A Pruetieul Guid,e

tor the Fresh Water

Fish Farmer

This guide was originally producedfor fish farmers in North West Germanyby the STATE FISH EPIDEMICS
CONTROL SERVICE of LOWER SAXONY and Fish Health Serviceand,as such,appearedrnl99l.
It originated as a developmentof a seriesof very simple informative leaflets on main fish diseasesfor pond
farrners published at irreguiar intervals in the (atthat time West-German)monthly periodical "Fisherman and
Pond Farmer" in the late seventies/ enly eighties.The 1991booklet gained an unexpectedacceptanceand
more than 4,000 copies were distributed in Germany,Austria and in the Germanspeakingcantonsof
Switzerland. The original German version is now out of print.
The EAFP would like to acknowledgethe support of the EuropeanCommission,FAR prograrnmewhich has
made the productionof this English versionpossible.

w88&r srt{twx,,xts IX}?

A Pruetieul

Guid,e tor the Fresh Water Fish Farmer

Publishedby the EuropeanAssociationof Fish Pathologists

as a Supplementto Bulletin of The EuropeanAssociationof Fish Pathologists15(4),1995
ISSN : 1024-9494
I S BN : 0 9 5 2 6 2 4 2 0 6
H.-J. Schlotfeld
and
D. J. Alderman
with
F. Baudin-Laurencin
E. M. Bemoth
D. W. Bruno
W. Daelman

E. Lorenzen
K. Thorud

STATE FISH EPIDEMICS CONTROL SERVICE OF LOWER SAXONY

and Fish Health Service,EintrachwegI7,D- 30173Hannover,FRG
MAFF, Fish DiseasesLaboratory,Weymouth,UK

CNEVA - LPAA, PIouzanl, France

CSIRO-AAHL" Geelong.Australia
SOAFD Marine Laboratory,Aberdeen,UK
DG VI, Commissionof the EuropeanCommunity,Brussels,Belgium
STATE FISH EPIDEMICS CONTROL SERVICE of LOWER SAXONY,
and Fish Health Service,Eintrachwegl7,D- 30113Hannover,FRG
Danish Veterinary Laboratory,Arhus, Denmark
Central Veterinary Laboratory,Oslo, Norway

Kett to front cover illustrations

Furunculosis - a classic furuncle

Acanthocephalanproboscis
ED - Cary Erythrodermatitus,white rimmed lesion
SVC - Spring Viraemia of Carp - haemorrhagesin muscle
ERM - Enteric redmouth disease,Yersiniaruckeri
VHS - haemorrhagesin muscle
Gas bubble disease- small bubblesin gill tissue
VHS - exophthalmos- pop eye
Fresh water fish farm in central Europe with hatchery earth ponds and fishing pond.

The Europea,ro Assoeia,teorl- ot

Fish Pathol,ogists

WHAT
SIil.OUM
I DO?

-*11
.^ fl)
[''i
{::

r'*'
'4-'

#' flflJ
<r

')1

1)

"-

ili L:.;

,fi lri
rti (fi ':L
):; {l)
*.,
'"f! $r- (:tl

s"T .(

,^ f ;::,o

lf

tl."

,; ffi il"Lt
{l :i l
. *: . * "
(-l *" ;;

*ifl(.u
"-1 {'j'}
-li
,J,

"-.i'
f'

t lj

i- -

A P.ro,eti,eaUGuid,e
for the Fresh Wuter
Fish Farmer

frl ,3" ffi

i{l 1:;, rs
I":r

0l "i:i:
i:Ji\ lrit

l. ;

'i - -

ih
tuli
*ii
(i)
ftn
q"

;:

tr": tll
*i -{
l;J *
fri fil
*: fl:l
ill 13r

Iil

s:: t...n.J,"i",
!-

t*J,.]

.)il
qf"
.,

fiJ

*:r

rt!
J:l:
l::
(,il

r,r"

r.J

. j: :

Y1

.[']
trr Lt-

fl!

,!" ,-

"-r'

il)

By H.-J. Schlotfeldtand D. J. Alderman

with
F. Baudin-Lantrencin
E. M. Bernoth
D. W. Bruno
W. Daelman

l:h
'il!

