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Mark A. Mitchell DVM, MS, PhD
University of Illinois
College of Veterinary Medicine
Non-Infectious Diseases
 Ammonia:
 Most commonly
observed in new
systems
 More problematic in
cold weather


Bacteria decreased
function
Check regularly in the
winter
Non-Infectious Diseases

Ammonia toxicity

More problematic with
small fish


Toxic levels build up faster
Toxic levels vary with pH
 Un-ionized form highly
fatal at 0.2 ppm
 1 ppb- 0.02 ppm
 Chronic problems
Non-Infectious Diseases

Ammonia toxicity

Clinical signs





Dyspnea
Telangiectasia
Gill damage
Mucous production

Gills and body
Lethargy
Non-Infectious Diseases

Ammonia toxicity

Treatment

Acute toxicity



Remove fish to
ammonia-free system
Lower system pH
Chronic toxicity

Water changes

Correct inciting cause
Non-Infectious Diseases

Ammonia toxicity

Treatment

Chronic toxicity


Water changes
Correct inciting cause
 Evaluate filtration

Often insufficient
capacity
 System burden


Fish density
Organic load
 Detritus
 Diet
Non-Infectious Diseases
 Nitrite toxicity
 Clinical signs
 Similar to ammonia
 Methemoglobinemia


Brown blood
Muddy gills
 Diagnosis
 Test water
 Blood sample
 Histopathology
Non-Infectious Diseases
 Nitrite toxicity
 Treatment


Acute toxicity
 Remove fish to ammonia and nitrite-free water
 Oxygenate water
 Increase salt
 Chloride competes with nitrite at gill
 3 ppt
Chronic toxicity
 Evaluate biological filter, stocking density, feeding practices
Non-Infectious Diseases
 Hypoxia
 Low oxygen levels


How can oxygen levels become depleted in a system?
Start by thinking about its usage through the system…..
 What requires oxygen?
 What is the highest biomass that requires oxygen?
Non-Infectious Diseases
 Hypoxia
 Low oxygen levels


Rare in aquariums because of aeration
More common in ponds
 Oxygen depletion occurs during the hours when the sun is
down
 Phytoplankton biomass can consume huge amounts of
oxygen
 High mortalities noted at dawn or early morning
 Largest fish typically go first
Non-Infectious Diseases
 Hypoxia
 Diagnosis

Measure dissolved oxygen levels
 Treatment


Acute toxicity
 Move fish to well oxygenated/aerated water
Prophylactically
 Aerate water- especially at night
 Manage phytoplankton blooms
 Reduce nitrogen in system
Non-Infectious Diseases
 Hypercapnia
 Clinical signs
 Narcosis
 Lethargy/depression
 Slowed respirations
 Diagnosis
 Test water, pH
 Treatment
 Increase pH
 Increase oxygen
 Stop supplemental CO2
Non-Infectious Diseases
 Super saturation (gas-bubble disease)
 Nitrogen gas most common
 Clinical signs

Gas bubbles under skin and fins, ischemia and necrosis
 Diagnosis

Physical exam, evaluate water source
 Treatment

Stop supplemental gas (CO2, pumps), evaluate water source
(deep well), minimize venturi’s
Non-Infectious Diseases
 Acidosis and Alkalosis
 Alterations in pH can lead to problems for fish

Log scale
 Small changes are actually BIG changes
 Fortunately most fish adaptable
 Immunocompromised/stressed fish less likely to handle
 pH varies based on native system
Non-Infectious Diseases
 Acidosis and Alkalosis
 Common causes for pH fluctuations



Carbon dioxide: acidic water
Heavy plant life- alkaline water
Concrete ponds- alkaline water
 Calcium compounds- pH: 10-11
 Seal with appropriate compounds: bituminous based paints
 Cheaper paints can be toxic
 Mix in muriatic acid with concrete to prevent leeching
Non-Infectious Diseases
 Acidosis and Alkalosis
 Signs:

Acidosis: darting, jumping from water, increased mucous
production, gill hemorrhages

Alkalosis: skin and fin erosions, mucous production- milky
white appearance
Non-Infectious Diseases
 Acidosis and Alkalosis
 Diagnosis: test pH
 Treatment:
 Remove fish to aquarium/pond with neutral water
 Titrate pH to appropriate level
Non-Infectious Diseases
 Chlorine Toxicity
 Addition to water as an oxidizing agent

