Fish & Invertebrate Mycology

Question 1

Describe the effects of saprolegniasis infections in fish.

What fish are typically affected? What age groups are more susceptible? Are any fish more resistant?

What are the typical clinical signs?

How is this transmitted? Are there any known risk factors?

How is this diagnosed?

What are the typical lesions on necropsy?

How is it treated?

Answer 1

• Oomycota (Saprolegniasis)
  
  • Water mold or fungal like organisms that can infect the skin or gills of fish, fish eggs and any decaying matter.
    
    • More closely related to diatoms and brown algae
  • Opportunistic pathogens of freshwater and brackish fish, particular issue for catfish
  • Infection often secondary to trauma or temperature stressors
  • Typical oomycetes – infect the skin fins or gills
    
    • Treated using medial and husbandry management, recurrence common
    • Common in all freshwater bony fish and reported in brackish water bony fish and fish eggs
    • Signs – Lesions start on wounds, peduncle or head. Early lesions gray-white, circular, raised with cotton wool appearance and become brown or green as debris and algae accumulate. Rarely extend below superficial muscle. Dyspnea or tachypnea if gills lesions severe, systemic signs (inappetence) rare. Mortality higher with Branchiomyces due to gill damage
  • Transmission – horizontal through direct and indirect contact. Oomycetes show sexual and asexual reproduction
    
    • Require water for growth and sporulation and can survive in the biofilm
  • Juveniles more susceptible than adults, some fish resistant to infection (carp, milk fish, European eel, nile tilapia)
  • Risk factors – trauma to mucus, skin, fins or gills (recent handling/transport), permissive water temperature (64-77F), poor food storage high organic loads, low flow rates, and stressors (high stocking, poor water quality, changes in water temp, other diseases – ectoparasites, virus, bacteria)
  • Diagnosis – fungal hyphae seen on skin scrap or gill biopsy. Atypical oomycetes require histology, culture or PCR.
    
    • Hyphae are broad, transparent with irregular walls and occasional branching and aseptate. Stain with PAS and silver.
    • Typical oomycetes may lose superficial hyphae in processing, but some hyphae are usually seen. May have little to no inflammatory response. In Atypical oomycetes, hyphae seen invading into muscle and viscera with granulomatous inflammation and necrosis
    • Culture and PCR available
    • In cyprinids, if infection limited to the gills, Branchiomyces most likely
  • Management – reduce sources of trauma, remove organics, increase mechanical cleaning/disinfection, increase water flow and water quality. No treatment for A. invadens, euthanasia followed by cleaning (dry in sunlight) recommended.
    
    • Debridement of fungal material recommended along with formalin immersion, increased salinity, hydrogen peroxide immersion, and systemic antibiotics. Prognosis good if lesions treated and risk factors resolved. If located deep within gill lamellae or biofilm, difficult to treat.
  • Prevention - pathogen free water source, disinfection with fine filtration followed by UV and/or Ozone, high water flow rate, good cleaning and disinfection (including of eggs)

Problem 34 – Water Mold (Oomycte) Infection - Saprolegnia

• Host/location: Freshwater fish, skin, fins, gills
• Clinical Signs/Pathology:
  
  • White, brown, red, or green cottony mass on skin or gills
  • Acute stress (often temperature drop, recent transport, or trauma)
• Life Cycle: Water molds are opportunists that feed on dead organic matter – infections in fish are usually associated with immunosuppression (often associated with low temperatures). Handling, crowding, heavy feeding, high organic loads predispose. Wounds serve as a portal of entry for water molds. Transmission occurs from motile zoospores.
• Diagnosis: Wet mounts with broad, aseptate hyphae of varying width. Hyphae stain strongly with silver (GMS).
• Treatment:
  
  • Increased salinity – kills mold, reduces osmotic stress from the associated wounds.
  • Copper – also can be used as a preventative
  • Malachite green (not for food fish)

Oomycete - ZP

• Aka water molds – not true fungi, classified as Stramenopiles (Heterokonts).
  
  • Includes golden-brown algae, diatoms.
• Three subclasses: Saprolegniomycetidae, Rhipidiomycetidae, Peronosporomycetidae.
  
  • Saprolegniomycetidae contains two orders – Saprolegniales, Leptomitales.
    