{/}

r-

Hi"s:l ffi
(,1,t
:*:

i\
LJ

g:
II

lfil

s'
""{_'

l*
I

E. Lorenzen
K. Thorud

Contents
Section
1
z

3
5
6
1
8
9
10
11
12
I3
I4
15
16
t7
18
I9
20
2l
22
z3

24
25
26
2l
28
29
30
31
32
.4
JJ

34
35
36
)t

38
39
40

4r
42
43
44
45
46
41
48
49
50

Page

Titte
Introduction
Some General Points
Treatments
General hygiene
Recommendationsfor submissionof samples
The Gill
Gas Bubble Disease
Viral Haemorrhagic Septicaemia(VHS)
Infectious HaematopoieticNecrosis (IHN)
Infectious PancreaticNecrosis OPN)
Spring Viraemia of Carp (SVC)
SleepingDisease(SD)
Enteric Redmouth Disease- ERM
Furunculosis
Erythrodermatitus - ED
Motile Aeromonas Septicaemia- MAS
Bacterial Kidney Disease- BKD
Rainbow Trout Fry Syndrome (RIFS)
/ Cold Water Disease(CWD)
Edwardsiella Septicaemia
Enteric Septicaemiaof Catfish (ESC)
Saprolegnia
Branchiomycosis
Crayfish Plague
Major ecto and endo- parasil.es:
Costia
Hexamita
Ichthyophthirlzs - White spot
Chilodonella
Trichodina
Glossatella / Apiosoma
Proliferative Kidney Disease(PKD)
Whirling Disease(WD)
Dactylogyrus
Gyrodactylus
Eye Fluke
Anguillicosis
Tape Worms
Acanthocephalans
Fish Louse - Argulus
Ergqsilus
Piscicola- Leeches
Warm Water Recirculation Systems
Koi and other cold water ornamentalfish
Disinfection in Aquaculture
Water Quality Parameters
Heavy Metals and Pesticides
Use of VeterinaryMedicines
Glossary of Terms
Disease Control at EC Level
Fish Health Laboratoriesin Europe

F. Baudin-Laurencin

E. M. Bernoth
E.Lorenzen
E. M. Bernoth
E. M. Bernoth

D. J. Alderman

4
4
5
5
7
8
10
11
12
t3
I4
16
T7
18
t9
20
22
ZJ

25
26
26
21
28
28
29
30
3I
az
aa
JJ

34
35
36
37
37
39
39
40
4I
4)

D. Bruno

W. Daelman

This t
tific I
patho
Instea
and t
which
able I
with r
fish d

Fish
mean
anim
afure
their
respo
wate
Patho
much
Asar
plex 1
in cor
t yof r
Oner
envir<
of fis
tions
batio
encei
not cc
batio

+J

SEVEN

47
48
50
51
51
52
53
58

Fishl
quali
mana
mean
reduc
the pr
provi
paran
Figur
ing t
ment

Authors specifically responsible for the contents of an individual Section are listed against that section
in the Contents list above.

Section1
Introduction
This handbook is not written as a scientific publication for professional fish
pathologists or fish parasitologists.
Instead the most important fish diseases
and parasites are described in a way
which we hope will be easily understandable for the layman and provide them
with a guide to help in discussion with
fish diseasespecialists.

Section2
Somegeneral
points to aid
understanding
Fish are cold blooded animals. This
means that, in contrast to warm blooded
animals with their con'stantbody temperature, fish body temperature and thus
their whole metabolism including
responseto infection is dependenton the
water temperature.
Pathogenic'organismscan be transmitted
much more easily through water than air.
As a medium water has much more complex biological and chemical properties
in comparison with air and the availability of oxygen in water is less.
One major effect of thesefacts is that the
environmental temperature dependence
of fish and pathogens means that infections in fish are not subject to fixed incubation times. The environmental influence is too great and incubation times are
not constant. Thus foi example, the incubation time for VHS can range from
sevendays to six months.
Fish health also dependsheavily on water
quality, nutrition and husbandry and
management policies. Better husbandry
means better health conditions and
reduced morlalities. Fish can survive in
the presenceof many different pathogens
provided that the critical environmental
parametersare correct.
Figure 2.L is a classic diagram illustrating the most important relationships
mentionedabove.

a) diseaseis the result of the interaction

between host pathogen and environment.
b) the influence of environment (water
quality) on fish is given by the formula :Disease(D) = Host (H) + Pathogen(P) +
Environment (E).

