Está en la página 1de 79

Institute of Breeding and Diseases of Game and Fish

University of Veterinary Medicine and Pharmacy


2011/12

IN FEC TIO U S D IS EA S ES O F
FIS H : V IR A L, B A C TER IA L
A N D M YC O TIC D IS EA S ES

Why Do Fish Diseases


Occur?
Predisposing
Environment

Susceptible
Host

Virulent
Pathogen

I. Viral fish diseases

Rule - out diagnoses (viral infections):


Presumptive diagnosis is based on the absence of other etiologies
combined with a diagnostically appropriate history, clinical signs,
and/or pathology.
Definitive diagnosis is based on presumptive diagnosis combined
with confirmation of viral presence (e.g., antibody probe, gene
probe)
EHN - epizootic haemopoietic necrosis (OIE)
IHN - infectious haemopoietic necrosis (OIE)
SVC - spring viraemia of carp (OIE)
IPN - infectious pancreatic necrosis (OIE)
Red sea bream iridoviral diseases (OIE)
ISA - infectious salmon anaemia
VHS - viral haemorhagic septicaemia (OIE)
CCVD - channel catfish virus disease
KHVD - koi herpes virus disease
PFRD - pike fry rhabdovirus disease
EPa - epitelioma papulosum (carp pox, fish pox)
LC - lymphocystis (LD - lymphocystis disease)

Systemic Viral Diseases: General Features


Method of Diagnosis
Clinical signs characteristic of the disease combined
with either or both:
1. Antibody or gene test of tissue or cultured virus
2. Histopathology of diagnostic lesions
History
Varies with etiological agent and environmental
conditions
(especially temperature)
Physical Examination
Varies with etiological agent and environment
Treatment
1. Disinfect and quarantine
2. Eliminate source of contamination (i.e., water or

General characteristics of viral diseases of fish


include:
Often temperature - dependent pathogenicity
Host - specific (usually affecting only one species
or a
closely related group of species)
Usually young fish get sick, while older fish
become carriers
Common clinical signs include:
Exophthalmos
Abdominal distension
Hemorrhage
Common microscopic lesions include:
Organ necrosis
Intracellular inclusions

No medications are available to treat any fish viral


disease.
Various antiviral compounds have been tried with
varying success, but none are commercially available
for use in fish. Thus, one must rely upon disinfection
and quarantine, or sometimes environmental
manipulation (e.g., temperature) for management.
Avoidance is the best method of control. This includes
obtaining
fish only from certified virus - free stocks and raising
Definitive diagnosis of systemic viral disease is
fish in virus - free water (spring, well, or disinfected).
based on observation of relevant history, clinical
signs and/or
pathology in combination with virus identification/
detection via either an antibody or a gene test.
Some
viruses may be present in low numbers without

CCVD - Channel Catfish Virus disease


causative agent: HERPESVIRUS
host: channel catfish Ictalurus punctatus (fry and
fingerlings)
geographical distribution: USA (possibly Europe, Asia)
pat-anatomical changes:
exophtalmus, pale gills, ascites, haemorrhages in the skin,
fins, muscles, liver, kidney, spleen

Clinical Signs
spiralling or swimming abnormally
convulsions
just before death at surface with tail down
fin base hemorrhage
internal also

Often obscured by columnaris


Appears to be host specific for catfish

Channel Catfish Virus


Disease
( CCVD )
Method of Diagnosis
Identifi cation of channel catfish virus
infection in fi sh displaying typical
clinical signs and pathology
History
Acute to chronic morbidity/mortality;
corkscrew spiral swimming
Physical Examination
Reddening on body and base of fi ns;
depression; exophthalmos;
swollen abdomen; equilibrium deficit
Treatment
1. Disinfect and quarantine
2. Reduce temperature to less than
15 C

Channel catfish virus is the


most important viral disease
affecting channel catfish.
Except for its accidental
introduction
into Honduras, it is restricted
to the channel catfi sh producing areas of the United
States .
It is a highly species - specific
herpesvirus and only naturally
affects channel catfish,
although it can experimentally
infect some other ictalurids

During CCVD epidemics, the


younger, more robust fish
typically die first. While older
fish can become clinically
sick, epidemics occur almost
exclusively in young
( < 1 year) and small ( < 15
cm) fish and most epidemics
are in fish < 4 months old.