Early 1900’s- cholera and typhoid fever
 Research with fish



4 ppm fatal within hours
0.2-0.3 ppm- fatal within hours in susceptible species, longer less susceptible species
0.002 ppm can cause chronic gill issues- hyperplasia
 Flushing of systems as pulse therapy is common

Alterations in dechlorination required
Non-Infectious Diseases
 Chlorine Toxicity
 Signs

dyspnea, gasping at surface
 Diagnosis:


water test
gill biopsy
 branchial epithelial hyperplasia
 Treatment


sodium thiosulfate
evaluate municipal water treatment schedules
Non-Infectious Diseases
 Hypothermia
 Clinical signs

Listless, clamped fins, non-progressive swimmers
 Hyperthermia
 Clinical signs

Hyperactive, tachypnea, rapid swimming, ruptured blood vessels
 Diagnosis
 Check temperature
 Return to normal temperature gradually
 2-3oF per hour
Non-Infectious Diseases
 Heavy metals
 Copper, Mercury, Zinc
 Clinical signs

Breaks down mucus coat, gill epithelial changes, anorexia,
edema, disoriented, protruded scales
 Treatment



Remove source
Increase pH- chelate compounds
Increase oxygen levels to assist gas transport
Bacteria
 General considerations:
 bacterial infections in fish can rapidly become systemic
 most infections are caused by Gram-negative bacteria
 most infections are stress mediated

poor water quality, overcrowding, poor diet
Bacteria
 Gram negative opportunists
 Freshwater


Aeromonas spp., Pseudomonas spp.
Saltwater

Vibrio spp.
 Gram positive opportunists
 Erysipelothrix rhusiopathiae
 Ubiquitous
 Clinical signs: skin ulcers, hemorrhages on skin and fins,
sepsis
Bacteria
 Diagnosis:




culture
incubation temperature
add salt for saltwater
cultures
sensitivity
 Treatment:
 systemic antibiotics
 reduce stress
 water changes
Aeromonas
 Aeromonas septicemia, red sore
 Most common bacterial disease of freshwater fish
 Clinical signs
 Generalized
 Pathogen
 Aeromonas hydrophila
 Aeromonas salmonicida achromogenes
Aeromonas
 Predisposing factors
 High temperatures, overcrowding, organic pollution,
hypoxia, skin lesions from primary pathogen (Epistylis)
 Diagnosis
 Biochemical identification of clinically significant
numbers associated with lesion
 Treatment
 Initial

Oxytetracycline
Bacteria
 Edwardsiella ictaluri
 “Hole in the head disease”
 Enteric Septicemia of
Catfish
 1976 first case


1981- isolated
Primary financial losses
 Seasonal
 Spring and fall

72-82F (22-28C)
Bacteria
 Clinical signs
 Decreased appetite
 “spiraling” and “surfing”
 Ulcer between eyes
 Ascites
 Hemorrhage internally
 Treatment
 Medicated feed-Oxytetracycline
 Vaccine
Flavobacterium columnare
 Clinical signs
 Erosive lesions of skin and gill
 Transmission
 >15C
 70ppm hardness is ideal for
growth
 Risk factors
 Physical injury, low oxygen,
organic pollution, high nitrate,
high arsenic
Flavobacterium columnare
 Diagnosis
 Wet mount – flexing or gliding motion
 Biochemical tests or agglutination
 Treatment
 Surfactant baths
 Potassium permanganate prolonged immersion
 Copper sulfate
 Antibiotics
Bacteria
 Streptococcus iniae
 1976: FW dolphin
 1996: Ontario
 4 cases


Bacterimic
16 h-2 d
 Tilapia
 Hybrid striped bass, RBT, YF
turbot
 Meningioencephalitis
 Diagnosis
 Culture
 Pulse-field electrophoresis
 Treatment
 Antibiotics
 Vaccine
Bacteria
 Mycobacterium
 M. fortuitum, M. marinum
 non-motile, acid fast
 cosmopolitan distribution
 transmission: oral-fecal, water
 signs: chronic progressive disease, lethargy, anorexia,
skin ulcers, edema, granuloma formation
Bacteria
 Mycobacteriosis
 diagnosis:
 squash preps at necropsy or
biopsy
 culture
 treatment:
 poor success
 depopulate, disinfect
 ZOONOTIC
Yersinia ruckeri
 Enteric redmouth
 Pathogen
 Gram negative
 Pathogenesis
 Warm water
 Transmission
 Fecal-oral
 Vertical?
Yersinia ruckeri
 Clinical signs