Fig. 2.1 Relationbetweenhost,pathogen

snd environmentin regardto the
(Sniezko,1971)
occurrenceofjl.sh diseases
Pathogen : The severity in fish of infections with bacteria, viruses, fungi and
parasites is strongly dependent on the
environment. In the case of a viral or
bacterial infection a septicaemicprocess
follows if the immune system breaks
down. The pathogenor its toxins spread
throughout the blood circulation (septicaemia), leading to a range of largely
similar gross signs, frequently including
haemorrhageson the internal organsor in
the musculature, ascites (liquid in the

Fig.2.2

abdomen) and exophthalmos (pop eye)

with haemorrhagesin and around the eye.
Such fish show dark colour, swimming at
the pond margin separatedfrom the rest.
Haemorrhages, mainly on the pectoral
and pelvic fins (Figure 2.2) are a distinct
sign of a septicaemic infectious disease
due to bacteria or viruses.
The number of different bacteria and
viruses which can cause diseaseis surprisingly small. Outbreaks of clinical
disease are often associated with clear
decreasein quality of environment or fish
health.
It is often possible to isolate specific fish
pathogens from apparently healthy fish
without evidenceof any clinical disease.
There are also many oofacultativettfish
pathogenic bacteria and viruses whose
pathogenicity depends directly on environmental quality and which in casesof
decreasing quality can lead to similar
septicaemiasto those causedby specific
fish pathogenic agents.
Therefore the identification of the
pathogenis important. Such diagnoses
are normally only possible in adequately
equippedfish healthlaboratories.
Tests for the presence of different
pathogenstake on average:
Virological : One to two days for
immunofluorescence,ELISA (Enzyme
Linked ImmunoadsorbentAssay) or PCR
(Polymerase Chain Reaction) methods.
If thesemethods are not possible,up to
2I daysusing cell culture methods which
are then essential.
Bacteriology and antibiotic sensitivity
tests : five to ten days. In exceptional

which are permissible in different countries varies considerably. For this reason,
although the treatments recommended
represent best available information,
their recommendation here does not
mean that they may be used legally in the
readers own country or even in anY
European country, EuropeanUnion (EU)
member state or otherwise.
It must be rememberedthat all treatments
to control or prevent disease are treatments with veterinary medicines, strictly
even including a treatment employing
common salt. Some suchtreatmentproducts are legally only available under veterinary prescription, others are readily
obtainable over the counter in pharmacies and from laboratory chemical suppliers. Which treatment belongs to each
group will vary between countries and
will changewith time.
Within the European Union the range of
these variations between Member States
are slowly being reduced, both by
increased uniformity in the licensing of
veterinary medicinesfor aquaculturaluse
and as a result of moves towards controls
of residues of veterinary medicines in
fish meat. In particular there is the effect
of Regulation 2311/90 which requires
that no veterinary medicine may be
licensed for use in a food animal species
in the EU unless a Maximum Residue
Level (MRL) has been set for the species
and tissuesconcerned. For all new molecules this has applied since the lst
January 1992 and existing licenses will
have to be withdrawn if no MRL has
been set by 3lst December1996. This,
together with new more centralised procedures for the licensing of veterinary
medicines, means that more uniform
standards will exist across Europe in
regard to which treatments may legally
be used for fish. When residue monitoring is introduced a more level playing
field may be expected in that countries
exporting fish to the EU will have to
demonstratethat programmesto monitor
and control residues exist which will
enable compliance with the MRL
Regulation.
In addition to constraintson the availability of treatments,in many casesadditional limits apply on the ability to release
In each section of this book, up to date water containing the treatment chemicals
after use. Such constraintsmay vary not
information on the most effective methods for the treatment or prevention of the just between countries but also between
areaswithin countries. Such local variadiseasedescribedis given. However, this
tions will often depend on the potential
book is intended to cover the whole of
Europe, and the range of treatments for environmental damage.