During epidemics, virus is


transmitted horizontally in
the feces and urine of
clinically affected fish. There
is also evidence for vertical
transmission .

Mortalities are most rapid


and severe with higher
temperatures, being highest
at 25 30 C .
Many CCVD epidemics are accompanied by secondary bacterial
infections ( Aeromonas , Flavobacterium , Edwardsiella ), which can
mask the primary diagnosis.

Clinical Signs/Pathogenesis
GROSS LESIONS
Clinical signs include hanging head up in the water, disorientation
(corkscrew spiral swimming), abdominal distension, exophthalmos,
and hemorrhages on the body, gills, and at the bases of the fins.
Internally, there is a yellowish fluid in the peritoneal cavity and
punctate hemorrhage in the viscera.
HISTOPATHOLOGY
Channel catfish virus attacks
all major organ systems.
Focal necrosis begins in the
posterior kidney and quickly
develops into diffuse necrosis
of both hematopoietic and
excretory tissues,
accompanied by hemorrhage
and edema . Necrosis also
affects the liver, spleen,
gastrointestinal tract,
pancreas, and skeletal muscle.

Diagnosis
The typical presentation of a CCVD
epidemic is a rapid, abrupt increase in
mortality in young - of year channel catfi
sh when the temperature is at least 25
C . Definitive diagnosis of clinical CCVD
requires identification of virus from target
tissues, with appropriate clinical signs.
Many CCVD epidemics are
accompanied by secondary bacterial
infections ( Aeromonas ,
Flavobacterium , Edwardsiella ),
which can mask the primary
diagnosis.
Treatment

Disinfection and quarantine is the most


effective means of controlling CCVD
epidemics. The virus can persist in water
up to 1 or 2 months at 4 C but less
than 2 weeks at 25 C .
Treating ponds with 20 50 mg/l chlorine
will ensure that the virus is eliminated.
Thorough drying also inactivates it. All
fish surviving an outbreak should be

The CCVD
virus is also relatively
unstable in the
environment.
There is a 50% loss of
infectivity in fish stored
for 100 days at
approximately 20 C
and 90% loss after 3
days on ice.
It survives for less than
3 days in dead fi sh at
room temperature.
Freezing and thawing
rapidly
destroys activity.

IPN - Infectious Pancreatic Necrosis


causative agents: BIRNAVIRUS
host: salmonids (not older than 6 months)!
clinical and pat-anatomical changes:
dark colour, stop feeding, cork-screw swimming, ascites,
exophtalmus, trailing faecal casts, haemorrhages in the skin, fin
bases, pyloric region, intestine filled with yellow catarhal exudate,
pancreatic necrosis (histologically)
geographical distribution: Europe, North America, Asia
transmission: by water (faeces), infected fish

Notifiable to
OIE

History
Usually acute,
sometimes chronic,
morbidity/mortality
Physical
Examination
Neurological signs;
trailing white feces;
dorsal darkening;
abdominal distension;
exophthalmos;
hemorrhage; pale gills;
catarrhal exudate in
stomach
Treatment
1. Disinfect and
quarantine
2. Raise fish in virus -

IPN

Only young fish become clinically ill (mortality in fish >


6months old is rare),
but any age fish can become infected, forming chronic
The virus is highly
Clinical Signs/Pathology
carriers.
contagious.
During epidemics, virus is
readily transmitted horizontally
by contact and by ingestion of
infected tissue; the fecal
pseudocast is a major source
of virus.
Virus can also be shed in the
feces of piscivorous birds.
Vertical transmission readily
occurs via transport in
reproductive fluids and on (or
possibly in) the egg.