    • Within Saprolegniales -> Saprolegnia, Branchiomyces, Achlya, Aphanomyces.
• Saprolegnia parasitica.
  
  • Wild and cultured FW fish.
  • Substantial losses in salmon and catfish aquaculture.
    
    • Catfish aka winter kill.
    • Serious pathogen of eggs in culture. Mycelial growth and death.
  • Gross – focal or focally extensive, raseid, white to gray, cotton-like plaques on external surface.
  • Microscopic – restricted to epidermis, dermis, occ superficial muscle.
    
    • Focal to focally extensive epidermal necrosis, erosion, and ulceration with hyphal invasion of the demis and occ muscle may be necrotic.
  • Hyphae cover gills, necrosis and hyperplasia.
  • Inflammation is minimal unless secondary bacterial infection.
  • Wet mount – hyphae nonseptate, multinucleate, variably branching, transparent.
  • Death from hemodilution and osmoregulatory failure.

Question 2

What is the etiologic agent of epizootic ulcerative syndrome?

Does this disease have other names? Is it reportable?

What fish are typically affected?

What are the clinical signs?

How is it diagnosed?

What are the lesions seen on necropsy?

How is it treated?

Answer 2

• Atypical oomycetes – more invasive and result in severe chronic inflammation
  
  • Aphanomyces invadans is atypical oomycete that can cause seasonal epizootics in wild and cultures freshwater and brackish fish (reportable in some states)
  • Less common but reported in a variety of freshwater and brackish fish
  • Signs – usually multiple fish affected, deep irregular, multifocal skin ulcer develop rapidly often behind the head and in perianal region. Fin erosion, petechiae, depigmentation are often seen. Inappetence, reduced feeding or weight loss common. Erratic swimming, loss of equilibrium, corneal opacity (edema/keratitis), dyspnea/tachypnea seen. High morbidity and mortality.

Problem 35 – Epizootic Ulcerative Syndrome – Aphanomyces invadens & A. piscicida

• Host/location: Freshwater and estuarine fish – skin and gills
• Clinical Signs/Pathology:
  
  • Shallow to deep skin ulcers
  • Morbidity and mortality can be high, epidemics can develop rapidly
• Life Cycle:
  
  • Some sort of skin damage is necessary for infection to begin
• Diagnosis:
  
  • Aseptate hyphae with severe, chronic inflammation – inflammatory cells are often seen on wet mounts, easily stain with silver (GMS)
  • Definitive – culture on nutrient poor medium
• Treatment: No known treatment supported with efficacy. Empirical reports of improving water quality and adding some salt.

Aphanomyces invadans. (ZP)

• Cause of epizootic ulcerative syndrome EUS (OIE reportable).
• Aka red spot disease (RSD), mycotic granulomatosis (MG), ulcerative mycosis (UM).
• Wild, farmed FW and brackish.
• Disease at temps 18-22 deg C, often after heavy rainfall.
  
  • High morbidity and mortality in young adult fish.
  • Infections of egg, fry, and larvae not reported.
• Ddx dinoflagellate Pfiesteria piscicida in estruarine fish.
• Gross – red spots on skin of head, operculum, body, caudal peduncle.
  
  • Progresses to focally more extensive, shallow red to gray skin ulcers with brown, necrotic centers and assoc with waves of acute mortality.
    
    • Some spp i.e. menhaden – circumscribed, deep ulcers in ventral perianal region that penetrate coelom.
    • Snakeheads – skin ulcers can involve body and head, exposing the brain.
• Histo – Extensive ulceration overlying deeply penetrating myonecrosis.
  
  • Erythematous dermatitis progresses to severe, locally extensive necrotizing and granulomatous dermatitis and myositis.
  • Hyphae penetrate dermis, extend deeply into muscle.

Question 3

What are the fungal organisms that cause phaeohphyomycosis?

What fish are typically affected?

How are these organisms transmitted? What risk factors have been identified?

What are the typical clinical signs? What are the three lesional patterns? What is the mortality rate like?

How does phomamycosis differ from exophiala?

How is this diagnosed?

What lesions are present on necropsy?

How is this managed?