casessuch as BKD up to ten weeks may

be necessary. If using immunofluorescence or ELISA methods, identification
can be made in two to three hours, but
this is without carryingout very important antibiotic sensitivity tests, which
take an additional two to ten days once
the organismhas been cultured. The bacteria first have to be grown in culture
before the testing of the different active
substances(antibiotics) can take place.
NOTE : It is essentialthat only untreated fish are tested becauseof the risk of
missing the true pathogen. The best
approachis to immediately separate10 to
15 fish for examination.
Histological examinations usually take
three to five days.
Water analyseswill take one or two days
- 5 days if tests like BOD5 (Biological
Oxygen Demand) are required.
The fish organ which is most exposedto
the environment is the gill. Its most sensitive structure (a single cell layer - the
respiratory epithelium) is in direct contact with the aquatic environment which
contains all kinds of possible pollutants
without the sort of protection as seen in
air breathing animals. It is as if human
lungs were hanging on the outside of the
neck exposing all' functioning pafis epithelium, lung alveoli etc. - directly to
the air with all its polluting parlicles.
Therefore the gill can be described as a
otmirror of fish health".
A clinical examination of the gill can
therefore be very valuable, especially in
cases of suspectedwater pollution. Fish
must therefore arrive alive and untreated
before examination becauseautolysis of
the gill and other organs begins within
15-30 minutes of death, resulting in
changes which make a good diagnosis
impossible.
Even at five minutes post rnortem the
very sensitive gill epithelium may have
become unsuitable for detailed examination.

Section3
Treatments

To reiterate. therefore. the recommendation of a treatment in this book does not

mean that you can obtain it or use it if
you do.

Section4
GeneralHygiene
Fish diseasescan be spreadseveralways.
Diseasesare often introduced by the inlet
water, which is unavoidable, but mostly
diseasesare transmitted or introduced by
purchased eggs and fish, by birds and
their faeces,by customersor visitors, by
transportvehicles and farm equipment or
even by a farm's own employees.
Therefore following hygiene rules should
be seenas the minimum.
Eggs should be purchasedonly from disease free farms. They should be disinfected routinely on ar:rival.
Fish : where purchaseof fish is unavoidable, they should ifpossible be purchased
from the samesourcesas the eggs. If this
is not possible the fish should be kept in
quarantinefor at least 2 weeks, separated
from the farm stock and using separate
equipment.
Visitors and customers: because many
of these work with fish themselves they
are possible transmitters of disease. If
they have to come on the farm, then they
should only do so after adequatedisinfection.
Employees: also representa diseasehazard, mainly after making deliveries to
other farms. Hands and boots at least
should be disinfected.
Transport vehicles: must be disinfected
before being driven onto the farm. Keep
cars and visitors vehicles off the farm.
Equipment: should be kept separate(for
each pond if possible) and be disinfected
after each use, if this is not possible at
leastonce a week.
Ponds / basins: clean and disinfect
before using if the nature of the pond permits.
Moving fish from time to time is necessary to grade them, but the different fish
populations/groupsshould not be mixed
up. If one group shows signs of disease
(often observed during grading) this
group should be kept in individual ponds
and not be spreadall over the farm.
Dead fish should be removed dailY.

Loss
nurn
quat
Nett
long
Wes
lega
t ob
inve
yeaf
surv
tant
miss
cour
infec
bvb
tem.

Fish
prof
that
can

AI9 I

take
fam
eas
still
Dea
bec
stan
cau
imp
mor
to br
pern
beg
mak
the r
teric
don
Not,
som
The
mal
bac
resi
test
fish
Whr
fish
ilv,

Losses must be recorded. Increasing

numbers of dead fish are a sign of inadequate conditions or disease.
Netting over the farm. The results of
long experience in Denmark and North
West Germany (where netting is now a
legal requirement) makes this an action
to be strongly recommended. The
investment will be repaid in two or three
years by the fact that more fingerlings
survive (no predator birds). Most important is reduced hazard of disease transmission. The converse view may of
course be taken, that more lethargic
infected fish which would be eliminated
by bird predators, will remain in the system.

Section 5
Recommendations
for submission of
samples
Fish mortalities are best examined by a
professionalfish diseaseexperton site so
that a full range of iippropriate samples
can be taken. In the event that samples
are submitted to a laboratory rather than
taken by the laboratory expert on the
farm, then for proper diagnosis of diseasedfish, it is essential that diseasedbut
still living fish are received.
Dead fish are useless for diagnosis
becausebreakdown (autolysis) of tissues
starts within 15-30 minutes of death,
causing changes which make diagnosis
impossible. Indeed at five minutes post
mortem the gills are already too damaged
to be examined properly, the gut becomes
permeable and large numbers of bacteria
begin to spreadinside the fish. This can
make it impossible to isolate into culture
the real pathogen so fhat an adequatebacteriological examination cannot then be
done.
Note: Whilst the gill colour is still red
some useable results may be obtained.
The process of freezing and thawing
makes fish unusable for histology and
bacteriology. Only some virological and
residues (pesticides, heavy metals etc.)
tests can be made on dead and/or frozen
fish samples.
When fish mortalities occur in rivers, live
fish samplescannot be obtained very easily, but since tests for residues are possi-