Clinical signs include dorsal


darkening, trailing white feces,
abdominal
distensionexophthalmos,
hemorrhage on the ventrum,
and pale gills.
Neurological signs (corkscrew spiral
swimming, whirling) can often be
initiated by startling the fish.
In older fi ngerling trout, there may
be many petechial hemorrhages in
the viscera . In contrast, fry have
pale viscera with few petechiae. A
catarrhal exudate in the stomach
and intestine produces the mucoid,
cohesive fecal pseudocast.

HISTOPATHOLOGY
The prime target of viral
infection is the pancreatic
acinar cells, which undergo
acute necrosis and have
basophilic,
intracytoplasmic
inclusions
( inclusions are actually
products of cell
Treatment
degeneration).
Disinfection and quarantine
are the only practical
methods of controlling an IPN
epidemic.
Extreme caution should be
taken to avoid spreading virus
to uncontaminated areas,
both on and outside the farm.
The IPN virus is one of the
most stable fish viruses. It
can survive for months in
frozen viscera.

Rainbow trout with IPN.


Note the swollen abdomen
caused by accumulation of
fluid in the peritoneal cavity.

IHN - Infectious Haematopoetic Necrosis


Causative agent: RHABDOVIRUS sp.
Notifiable to OIE
host: salmonids
clinical manifestation: at water temperature below 15 oC
mortality: up to 100 % (in young population)
clinical and pat-anatomical changes:
lethargy, abdominal swelling ascites, exophthalmus pop-eye,
anaemia, pale gills, haemorrhages on the fin bases, dark coloration,
distended stomach with a milky fluid, intestine filled with a yellow fluid,
petechial haemorrhages in the haematopoetic organs, which are paleanaemia, necrosis in the anterior kidney, spleen and submucosa of the
intestine (histologicaly)
geographical distribution: USA, Japan, Europe
transmission: via infected water, urine, faeces, food

Infectious Hematopoietic Necrosis ( IHN ; Chinook


Salmon
Disease Virus, Sacramento River Chinook Disease,
Columbia River Sockeye Disease, Oregon Sockeye
Disease)

History
Variable; acute to chronic
morbidity/mortality
Treatment
1. Disinfect and quarantine
2. Raise temperature above 15 C
3. Treat eggs with povidone iodine

Epidemiolog
y
Infectious
hematopoietic
necrosis virus,
a
rhabdovirus,
is a major
cause of
mortality in
salmonids

IHN is most serious as a disease


of cultured rainbow trout in
freshwater.
During IHN epidemics,
only young ( < 2 years old) fish
become clinically ill.

High mortality can occur in fish less


than 6 months old, while older fish
have lower mortality and may not
show clinical signs

Temperature has an important


influence on epidemics.
Peak mortalities (to 100%) occur
at 10 C;
fewer and more chronic
mortalities occur at less than 10
C, while fewer and more acute
mortalities occur above 10 C.
No disease occurs above 15
C.

During epidemics, virus


is readily transmitted
horizontally
by ingestion of infected
tissue, as well as by the
feces,
urine, and mucus of
infected fish.

Survivors have strong


protective
immunity and can
become carriers.

Clinical Signs/Pathology
The typical presentation of IHN is
increased mortality among fry or
fingerlings of susceptible species at the
appropriate temperature.
Larger, more robust individuals die
first.
A long, thick, off - white fecal pseudocast
trailing from the rectum is diagnostic.
The most diagnostic
change is the presence of
remnants
of necrotic cells (
necrobiotic bodies ),
probably erythrocytes, in
kidney smears
Avoidance is the most useful
prophylactic measure.