Answer 3

• Exophiala spp - ZP
  
  • Opportunistic fungal pathogens, cause chronic necrotizing granulomatous disease
  • Usually sporadic problem for individual/small group of same species in aquariums, but epizootics reported in aquaculture.
  • No successful treatment reported
  • Most common species that infects fish – Exophiala salmonis, Exophiala pisciphila, and Exophiala psychrophile.
  • Causes phaeohyphomycosis, along with Phoma, Wangiella and Veronaea spp.
  • Transmission – primary route is through inoculation though ingestion of contaminated food can also occur. Not highly contagious
    
    • Same species found in amphibians and aquatic invertebrates – may play a role in transmission
  • Disease reported primarily from farmed salmonids, demersal teleosts (flounder, cod, halibut, lumpfish) and syngnathids (sea dragons). Rare reports in elasmobranch.
    
    • Suspect that Exophiala spp or strains are species specific
  • Risk factors: Trauma, permissive water temp, poor food storage, high organic load, stressors
  • Signs – Typically chronic disease lasting weeks to months
    
    • Lethargy, inappetence, weight loss, dyspnea/tachypnea, abnormal buoyancy or swimming (spiraling or circling) due to neurologic or swim bladder involvement, coelomic distention, skin lesions (dermal mass, skin ulcer, lesions with black margins)
      
      • Sometimes skin lesions are only clinical sign
      • Mortality usually low, though epizootics in salmonids may have up to 50% mortality.
  • Diagnosis – cytology, histology, culture and sequencing
    
    • Sample the skin (if lesions present), gill, brain, and kidney
    • Cytology – thin fungal hyphae dark yellow to brown with acute or right angled branching
    • Nx/Histo – multifocal black, (sometimes tan or white foci) throughout the viscera that can develop into multinodular masses. See necrotizing granulomatous inflammation with intralesional fungal hyphae.
    • Culture – slow to grow but grow readily. Warm temp and antimicrobial agents may be needed. PCR/Sequencing needed for species identification.
  • Management – reduce or resolve stressors, especially water quality and temp. No effective treatments reported. Should continue antifungal therapy for several months if started. Consider surgical debridement.
  • Zoonosis - zoonotic potential of the species identified in fish is lower, although rare cases of cutaneous lesions in immune-suppressed humans have been reported
• Exophiala – black yeast-like fungi aka black yeasts
  
  • Produce yeast-like cells by unilateral budding, and melanized hyphae.
  • Orders Pleosporales, Ochroconiales, Chaetothyriales.
    
    • Factors contributing to pathogenicity – presence of melanin and carotene, formation of thick cell walls, thermos and osmotolerance, assimilation of aromatic hydrocarbons, production of extracellular polysaccharides, siderophores, and acidic or alkaline secondary metabolites.
  • Temperature influences host range.
    
    • Exophiala – nonthermotolerant, waterborne, cluster in the salmonis-clade.
      
      • Account for majority of recognized Exophiala spp infections of aquatic poikilotherms (fish, toads, crabs).
  • Three recognized lesional patterns:
    
    • Chromoblastomycosis.
      
      • Chronic subcutaneous mycosis, characterized by presence of verrucous plaques possessing sclerotic bodies (muriform fungal cells).
    • Eumycetoma.
      
      • Eumycotic mycetoma is a chronic subcutaneous nodular granulomatous inflammatory condition that may develop draining tracts.
        
        • Presence of ‘grains’ or sclerotia – mycelial aggregates surrounded by an extracellular matrix containing melanin-like compound.
    • Phaeohyphomycosis.
      
      • Melanized fungal elements in tissues.
      • i.e. yeasts, pseudohyphae, hyphae, any combination.
      • Can be cutaneous, SQ, or systemic.
      • Phaeohyphomycosis caused by Exophiala in FW and marine fish may be localized or systemic.
        
        • Varying in necrosis and intensity of inflammation.
        • Typically granulomatous response.
        • Fungal angioinvasion is common.
        • Vascular necrosis with or without ulcers with raised black margins are characteristic of disseminated phaeohyphomycosis of seadragons.
          
          • Exophiala angulospora, Exophiala aquamarina.
      • E. salmonis – granulomas in brain and cranial tissues with extension into gill and eyes.
      • E. pisciphila – Atl salmon, hyphal invasion of cranial structures, semicircular canals, lateral line.
        
        • Brown, slender, filamentous, septate with parallel walls and right-angle branching in tissues.
      • Histo insufficient for ID at species level.
      • Dx – wet mount initially.
        
