stage – released with feces

  3. Ingestion by fish – cysts excyst in stomach → trophonts colonize intestine

Clinical signs:

  • Inappetence, dark color, emaciation (“pinheads”)

  • Ascites, pale stringy feces, enteritis

  • Exophthalmos

  • Chronic mortality

Pathogenesis (species-specific):

  • S. salmonis: intestines → abdominal distension, emaciation

  • S. barkhanus: internal organs, muscle, skin

  • S. vortens: cachexia, gastroenteritis, peritonitis, “hole head vs lateral line” syndrome

Diagnosis:

  • Fecal exam (trophonts or cysts)

  • Necropsy more accurate → assess intensity (treatment if 15–30 organisms/fish)

Prevention / Therapy:

  • Metronidazole (oral or immersion)

  • Magnesium sulfate (oral)

  • Raise water temperature to 35 °C for 7 days

<p><strong>Causative agents:</strong><br><em><mark data-color="red" style="background-color: red; color: inherit;">Spironucleus salmonicida</mark></em><mark data-color="red" style="background-color: red; color: inherit;">, </mark><em><mark data-color="red" style="background-color: red; color: inherit;">S. salmonis</mark></em><mark data-color="red" style="background-color: red; color: inherit;">, </mark><em><mark data-color="red" style="background-color: red; color: inherit;">S. barkhanus</mark></em><mark data-color="red" style="background-color: red; color: inherit;">, </mark><em><mark data-color="red" style="background-color: red; color: inherit;">S. torosa</mark></em><mark data-color="red" style="background-color: red; color: inherit;">, </mark><em><mark data-color="red" style="background-color: red; color: inherit;">S. vortens</mark></em> (flagellated protozoans)</p><p><strong>Hosts:</strong></p><ul><li><p>Salmonids (freshwater, seawater, cage-cultured)</p></li><li><p>Aquarium fish</p></li></ul><p><strong>Localization:</strong></p><ul><li><p><strong>Intestine</strong> (primary)</p></li><li><p>Gall bladder, stomach</p></li><li><p>Some species: internal organs, muscle, skin</p></li></ul><p><strong>Life cycle:</strong></p><ol><li><p><strong>Trophont</strong> – reproduces by binary fission in intestinal mucosa</p></li><li><p><strong>Encysted stage</strong> – released with feces</p></li><li><p><strong>Ingestion by fish</strong> – cysts excyst in stomach → trophonts colonize intestine</p></li></ol><p><strong>Clinical signs:</strong></p><ul><li><p>Inappetence, dark color, emaciation (“pinheads”)</p></li><li><p>Ascites, pale stringy feces, enteritis</p></li><li><p>Exophthalmos</p></li><li><p>Chronic mortality</p></li></ul><p><strong>Pathogenesis (species-specific):</strong></p><ul><li><p><em>S. salmonis</em>: intestines → abdominal distension, emaciation</p></li><li><p><em>S. barkhanus</em>: internal organs, muscle, skin</p></li><li><p><em>S. vortens</em>: cachexia, gastroenteritis, peritonitis, “hole head vs lateral line” syndrome</p></li></ul><p><strong>Diagnosis:</strong></p><ul><li><p>Fecal exam (trophonts or cysts)</p></li><li><p>Necropsy more accurate → assess intensity (<strong>treatment if 15–30 organisms/fish</strong>)</p></li></ul><p><strong>Prevention / Therapy:</strong></p><ul><li><p><strong>Metronidazole</strong> (oral or immersion)</p></li><li><p><strong>Magnesium sulfate</strong> (oral)</p></li><li><p>Raise water temperature to <strong>35 °C for 7 days</strong></p></li></ul><p></p>
7
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Gill Amoebic Infestation; Nodular Gill Amoebic Infestation

Pathogen

Susceptible hosts

Localization

Life cycle

Clinical signs

Pathological changes

Prevention and therapy

Diagnosis

Amoebic Gill Disease (AGD)

Causative agent:
Neoparamoeba perurans

Hosts:
Marine fish, especially Atlantic salmon (other salmonids)

Localization:
Gills → may become systemic in chronic cases

Life cycle (important exam clarification)

  • Exists mainly as a trophozoite (trophont)

  • Divides by binary fission

  • Can survive freely in seawater

  • No well-defined cyst → theront cycle like Ich or Velvet
    👉 Examiners usually accept:

“Direct life cycle with free-living and parasitic trophozoites”

Clinical signs:

  • Lethargy, ↓ swimming, ↓ feeding & growth

  • Respiratory distress

  • Progressive epithelial hyperplasia and ↑ mucus on gills

Pathogenesis:

  • Chronic but rapidly progressive

  • Severe gill hyperplasia → impaired respiration, osmoregulation & circulation

  • High mortality (up to 85%)

Diagnosis:

  • Macroscopic gill lesions

  • Microscopic examination of gill scrapings

Prevention / Therapy:

  • Freshwater baths, hydrogen peroxide baths

  • Management: functional feeds, selective breeding

  • No effective commercial vaccine

Nodular Gill Amoebic Infestation (NGD)