VHS - Viral Haemorhagic Septicaemia

Notifiable to OIE

causative agent: family RHABDOVIRIDAE genus LYSSAVIRUS


host: salmonids
clinical manifestation: at water temperature below 8 oC
mortality: up to 80 %
clinical and pat-anatomical changes:
acute form poor feeding, erratic spiral swimming, dark skin, exophthalmus,
pale gills, anaemia, multiple haemorrhages in skeletal muscles, serosa and
parenchymatous organs, swollen kidneys, hyperaemic liver high mortality
chronic form dark skin, exophthalmus, swollen abdomen ascites,
swollen kidney, pale liver, haemorrhages of internal organs lower mortality
nervous form ataxia, circular (spiral) swimming, retracted abdomen high
mortality
geographical distribution: Europe
transmission: virus laden water, infected fry and eggs

Clinical Signs/Pathology
The range of gross lesions seen with VHS in salmonids is great. There
are three phases to VHS outbreaks, which refl ect the severity of
infection, not the chronological
stages.
The acute phase (typically at 15 18 C) involves rapid, initially high
mortality, but lower cumulative mortality. Fish are dark and lethargic
(congregate away from the current on the edges of the pond or
raceway, eventually massing near the outlet screen), with reddening
at the base of the fi ns and gills caused by injection
of vessels and punctate hemorrhage. There is also hemorrhage in the
abdominal cavity and a leucopenia
In the chronic phase (typically at 1 5 C), there are moderate,
mainly protracted deaths that eventually result in high cumulative
mortality. Fish are black, with anemia, exophthalmos, and a swollen
abdomen. The organs are pale from severe anemia, with organizing
hemorrhages.
In the nervous phase, there are low mortalities. Fish do not have gross
lesions but exhibit a looping swimming behavior, darting through the
water and spiraling at the bottom of the pond.

Epidemics occur at
3 12 C,
with highest
mortalities at about
8 10 C.
Outbreaks rarely
occur above 15 C
and never above 18
C

Epidemiology
It is primarily a disease of
rainbow trout and brown trout.
During VHS epidemics, any
age salmonid can become
clinically ill, but young fi sh
are most severely affected.
Mortality can be up to 100%
in fry and often 30 70% in
older fi sh.

abnorm lne plvanie v bonej


polohe ,alebo okolo svojejosi

Abnorm lne plvanie

Abnorm lne plvanie

Abnorm lne plvanie -hyn

hem orgie na bze plutiev

exoftalm us

Exoftalm us

Patologicko anatom ick zm eny

Patologicko anatom ick zm eny

D etail-patologicko anatom ick zm eny

Patologicko anatom ick zm eny

SVC Spring Viraemia of Carps

Notifiable to
pvodca RHABDOVIRUS CARPIOOIE
bulletshape
Vnmav druhy: common carp, koi carp, etc.
rarely bighead carp, crucian carp
Klinick manifestcia: JAR teplota vody pod 15 oC
mortalita: do 90 %
Klnick a pat-anatomick zmeny:
dark colour, uncoordinated swimming, slowed respiration, gathering
at the water outflow, gross abdominal distension ascites, oedema
and inflammation of anal papilla, uni- or bilateral exophtalmus,
haemorrhages on the skin and gills, peritonitis, catarrhal or
haemorrhagic inflammation on the heart, kidneys, swim bladder and
skeletal muscle
geographical distribution: Europe
transmission: by water (faeces, urine), by mechanical vectors
leech, carp louse

Spring viraem ia (dropsy)


Rhabdovirus carpio
Notifiable disease!
EU: List III.

(91/67/EEC)

SVCV causes major losses in cultured carp in eastern


and western Europe as well as Israel.
In typical outbreaks, SVCV spreads horizontally during the winter when
water temperatures are low and host immunity is suppressed.

