Documentos de Académico
Documentos de Profesional
Documentos de Cultura
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
Susceptible
Host
Virulent
Pathogen
Clinical Signs
spiralling or swimming abnormally
convulsions
just before death at surface with tail down
fin base hemorrhage
internal also
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
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.
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
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.
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
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.
Notifiable to OIE
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.
exoftalm us
Exoftalm us
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
(91/67/EEC)
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.
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
Mortality is
generally
low but can
be up to
100%.
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,
Iridoviral Diseases
Notifiable to
OIE
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.
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
( 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.
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
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
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
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
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