        • Histo.
        • In vitro culture, molecular analysis.
      • Phomamycosis – phaeohyphomycosis of hatchery-reared fish.
        
        • Salmon.
        • Fry and fingerlings with variable mortality.
        • Etiologic agent – Phoma herbarum.
          
          • Ubiquitous in environment.
          • Saphrophyte and plant pathogen, also infects fish.
          • Transmission via inhalation or ingestion of conidia.
          • Dz of intensive aquaculture.
          • Limiting fungal contamination of food important.
        • Primarily targets swim bladder.
        • May lead to angioinvasion, other ograns.
        • Gross – caseous material and plaques of fungus in swim bladder lumen.
          
          • Adjacent hypaxial muscles and kidney may be hemorrhagic.
        • Histo – necrotizing, granulomatous aerocystitis.
        • Vasculitis, intravascular melanized septate and branching fungal hyphae.
        • Most severe lesions swim bladder and GIT.
        • Definitive ID by culture followed by PCR and sequencing.

Question 4

Describe the effects of fusarium infection in fish.

What is the etiologic agent?

What species are particularly affected?

How is this transmitted? What risk factors have been identified?

What are the typical clinical signs?

What differentials should be considered?

How is this diagnosed?

WHat lesions are present on necropsy?

How is fusarium treated?

Answer 4

• Fusarium spp.
  
  • Environmental saprophytes common in soil and plants
    
    • Opportunistic infections in fish, especially marine fish
  • Necrotizing granulomatous dermatitis – treatment rarely successful once fungi invade deeper tissues
  • Fusarium solani most common infection in fish
  • Produce mycotoxins that can contaminate feeds and lead to developmental abnormalities and reduced growth rates
  • Primarily horizontal transmission through inoculation. Identified in plants, inverts, amphibians, reptiles and mammals which may play a role in transmission.
  • Signalment – mostly marine species – marine elasmobranchs (bonnethead, scalloped hammerhead), marine teleosts (parrotfish, pufferfish) – problem of managed fish
  • Trauma to mucus, skin, fins or other stressors (density, water, transport, enclosure) are risk factors.
  • Signs – lethargy, abnormal swimming (slow interspersed with burst swimming and spiral swimming), inappetence, weight loss, skin lesions (along head, lateral line, fin edges and tail – white, pink or red pustules, swollen lateral line pores, erythema, depigmentation. White viscous fluid or blood may be seen and the lesions may ulcerate exposing muscle, cartilage or bone
  • Differentials for fungal hyphae associated with skin ulcers – Fusarium, and other causes of hyphalomycosis (e.g. Aspergillus, Paecilomycosis, Penicillium spp.) and phaeohyphomycosis (e.g. Exophiala spp.).
  • Diagnosis – cytology or histology of gill, skin or tissue and culture followed by molecular testing
    
    • Thin walled hyphae, acute and right angled branching, characteristic large, sickle-shaped macroconidia with numerous septa
    • Necropsy – necrotizing hemorrhagic dermatitis with intralesional fungi invading into muscles, nerves, vessels, cartilage, bone
    • Grow on culture media but slowly. PCR and sequencing needed for definitive ID.
  • Management – remove sources of trauma, resolve stressors, increase water temp > 82F for bonnethead sharks
    
    • Treatment – supportive care (fluids and nutrition), voriconazole for months. Potentially Posaconazole and amphotericin B
    • Reduce stressors – pelagic sharks in large oval systems with smooth clearly marked walls, pathogen free water source (UV and/or ozone)
    • Zoonotic but not reported from fish exposure

Question 5

What is the etiologic agent of gill rot?

What fish are typically affected?

What are the typical signs and lesions?

How is it treated?

Answer 5

Problem 36 - Branchiomycosis

• Host/location: Freshwater fish - gills
• Clinical Signs/Pathology:
  
  • Mottled Gills from thrombosis and ischemia
• Diagnosis:
  
  • Branched aseptate hyphae with intrahyphal round bodies (aplanospores) – looks like Saprolegnia sporangia.
  • Often infects proximal gill lamellae
• Treatment: No known treatment

Branchiomyces spp. - ZP

• Branchiomycosis aka gill rot.
• Cultured, wild FW fish.
• Major problem in European aquaculture.
• Two spp – B. sanguinis, B. demigrans.
  