In spring, as temperatures approach 10 C, fish develop clinical


signs of SVC.
Outbreaks are most severe within a very narrow temperature range,
when temperatures begin to reach 15 18 C

When overwintering fi sh are in poor condition, they are more


susceptible. When clinical disease is present, mortality ranges
from 30% to 70%.
Any age fish is susceptible (including broodstock), but disease is
most severe in young fish.
Horizontal transmission can occur via exposure to infected
feces, urine, or skin/gill mucus.
The gill is the most common portal of entry.

Clinical Signs/Pathology
Affected fish often seek slow moving
water or lie on the bottom.
As the disease progresses, fish become
dark, sluggish, nonresponsive to
external stimuli; they often swim on
their side and rest in abnormal
positions. There may be exophthalmos
and abdominal distension, as well as
skin, gill, vent, or ocular hemorrhages .
The gills may be pale. There is also
internal hemorrhage and inflammation,
especially in the swim bladder, but also
in the intestine, peritoneum and
muscle.
Secondary infections, especially with
Aeromonas hydrophila , are very
common.

Treatment
Disinfection and
quarantine are the
only proven means
of controlling SVC
epidemics.

Minimizing stress
and overcrowding, and sanitary disposal of dead fish are
also recommended. Reducing fish stocking density in
winter and early spring can reduce virus spread.

Infectious Salmon Anemia (ISA ;


Hemorrhagic Kidney
Syndrome [ HKS ])

ISA

Notifiable to OIE
Method of Diagnosis
Identifi cation of ISA virus infection in
fi sh displaying typical clinical signs
and pathology
History
Mainly chronic but sometimes acute
morbidity/mortality
Physical Examination
Lethargy; hanging head up; dyspnea;
abdominal distension; exophthalmos;
skin hemorrhage; pale gills
Treatment
Disinfect and quarantine

ISA is most often diagnosed in


spring.

Infectious salmon anemia (ISA), also called


hemorrhagic
kidney syndrome (HKS), is caused by an
orthomyxovirus
in the genus Isavirus . ISA is a major worldwide threat
to
Atlantic salmon farming.

Mortality is
generally
low but can
be up to
100%.

Initially observed in Norway and then identified in


Atlantic Canada , Scotland, Faroe Islands,Denmark ,
Maine, Nova Scotia, Shetland
Islands, Chile.
The epidemic typically spreads slowly within a farm.
Transmission occurs from fish to fish by contact with
infected fish (infectious virus is present in skin
mucus, feces, urine, and blood), parts from infected
fish (including viscera, trimmings, and muscle).

Clinical Signs/Pathology
Pathology is highly variable.
The uncommon, peracute form of the disease often presents
with no clinical signs.
Chronic disease is typical, and fi sh may display anorexia,
dyspnea, and lethargy. Fish may congregate in the upper parts
of a cage and hang motionless on the cage wall before sinking
to the bottom.
ISAV primarily infects blood cells (e.g., kidney) and endothelial
cells (such as those lining the liver and heart), typically causing
severe anemia, vascular damage and hepatocellular
degeneration.
Thus, typical gross lesions include exophthalmos, distended
abdomen, scale edema (vascular collapse), skin hemorrhage
and pale gills (anemia). Internally, there may be straw - colored
or hemorrhagic ascites, hemmorhages in the peritoneal cavity,

Gross lesions in salmon


infected with ISAV,
showing severe anemia
(pale gills), dark
congested liver and
petechiation of the
visceral fat.

Salmon with ISA


having
ascites.

Infectious Salmon Anemia


( ISA ; Hemorrhagic Kidney Syndrome [ HKS ])

Iridoviral Diseases

Notifiable to
OIE

Only epizootic hematopoetic necrosis (EHN)


and red sea bream Iridovirus
History
Acute to chronic morbidity/mortality
Physical Examination
Varies greatly with affected species: abnormal
swimming,
reddening of body, skin ulcers, anemia and/or
abdominal
distension
Treatment
Disinfect and quarantine

Disease occurs at 11 17 C . Other environmental factors


affecting epidemics are poorly understood, although outbreaks
are associated with poor water quality.
The virus is very persistent in the environment and it might
possibly cycle through insects or amphibians.