ble using deadfish, reasonablyfresh dead

should be kept as cool as possible before
freezing and frozen as quickly as possible
after collection.
Transporl of small fish can be simple,
using water/air (or preferably oxygen)
filled plastic bags (heavy gradefood bags
may be suitable). In this way even small
numbers of small salmonids can survive
quite long distancetransport. Inevitably,
with diseasedfish in particular, transport
creates additional stress.The bigger the
fish the fewer can be put in each bag.
Bags should be filled one third with
water and if possible two thirds pure
oxygen. Alternately, a battery operated
portable pump may be used, either from
the vehicle battery or from a separatebattery. For short distancesan air filled bag
may be adequateespecially for cyprinids.
In summer ice or ice packs should always
be used and are always advisable when
bags are carried inside vehicles.
If fish must be sent by commercial carriers, then contact the carrier in advance,
make sure that the carier is prepared to
accept live animals and provide good
external packaging around the bags - a
tough cardboard outer box with polystyrene bead or solid inside around the
bag to stop movement. Even better is a
commercial or a picnic cool box.
Labels should be applied with an indelible marker to the bags and duplicated
insidethe box. Agreedeliverytime with
the carrier and make certain that there
will be someoneto receive the fish when
they are delivered.
Water sampling
In the UK, water samples are normally
best left to be collected by the local officers of the National Rivers Authority or
River Purification Board (in Scotland).
In France regular samplings are made by
the Agences de leau (Water agencies)
every month for chemical and bacterial
parameters.
In Gerrnany suitability of fish-holding
water is controlled by Fish Health
Servicesand/or environmentalprotection
departmentsof police. In emergencyor if
independentsamplesare needed,the following proceduresshould be followed.
Water samples should have a volume of
between 750 ml to a litre in clean bottles
rinsed several times with sample water
before the final fill. If very well washed,
plastic soft drink bottles are suitable
The following points should be noted:
- keep the bottle about 10 cm below the

surface,avoiding air bubbles

-do not let solids (plants, sediment, etc.)
get into the bottle with the water sample
- close the bottle whilst the rim is still
below the water surfaceand send as soon
as possible, meanwhile keep cool at a
Pack
temperature of about 4"C.
describedas for fish
- record sampling time, water temperature and date
- bottles must be fully labelled using
waterproof marker.
Pond water should be sampled as inflow
water and outflow water separately,for
ponds without flow through one sample
is enough.
In casesof suspicion of water pollution
(fish dying in rivers) at least three samples of 3-10 litre each should be taken
and fish samples should also be taken.
Names and statementsof any witnesses
as well as samplesof the possible contaminating substancecan also be very valuable.
Additional water samples should be
taken from:
a) suspectdischarges
b) contaminated water from river or
stream
c) uncontaminated water from river
upstreamof the suspectdischarge.
Immediate collection and dispatch of
samples is critical.

Section6
The Gill : Gill
inflammation
1. Cause : gill ir:ritation caused by
poor water quality (often: relating to
excessively high stocking densities) or
incorrect use of chemotherapeutantsfor
ectoparasitetreatment (immersion bath)
followed by (secondary)bacterial growth
on the gill surface. This results in excess
mucus production (which can be an
excellent culture medium for ubiquitous
water bacteria) and encouragesparasites
(mainly ciliates, flagellates or monogeans).
The gilt reacts quickly to changesin the
water environment because of its direct
exposure to the water. Therefore, in a
way, the gill can be regarded as a ttmirror of fish health". Gill inflammation

4.
Clinical signs: fish swim at the surface of the water near the inlet (where the
water will contain more oxygen), showing respiratory problems (gasping), and
are easily startled. Gill operculae are
held open (Figure 6.3). Animals loose
appetite and acceptlittle or no food.
5. Mortality: can range from individual fish to total loss.
6. Diagnosis: gill inflammation can be
seen with the naked eye, developing
through a progression of stages : gill
operculaeare open.excessmucusis produced, gills are pale, telangiectasia
(exploded secondary lamellae), visible
bleeding and blood clots (Figure 6.4).It
is very important to recognisegill inflammation at an early stage,by microscopical examination (at low magnification).
A gill arch should be dissectedcarefully
and examined under the microscope.
Particularly in salmonidsthe primary and
secondarylamellaeshouldbe visible separately (giving a pine tree like structure),
cyprinid gills have a more "bushy" structure.
With severegill inflammation, secondary
lamellae "melt" together leaving club
shapedprimary lamellae (Figure 6.5).