  • Dz at water temps > 20 deg C, develops rapidly, high mortality.
  • Exacerbated by crowding, algal blooms, or increased levels of unionized ammonia.
• Lesions in gill – necrosis, infarctive.
  
  • Due to invasion of branchial blood vessels.
  • Thrombosis, vascular necrosis, hyperplasia of gill lamellar epithelium, telangiectasis.
  • Granulomatous reaction to hyphae.
• Hyphae – branched and nonseptate, B. sanguinis smaller than B. demigrans.

Question 6

Describe microsporidiosis in fish.

What are microsporidia?

How are they transmitted?

What clinical signs do they cause?

What differentials should be considered?

How are they diagnosed?

How are they treated?

Answer 6

• Microsporidia
  
  • Obligate intracellular parasites infecting invertebrates and fish – most are species, tissue or cell specific
  • Form spore filled cysts (xenomas) but some cause diffuse infection
  • Often carried asymptomatically but may cause morbidity and mortality
  • Direct life cycle – horizontal transmission common with vertical transmission in some. Spores released when fish dies or lesions rupture
    
    • Spores very hardy and survive for months
    • Found in freshwater and saltwater worldwide, common in temperate freshwater teleosts
  • Most infect a single species or closely related group but few have wider host ranges
  • Risk factors – exposure (poor biosecurity), permissive water temperature, low flow rate, stressors
  • Signs – typically carried asymptomatically
    
    • If signs seen, develop weeks to months after infection – lethargy, inappetence, weight loss, poor growth, dark coloration (may be focal), dyspnea/tachypnea, coelomic distention
    • Some cause white, yellow, brown or black cysts – xenomas
      
      • L salmonae – affects gills causing nodule and congestion
      • Pseudoloma – affects brain and spinal cord – scoliosis, weight loss, decreased fecundity
      • D. levantinae – affects skeletal muscle producing long thin swellings
      • Ovipleistophora ovariae affects the ovaries, causing reduced fecundity.
      • P. hyphessobryconis affects skeletal muscle, causing muscle wasting and abnormal swimming.
    • Signs may resolve over time, protective immunity seen in some cases
  • Diagnosis – wet mount or impression smear of ruptured xenomas or histology sufficient to confirm microsporidian spores
    
    • Spores are small, often 1–6 μm in length and ~2 μm in width, egg-shaped, each with a prominent, clear posterior vacuole creating a clog-like appearance. Birefringent walls.
    • Species identification often based on host species and tissue location. PCR and ISH available.
  • Management – can help reduce clinical signs if present.
    
    • Isolate fish to reduce transmission, increase aeration, increase water flow, change temp, increase UV and ozone, depopulation (inactivation or spores with 70% alcohol, and chlorine)
    • Treatment can reduce new xenoma formation and improve clinical signs, but limited effect on existing xenomas with recurrence common
      
      • Fumagillin orally and supportive care recommended. Other treatments (albendazole, toltrazuril, monensin, Nitazoxanide, salinomycin and amprolium
      • Inflammation highest after rupture of xenomas – consider NSAID
    • Spore viability unknown and some spores may survive freezing (recommended to feed frozen thawed diet.
      
      • Disinfection of eggs (iodine or chlorine) ineffective at stopping transmission in salmonids and zebrafish
      • Immune stimulants may decrease severity of signs
    • Zoonosis – fish are not a common source of microsporidiosis in humans

Problem 70 – Microsporidian Infection

Method of Diagnosis

• Wet mount of affected tissue having typical spores
• Histology of affected tissue having typical spores

History

• Usually wild - caught or pond - raised fish; variously sized nodules that enlarge slowly, if at all

Physical Examination

• Usually white or yellowish, variously sized nodules having fi rm to soft material; other clinical signs depend on the organ system(s) affected

Treatment

• Disinfect and quarantine
• Toltrazuril bath
• Fumagillin oral

Life cycle

• Often infections are species specific
• All microsporidians of fish are intracellular parasites with a direct life cycle
• They form a characteristic, thick - walled spore, which contains a sporoplasm.
• Host ingests the spsore—sporoplasm is discharged and migrates to the target organ and starts a proliferative phase (merogeny), producing a large number of cells (meronts)
• Mature spores may be released from lesions on body surface or after death of the host