Epidemiology
Iridoviral diseases (family Iridoviridae) can cause
acute to chronic morbidity and mortality in many fish
species
Clinical Signs/Pathology
Clinical signs are nonspecific.
In perch, sudden death is the most common
sign. Perch may display nervous signs
(ataxia, lethargy), as well as a darkened body,
and reddening around the nostrils, gills and base
of the fins.
Rainbow trout may also display skin ulcers and
abdominal distension.
In both species, the kidney and spleen may be
swollen, with petechial hemorrhage on the
viscera.

Koi Herpesvirus Disease


( KHVD ; Carp Nephritis and Gill Necrosis Virus [
CNGV ])
It has caused major losses in koi and mass
mortalities in common carp

History
Acute morbidity/mortality
Physical Examination
Pale, swollen, mottled gills;
abnormal coloration, skin
lesions, enophthalmos,
dyspnea, erratic swimming
Treatment
Disinfect and quarantine

Notifiable to
OIE

First identified in 1998 in


Israel and the United States ,
it has subsequently been
reported in an ever greater
number of countries in Asia
(Japan, China, Indonesia,
Taiwan, probably Malaysia)
and Europe (United Kingdom,
Belgium, Denmark, the
Netherlands, Germany, Italy,
Austria, Switzerland,
Luxembourg, and France), in
some Eastern European
countries (Poland and the

Typical lesions of koi


herpesvirus (KHV). Arrows
indicate skin lesions
presenting as blanched,
circular to diffuse
areas, characteristically seen
during acute episodes of KHV
disease.
Clinical Signs/Pathology

Affected populations can exhibit up to


100% mortality

Temperature is the single most


important determinant of
pathogenicity. Outbreaks are
most severe and fish are most
susceptible at 18 28 C;
disease does not develop at <
13 C or > 30 C

Pale, swollen, mottled gills is


the most common gross
sign. Gill damage probably
signifi cantly contributes to
morbidity.
Other characteristic signs
include abnormal coloration,
skin lesions , enophthalmos
and dyspnea (increased
respiratory rate).

EPa - epitelioma papulosum (carp pox, fish


Carp pox
pox)
Carp pox lesions on common

( Herpesvirus
cyprinid disease, carp
epithelioma, Cyprinid
herpesvirus 1)
Hosts: common carp,
crucian carp, barbel,
bream, golden ide, rudd,
smelt, carp goldfi sh,
aquarium fi sh
Geo. range: Europe;
Asia; Russia; Great
Lakes, United
States; Israel,
History:
to Chronic
Smooth to rough, milky white to grey plaques up
to 2 Acute
mm thick;
may
cause scarring, retard growth, lead to skeletal deformities; hyperplastic
epithelium (may be papillomatous); lesions eventually slough but can
last for months; lesions may become dark pigmented, reducing value;
lesions develop in low temperatures (winter/spring) and regress with high
temperature (summer) but latent infection remains; transmission
probably from wounds; acute disease in young fi sh; experimentally
virulent to carp fry;
Dif.diagn. : koi herpesvirus
carp.

FRD - pike fry rhabdovirus disease


Pike fry rhabdovirus disease (hydrocephalus, red disease of
pike, grass carp

rhabdovirus)
Hosts: Northern pike, brown trout, grass carp, white bream,
gudgeon, tench
History: Subacute to Acute
Geographic range: Europe
Diagnostic features: Spontaneous disease only in young pike;
two syndromes: (a) swelling on skull (hydrocephalus) or
(b) hemorrhagic mass between pelvic fins and
hemorrhage on flanks; hemorrhagic necrosis of viscera

LC - lymphocystis (LD - lymphocystis


disease)

Lymphocystis is a viral disease characterized by multiple creamy-white


nodules on the skin and fins. It is probably the most common viral
disease of ornamental fish. Caused by an iridovirus, the disease has
been identified in over 100 species of fish. The disease is most
common in recently purchased/shipped fish, and is more prevalent in
brackish and marine species, as well as some New World cichlids.
Lymphocystitis is contagious from one fish to another, but all exposed
fish are not affected by the disease. Viral particles can survive for at
least several days in the water and sub-clinical carriers likely exist.
The viral particles cause a marked enlargement of the dermal
connective tissue cells resulting in cells up to one thousand times their
normal size.