Reddening around mouth and head
Darkening of dorsum
Anorexia
Exophthalmia, corneal opacity, blindness, loss of
melanin control
 Diagnosis
 Clinical signs, anemia, culture
 Treatment
 Oxytetracycline
 Control
 Avoid carriers (mammals and birds)
 Vaccine
Yersinia ruckeri
Water molds
 Saprolegnia spp.
 Cosmopolitan
 considered opportunist,
possibly primary invader
too
 associated with stress
 secondary invader
 prefer cooler temperatures
Water molds
 Signs:
 “cotton-growth” on skin
ulcers, trauma.
 can become internalized.
 Diagnosis:
 direct saline smear
 branching non-septate
hyphae
 Treatment:
 reduce organic load, salt,
formalin
Atypical Water Mold
 Ulcerative mycosis, red-spot disease
 Freshwater or estuarine
 Clinical signs
 Usually deep penetrating wound into body cavity
 Pathogen: Aphanomyces (most common)
 Evidence that skin damage by Pfeisteria (toxic dinoflagellate)
linked to infection
Atypical Water Mold
 Diagnosis
 Wet mount
 Culture on corn-meal agar
 Treatment
 None proven
 Improve water quality
 Limit access to Pfeisteria
Viruses
 Current status
 Knowledge of
epidemiology of many
viruses is limited
 Aquaculture and wild
populations: more
common

Emerging pathogens?
Virus diagnostics
 Historical
 Cell culture,
Histopathology, EM,
Serology
 Current
 Molecular techniques
 PCR, cDNA cloning,
restriction digestion
analysis
Viruses
 Characterizing viral genomes
 Determine gene organization, protein products,
regulatory strategies
 Generate clones
 Diagnostic and control methods
 Generate probes
 Diagnostics
 Investigate molecular epidemiology
 Immunological response and virus-cell interactions
Viruses
 Lymphocystis
 cosmopolitan
 iridovirus
 signs: macroscopic nodules on skin and fins (internal
possible)



chronic
often self-limiting
prognosis poor if affects certain areas of the body
Lymphocystis
Viruses
 Lymphocystis
 diagnosis
 gross examination
 wet mounts
 biopsy and histopath
 treatment:
 no specific treatment
 debulk, probably return
 spontaneous regression
Large Mouth Bass Virus
 Lake Weir, FL (1991)
 Unexplained die-off
 Santee- Cooper, SC (1995)
 1,000 mortalities
 Etiology: Iridovirus
 Identified other centrarchids
 Ornamental fish-release, escapes
Large Mouth Bass Virus
 Clinical signs
 Abnormal swimming patterns

Loss of equilibrium
 Epidemiology: Risk factors
 Adult fish
 Summer months
 Affected and unaffected populations
Channel Catfish Virus
 Herpesvirus
 1960’s
 Confirmed 1971
 Signalment
 Young fish

<1 year old
 Clinical signs
 Decreased appetite
 Ascites
 Renomegaly
Channel Catfish Virus
 Transmission
 Horizontal and vertical (presumed)
 Direct and indirect contact
 Not stabile: UVB, mud, chlorine
 Diagnosis
 Histopathology and culture
 Treatment: None, management
 Adult survivors are reservoir: don’t use as brood stock
Infectious Salmon Anemia
Orthomyxovirus
Norway, 1984
Canada, 1996
US, 2001
molecular differences between regions
Clinical signs
anemia, leukocytosis, pale gills, ascites, renomegaly
Infectious Salmon Anemia
 Mortality: significant
 Transmission: direct, indirect
 Diagnosis
 Serology
 RT-PCR
 Management
 Cull affected stocks
Protozoa
 Ichthyophthirus multifilis
 Ciliate (up tp 1.5 mm)
 Life cycle:

trophont on fish--> break off-> tomonts develop on
substrate-->theronts released
find fish
 Temperature dependent
 Diagnosis: skin scrape, gill
biopsy
 Treatment: many available
Conclusions