Fi g .6. 1

7. Prevention: improve envlronmental conditions by improving water quality. Increasewater flow rate, prevent accumulation of waste food and of faeces.
8.
What should I do? : find and
remove the primary causeof gill damage
by optimising the fish environment and
check for gill parasites. If parasites are
the problem then a medicated immersion
bath treatment may be tried. Many such
treatments actually work by producing
more initation with resultant mucus production which sloughsoff parasites. The
gill damageproduced by treatmentswith
compounds such as quaternary ammonium compounds can be worse than the
original problem. Good results have been
achieved wrth Chloramlne-Z (immersion
bath treatment) with an intial concentration of 5glm3. A one hour bath, treatment
which may be repeatedup to four times at
intervals of one day. As is the case with
almost all drugs used in bath treatmentsthe effective dosage regime depends
upon the local water chemistry. Thus, the
effective dose of Chloramine-T can be
four or more time the initial 5glm3. Start
with 5glm: - if fish do not show any reaction the concentrationis too low. Increase
with great care until fish show clear evi-

Fig.6.2

increases difficulties with exchange of

gas and electrolytes and so produces an
adverse effect on the health and the
immune status of the fish. Almost 957o
of nitrogen produced by the fish (NHa,
etc.) is excretedthrough the gills.
If gill inflammation remains untreated
and environmental eondiiions continue to
be unfavourable, the inflammation can
develop into necrosis when the gill structure is destroyed and only "naked" primary lamellae remain (Figure 6.1).
White spots of deadtissue are seenwhich
later turn black (necrosis,Figure 6.2).

Fig.6.3

denc
of b;
mor(
cent
chlo
ever
dure
priat
istry
The
desc
Saln
less
Bath
salt r

Gas
prob
whic
This
bubh
in th
bubb
sign
appe
sign
arch
bloo
seen
bubb
the e
swe
Note
the
prob
time
sels,
incre
even
taker

2. Susceptiblefish species:all species

and age groups are susceptible to poor
water conditions.
3. Temperature at outbreak:
water temperatufes.

all
Fig.6.4

Fig. 6.5

Fig.

dence of unrest and even try to jump out

shouldnot last
ofbasin. This restlessness
more than 30 seconds,otherwise the concentration is too high and a danger of
chlorine-burning of the gills arises.Thus
every farmer must carry out this procedure at least once to determine the appropriate dosage for his local water chemistry. Thus test baths are unavoidable.
The fish behaviour with Chloramine-T
described here refers essentially to
Salmonids.Other fish (e.g. eels) show a
lesserreaction.
Baths with formalin and with common
salt may also be effective.

Section7
Gasbubbtedisease
Gas bubble disease can be a significant
problem for fish farmers and is often one
which is not recognised immediately.
This is becausethe clinical signs (small
bubbles in the head area) are only present
in the acute stage of disease, when the
bubbles can be up to pea size. The first
sign is of apathetic fish showing reduced
appetite without any other clear disease
signs. Very small bubbles on the gill
arches (Figure 7.1) and gas emboli in
blood vessels(Figure 7.2) can only be
seenunder'a microscope.In chronic gas
bubble disease bubbles can be found in
the eyes (Figure 7"3), which can lead to
swelling and blindness(Figure 7.4).
Note: When.gas bubbles are visible to
the naked eye, this indicates that the
problem has already existed for some
time. Damage to tissuesand blood vessels will have already occurredleading to
increased risks of secondary infections
even after corrective measureshave been
ta ke n . I n t he ac ut es t a g e e. x tre mes i g n s

Fi g .7 .3

F i g .7 .l

Fig.7.2
of gas bubbles can occur in the head and
fin regions (Figure 7.5 and 7.6), which
must be very distressingto the fish.
Gas bubble diseaseis causedbv a super-

Bavarian FisheriesService,Grub

Fig.7.4

saturation of the water by gases. Its

occurence is often associatedwith water
drawn from boreholes. Fish can tolerate
oxygen saturation up to 300Vo.