Symptoms
Affected fish have multiple raised
epithelial (skin surface) nodules
1-2 mm in diameter ranging from
pure white to pink in color. These
nodules may be singular but
more commonly appear in
granular clusters of several dozen
or more. Affected fish usually
behave normally and mortality
(death) is usually low or nonexistent. The lesions are usually
restricted to opercula (gill plates),
skin, and fins and are rarely
found on the surfaces of internal
Diagnosis
organs.
A biopsy sample is examined using a standard laboratory microscope and
"grape-like" clusters of hypertrophied fibroblasts (enlarged connective
tissue cells) are seen in positive cases. Frequently, these cell clusters
appear light orange or yellow in color.
Since the disease is usually self-limiting, the prognosis tends to be good.
Severely infected individuals may succumb if the lesions are large enough
to interfere with eating or respiration. In such severe cases, they may

II. Bacterial fish diseases

Bacteria offi
shes
Gram-positive bacteria
MYCOBACTERIACEAE

Gram-negative bacteria
FLAVOBACTERIACEAE
Flavobacterium spp.
Flexibacter spp.

ENTEROBACTERIACEAE
VIBRIONACEAE
Vibrio spp.
Aeromonas spp.

PSEUDOMONACEAE

Chlamydia

Myxobacterial infection
order: Myxobacterales
genus: Flexibacter
Flexibacter columnaris
Columnaris disease world-wide
host: many species of fish
by water temperatures 15-20 oC
clinical and pat-anatomical changes: Skin lesion, usually on the head, back, gill
operculum and fins, haemorrhagic ulcers, necrotic lesions, destroyed fins
Treatment: antibiotic treatment is difficult affected fish rarely consume food,
improvement of water quality
oxygen, organic addition, temperature
Flexibacter psychrophila
Cold water disease
water temperature: below 12 oC (4-12 oC)
rainbow trout, salmonids
mortality 50 %
clinical and pat-anatomical changes: fin and tail lesions, necrotic lesions,
completely eroded tail
treatment: difficult

Aeromonas hydrophila
important cause of diseases of pond-cultured and wild freshwater fishes
CE Carp Erythrodermatitis
water temperature: over 18 oC
clinical and pat-anatomical changes:
dark colour, red irregular haemorrhages on the skin and fish,
ascites, ulcers and necrotic lesions, swollen spleen
treatment: antibiotics, sulphonamides, improvement of environmental
conditions
Aeromonas salmonicida
Furunculosis of salmonids
water temperature: 15-20 oC
clinical and pat-anatomical changes:
anorexia, gathering at pond outlets, ataxia, haemorrhages at bases of fins
and in the gills, hyperaemia in hypodermis, inflamation in dermis, furuncles
on the back or sides of the body, catharal enteritis
treatment: antibiotics, sulphonamides, improvement of water conditions

Family: ENTEROBACTERIACEAE
Edwardsiella ictaluri
Acute septicaemia disease of channel catfish fingerlings
water temperature: 20-30 oC
clinical and pat-anatomical changes:
Nerve signs, haemorrhagic lesions or ulcerations of the cranium,
exophthalmus, pale gill, ascites
treatment: oxytetracycline difficult, vaccination
Edwardsiella tarda
pathogen of catfish (USA), eells (Japan) and tilapia
clinical and pat-anatomical changes:
small cutaneous lesions extending down into the muscles, fibrinous
peritonitis, necrosis in the kidney and liver, ascites
treatment: sulphonamide, tetracycline, water quality improvement