Epidemiology

• Intracellular and often cell-specific (but may infect many organs if that cell type iss widespsread)
• Low temperatures significantly slow parasite growth
• Vertical transmission is suspected to occur with some species

Pathogenesis

• Clinical signs depend on the organ(s) infected
• Mild infections may be innocuous , heavy infections can cause severe organ dysfunction and death
• All microsporidians infect a host cell, but some (e.g., Glugea) also induce the formation of a tremendously hypertrophied cell that, together with the parasite, forms a xenoma

Taxonomy

• Classification of microsporidia has been divided into two major groups: pansporoblastina, where spores develop in membrane-bound packets and apansporoblastina, where spores are free within the host cell cytoplasma

Diagnosis

• Lesions may grossly resemble other pathogens that cause masses, including myxozoans, lymphocystis, dermal metacercaria, granulomas, and neoplasia
• Easily distinguished by examining wet mounts or histo for spores
• Microsporidia are gram positive, some are acid fast

Treatment

• Spore are typically resistant to environmental conditions and can survive for over a year at low temps
• High doses of chlorine depending on species
• Aside from quarantine and disinfection, no proved treatment though toltrazuril hass shown some efficacy against Glugea anomala
• Fumagillin has successfully treated several experimental infections
• Albendazole has potential for treating Loma ssalmonae and quinine hydrochloride delays xenoma formation
• Low temps can halt disease progression but is rarely feasible

Microsporidia - ZP

• Highly specialized, obligate intracellular eukaryotic parasites, wide host range.
  
  • Most recent phylogenetic data place them within fungi.
• In fish – simple, single-host lice cycles characterized by infection, merogony, sporogony, spore release, and presumed direct transmission.
  
  • Spore is the dispersal and infective stage.
    
    • Also the most relevant stage to diagnostics and only stage outside of host cell.
    • Also only stage that allows spp differentiation.
  • Spores have thick walls, cytoplasm containing nucleus but lacking mitochondria, Golgi complex and peroxisomes, and a coiled, extrudable polar tube.
    
    • Extrudes in response to environmental stimuli.
    • Polar tube is conduit for passage of sporoplasm into host cell cytoplasm.
      
      • Initiates infection, avoids host immunity.
    • Once inside, sporoplasm matures into meront.
      
      • Develops within host cell via proliferative phase that produces more meronts and sporogony aka spore development phase, meronts undergo conversion to spores.
  • Meronts in host cytoplasm except Nucleospora (host nucleoplasm).
    
    • Then grow into multinucleate plasmodia.
    • Sporogonial plasmodia arise from meronts.
    • Infected cells may develop at sites of primary infection or be transported to other tissues for development.
• Lesions variable – hypertrophy of infected target cells and transformation into xenoma or destruction of cytoplasm and necrosis of the cell.
  
  • Xenoma – enormously hypertrophied host cell replete with microspodian stages i.e. meronts and spores.
    
    • Cyst-like structure.
    • In xenoma inducing microsporidians i.e. Glugea spp, compression of surrounding tissue, pressure atrophy, and fibrosis.
    • Mature xenomas elicit granuloma formation.
    • Healing can occur as spores at center og granulomas are destroyed by MP.
  • MS that do not induce xenomas – destroy host cell cytoplasm and replace with developmental stages without hypertrophy.
    
    • i.e. Pleistophora spp.
    • Development of meronts and spores destroys sarcoplasm and results in degeneration and necrosis.
    • Release of spores results in granulomatous inflammation.
  • Ddx – mycobacteriosis, lymphocystis, ichthyophonus, metacercarial granulomas, cyst-like myxozoan plasmodia, neoplasia.
  • Dx confirmation with ID of spores in tissues through wet mounts or histo. Organism ID/PCR.

Question 7

What is the etiologic agent of Ichthyophonosis?

What fish are commonly affected?

How is it transmitted?

What are the lesions and clinical signs?

How is it diagnosed?

How is it treated?