Causative agents:
Various amoebae (not Neoparamoeba perurans)

Hosts:
Freshwater fish, especially rainbow trout

Localization:
Gills

Life cycle

  • Direct life cycle

  • Trophozoites divide by binary fission

  • Free-living and parasitic forms

  • No obligate cyst stage required for transmission

Clinical signs:

  • Reduced activity, abnormal swimming

  • Respiratory distress

  • Reduced growth

  • White nodular lesions on gill filaments

  • Increased mucus

Pathogenesis:

  • Chronic course

  • Epithelial hyperplasia → partial or complete lamellar fusion

  • Mortality occurs weeks after onset

Diagnosis:

  • Wet mount examination of gills

Prevention / Therapy:

  • Formalin treatments

  • Salt baths

extra for comparing: Amoebic gill disease is caused by Neoparamoeba perurans in marine salmonids and is highly lethal, whereas nodular gill disease affects freshwater fish, is caused by other amoebae, and is usually more chronic.

<p><strong>Amoebic Gill Disease (AGD)</strong></p><p><strong>Causative agent:</strong><br><strong><mark data-color="red" style="background-color: red; color: inherit;">Neoparamoeba perurans</mark></strong></p><p><strong>Hosts:</strong><br><strong>Marine fish</strong>, especially <strong>Atlantic salmon</strong> (other salmonids)</p><p><strong>Localization:</strong><br>Gills → may become <strong>systemic</strong> in chronic cases</p><p><strong>Life cycle (important exam clarification)</strong></p><ul><li><p>Exists mainly as a <strong>trophozoite (trophont)</strong></p></li><li><p><strong>Divides by binary fission</strong></p></li><li><p>Can <strong>survive freely in seawater</strong></p></li><li><p><strong>No well-defined cyst → theront cycle</strong> like Ich or Velvet<br><span>👉</span> Examiners usually accept:</p></li></ul><figure data-type="blockquoteFigure"><div><blockquote><p>“Direct life cycle with free-living and parasitic trophozoites”</p></blockquote><figcaption></figcaption></div></figure><p></p><p><strong>Clinical signs:</strong></p><ul><li><p>Lethargy, ↓ swimming, ↓ feeding &amp; growth</p></li><li><p>Respiratory distress</p></li><li><p>Progressive <strong>epithelial hyperplasia</strong> and ↑ mucus on gills</p></li></ul><p><strong>Pathogenesis:</strong></p><ul><li><p>Chronic but <strong>rapidly progressive</strong></p></li><li><p>Severe gill hyperplasia → impaired <strong>respiration, osmoregulation &amp; circulation</strong></p></li><li><p><strong>High mortality (up to 85%)</strong></p></li></ul><p><strong>Diagnosis:</strong></p><ul><li><p>Macroscopic gill lesions</p></li><li><p>Microscopic examination of gill scrapings</p></li></ul><p><strong>Prevention / Therapy:</strong></p><ul><li><p><strong>Freshwater baths</strong>, <strong>hydrogen peroxide baths</strong></p></li><li><p>Management: functional feeds, selective breeding</p></li><li><p><strong>No effective commercial vaccine</strong></p></li></ul><p></p><p><strong>Nodular Gill Amoebic Infestation (NGD)</strong></p><p><strong>Causative agents:</strong><br>Various <strong>amoebae</strong> (not <em>Neoparamoeba perurans</em>)</p><p><strong>Hosts:</strong><br><strong>Freshwater fish</strong>, especially <strong>rainbow trout</strong></p><p><strong>Localization:</strong><br>Gills</p><p><strong>Life cycle</strong></p><ul><li><p><strong>Direct life cycle</strong></p></li><li><p><strong>Trophozoites divide by binary fission</strong></p></li><li><p>Free-living and parasitic forms</p></li><li><p>No obligate cyst stage required for transmission</p></li></ul><p></p><p><strong>Clinical signs:</strong></p><ul><li><p>Reduced activity, abnormal swimming</p></li><li><p>Respiratory distress</p></li><li><p>Reduced growth</p></li><li><p><strong>White nodular lesions</strong> on gill filaments</p></li><li><p>Increased mucus</p></li></ul><p><strong>Pathogenesis:</strong></p><ul><li><p>Chronic course</p></li><li><p><strong>Epithelial hyperplasia</strong> → partial or complete <strong>lamellar fusion</strong></p></li><li><p>Mortality occurs <strong>weeks after onset</strong></p></li></ul><p><strong>Diagnosis:</strong></p><ul><li><p><strong>Wet mount examination</strong> of gills</p></li></ul><p><strong>Prevention / Therapy:</strong></p><ul><li><p><strong>Formalin treatments</strong></p></li><li><p><strong>Salt baths</strong></p></li></ul><p></p><p><span><span>extra for comparing: Amoebic gill disease is caused by </span></span><em>Neoparamoeba perurans</em><span><span> in marine salmonids and is highly lethal, whereas nodular gill disease affects freshwater fish, is caused by other amoebae, and is usually more chronic.</span></span></p>

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