Yersinia ruckeri
ERM enteric red mouth disease
host: younger rainbow trout, salmonids
water temperature: over 10 oC
clinical and pat-anatomical changes:
red mouth ulceration and haemorrhages in oral area, dark
colour, petechial haemorrhages in over abdominal organs,
swelling of the kidney and spleen
treatment: antibiotics, vaccination

The Vaccination against ERM


Bath for small fishes

Oral vaccination - pellets

Imunomodulation
- increase of the natural resistance of organism
- non-specific

CORYNEFORM GROUP
Renibacterium salmoninarum
BKD bacterial kidney disease
salmonids
water temperature: 13-18 oC, chronic disease
low levels of mortality
clinical and pat-anatomical changes:
Dark colour, exophthalmus, small haemorrhages at the bases
of the pectoral fins, whitish nodular lesions in the kidney with
red hyperaemic ring
treatment: not very effective

Family: MYCOBACTERIACEAE
Mycobacterium marinum
pathological agents for tropical marine and freshwater
fish chronic disease
clinical and pat-anatomical changes:
kachexia, dark colour, swelling of the abdomen, skin
lesions, exophthalmus, swimming disorder, eroded fins,
miliary tubercules in liver, spleen, kidney and other
organs
treatment: unknown
Mycobacterium fortuitium
pathological agents wide spread in tropical aquaria
infections are similar to M. marinum
treatment: unknown

Tuberculosis of fish contagious disease


transmitted
from sick ornamental fishes to human
Before treatment ...

... After treatment

II. Mykotic diseases diseases caused by fung

SAPROLEGNIA PARASITICA
saprolegniasis
surface fungal infection (skin, gill, fins) and fish
eggs
secondary pathogen after handling, netting and
traumatic, chemical, parasitical damage of the skin
clinical and pat-anatomical changes:
grey white patches on the skin, cotton-wool like
appearancehyphal filaments extend in to the water,
later stages-fungal patches are dark grey or brown,
growing is often circular
treatment: malachyte green, copper sulfate,
potassium permanganate, salt, formaline

BRANCHIOMYCES sp.
Branchiomyces sanquinis, Branchiomyces demigrans
branchiomycosis fungal disease of gill of freshwater fishes
mainly Cyprinids
mortality about 50 %
localisation blood vessels of the gill
clinical and pat-anatomical changes:
Gills rot areas of necrotic tissue necrotic gangrenous branchitis,
thrombosis of vessels by fungal hyphae, suffocation.
treatment: unknown

H istopathology ofgillrot
Circulatory disturbances
Hemorrhagic

inflamation
Deep necrosis
Incomplete
regeneration
Fusion of gill lamellae

ICHTHYOPHONUS HOFERI (syn. Ichthyosporidium hoferi)


ichthyophonosis
systemic granulomatosis in freshwater and marine fish of many
species
clinical and pat-anatomical changes:
anorhectic fishes, swimming disorder, skin lesions, exophthalmus,
ascites, desintegration of fins, white nodules (similar to the TBC) in all
organs, esspecially in heart, liver and spleen
treatment: unknown strict hygiene and optimal environmental
condition
Temperature
Dissolved oxygen
Total ammonianitrogen, NH3, NO-2
Alkalinity
Hardness
pH
Carbon dioxide

UDN - ULCERATIVE DERMAL NECROSIS


host: salmonids only adult fish
causative agents: unknown
water temperature: below 10 oC
clinical and pat-anatomical changes:
Grey erosions symmetrically placed on the skin mainly on the
head, adipose fin and gill operculum, lesions are often invaded by
fungi (Saprolegnia sp.), later ulceration of skin
treatment: unknown

THANK YOU FOR


YOUR ATTENTION

También podría gustarte