Answer 7

Problem 71 – Ichthyophonosis (Swinging Disease)

Method of Diagnosis

1. Culture of Ichthyophonus
2. Wet mount of lesion (skin or viscera) with sporulating organism
3. Histopathology of pathogen

History/Physical Examination

Emaciation; usually shallow skin ulcers; sandpaper – like texture to skin; vertebral curvature

Treatment

Avoid exposure to contaminated feed

Epidemiology

• Ichthyophonus is a fungus - like agent that causes a chronic, systemic, granulomatous disease.
• Endemic in many feral, cold water marine fish populations
• Rarely a problem in cultured fish but has infected freshwater fish that were fed contaminated marine offal

Life cycle

• Complicated life cycle involving production of multinucleated spores which produce endospores
• Hyphae may or may not be produced before endospore formation
• Obligate pathogen, but spores can survive in sweater for 2 years

Pathogenesis

• Lesions of ichthyophonosis are most common in highly vascularized organs, such as heart, spleen, kidney, and liver.
• The acute form, which takes several weeks to develop, involves invasion of tissue with little inflammatory response.
• In the chronic form, there is a strong, chronic inflammatory response to invasion
• White or dark nodules may be present on various organs
• Lesions on the skin may be rough or ulcerated
• Neuro signs are common in freshwater salmonids due to CNS involvement
• Fish may also have spinal curvature and darkening of the skin

Diagnosis

• Can be identified from fresh lesion wet mounts
• Thick-walled spores surrounded by granulomatous inflammation
• PAS and silver positive

Treatment

• None, avoid contaminated feed

Ichthyophonosis – systemic granulomatous dz, FW and SW. - ZP

• Ichthyophonus hoferi.
  
  • Fungus-like protistan microorganism.
  • Obligate pathogen.
  • Endemic in wild coldwater marine fish i.e. Atlantic herring.
  • Transmission is direct via oral – ingestion of contaminated feed, infected, fish, infected copepods.
• Lesions – in highly vascularized organs i.e. heart, spleen, kidney, liver.
  
  • Spores found in tissues of affected fish.
    
    • Round, double-walled, multinucleate spores, or flask-shaped germinating spores characteristic, considered pathognomonic.
    • Hyphae may also be seen.
• Spores elicit granuloma formation.
  
  • Dz often systemic.
  • Skin – roughened surface texture aka sandpaper effect resulting from elevation of epidermis overlying granulomas.
  • Neuro signs from involvement of brain and SC.
    
    • FW salmon aka swinging dz.
    • May also have spinal curvature and darkening of skin.
• Dx – culture or examination of wet mounts, histo.
  
  • I. hoferi can be cultured in vitro using fungal media i.e. Sabouraud dextrose agar with 1% serum or tissue culture media with 10% fetal bovine serum.
    
    • Unlike some of the other mesomycetozoea.
• Tx – None, lesions in muscle render fillets unmarketable.

Question 8

What are the effects of mesomycetozoea infections in fish?

What are these organisms?

How are they transmitted?

What fish do they affect?

What are teh typical clinical signs?

How are they diagnosed?

Answer 8

• Mesomycetozoea (DRIPs)
  
  • Chronic disease that may be associated with white nodules – thin cysts containing characteristic spores
  • Fungal-like organisms - No treatment but lesions may resolve over time
  • Horizontal transmission – ingestion of viable spores in prey, especially scavenging on dead fish or waterborne
  • Can survive in saltwater for up to 2 years – S. destruens has asymptomatic carriers (topmouth gudgeon)
  • Found in both salt and freshwater habitats and teleosts – koi, chinnok salmon, European eels, atlantic herring, pacific herring, rainbow trout
  • Signs – several conspecific affected with typically a chronic presentation
    
    • Skin and fin lesions common - white nodules, plaques, papules, linear tracts. May be red and ulcerative and tend to progress – similar gill lesions may be seen. Weight loss, exophthalmos (white nodules or tracts within conjunctiva), neurologic signs, and spinal curvature.
  • Diagnosis – usually identified on direct microscopy of lesions after rupturing of the cyst wall, releasing spores
    
    • Spores are uniform, round to elliptical, thick or double-walled, and signet-ring shaped with a prominent central refractile body. Central body is negative on acid-fast stain and positive on periodic acid–Schiff and silver stains. Spores may germinate after host death producing hyphae.
    • Necropsy – thin walled cysts within hypodermal tissue with spores. Granulomatous inflammation and necrosis possible, systemic spread less common. Culture is possible.
    • Identification to genus/species requires molecular diagnostics.
  • Treatment
    
    • Not indicated in incidental infections, but surgical removal may help individual fish if mass causing secondary issues. Antifungals may be considered.
  • Zoonosis – no known zoonotic potential