Bavarian FisheriesService,Grub

Fi g .7 . 5
Supersaturationby nitrogen however can
rapidly lead to severeproblems and starl
as low as I03-I04% supersaturation.
Nitrogen (N2) is therefore the main cause
of gas bubble disease. Carbon dioxide
(CO2) and some rare gases (argon) are
less important. Experience shows that
fish do not avoid areasof supersaturation
in natural water systems.
What should I do? If possible,check to
confirm that the water is supersaturated.
The saturation levels of nitrogen are the
most important.
This cannot be done with a standardoxygen meter which only indicates oxygen
saturation levels. A meter designed to
measuresupersaturalion
by any gas can
be used instead. An example of such
meters is the Tensionometer 300C produced by Novatech Designs of Victoria,
B.C., Canada,to measuretotal gas pressure.
A safe gas equilibrium can be restoredby
use of a de-aeration cascade system
which by freaking up the water equili-

bratesit with air. Where water is derived

from deepboreholessupersaturationmay
be a continuous problem. With such
water sources a properly designed cascade deaeration system will reduce the
supersaturationof the water to acceptable
Ievels. Occasionalsupersaturalion
may
be overcome by intensive stining of the
water or allowing it to stand for about 30
minutes in a "buffer basin" before passing to fish ponds. In practice due to space
limits this latter approach is not always
possible.

Section8
Fish Pathogenic
Viruses :
Viral Haemorrhagic
Septicaemia,VHS

also susceptible. Brown trout are susceptible to some sffains but in practice are
rarely found to be clinically infected.
Also
susceptible are
whitefish
(Coregonus). These speciesare potential
carriers and can therefore represent a
major infectionhazard for rainbow trout.
3.
Temperature at outbreak:
Critical water temperaturesare l-ll'C,
mainly in spring, sometimes in autumn.
Clinical disease is rarely observed
between I4-16'C. No VHS outbreaks
occur above 16oC.
4.
Clinical signs:
stagesare observed:

three main

4.1
The acute stage : External
signs: slight darkening of body colour,
pop eye (exophthalmos),bleeding around
the eyes (Figure 8.1) and on the fin bases
(mainly pectoral and pelvic fins), pale
gills with petechial (pin point) haemorrhages.

1.
Pathogen: Viral haemorrhagic
septicaemiavirus, VHS-virus (VHSV)
VHSV is a rhabdovirus, a member of the
largest group of fish pathogenic viruses,
and is related to the viruses causing
Infectious Haematopoietic Necrosis
(IHN) and Spring Viraemia of Carp
(SVC). In Europe three main subtypesof
VHSV are known.
2.
Susceptible fish species: rainbow trout, grayling and young pike.
Marine fish includine turbot and cod are

Fig.
Fig.8.1
Main internal signs: petechial haemorrhages on surfacesof fatty tissue, intestine, liver, swimbladder and in the muscle
(Figure 8.2, 8.3, 8.4), presenceof ascites
(accumulation of fluid in the abdominal
cavity). The fish are apathetic, separated
from the rest, swimming at pond edges.
High moftalities occur very rapidly.

Fi g .7 . 6

Fig.

4.2
The sub-acute or chronic stage
follows the acute stage; with more
intensedarkening of body colour and pop
eye. The gills turn grey-white, but haemorrhaging of the gills is rarely evident.
Fish are severely anaemic and the resulting palenessis particularly evident in the
abdomen (Figure 8.5). The liver is pale,
with numerous haemorrhages. Fewer
haemorrhages are seen on the other

orga
rotat
aris.

4.3
acco
colo
al th
sign
mali
seen

subt
men
to 5(

6.
cell ,
two
ods

in appropriate laboratories these may

enable confirmation of the presence of
the virus in only a few hours. Culture of
the virus is normally only successful in
the acute stage, identification of VHSV
from "carrier fish" mav not always be
successful.
Tran smi ss i on/outb r e ak:
VHSV can be transmitted by water, from
infected carrier fish which show no clinical signs, predator birds, equipment,
infected (transport) water, eggs or even
by blood sucking parasites. Stresssituations such as overfeeding, movement of
infected fish , high stocking densities,
grading or extreme water temperature
changes can lead to VHS outbreaks in
infected but apparently healthy populations.
The VHS-virus is heat and acid sensitive
- several warm summers in succession
(high water temperatures) might completely eradicate VHS from infected
farms. New outbreaks even in fish from
VHS free farms stocked into big lakes
can result from the survival of the virus in
the deep and therefore cold water layers
of such lakes.

Fig.8.2

Fis. 8.3
organs and in muscle. Fish swim with
rotating movements around the body
axis. Fish mortalities reduce.

Antibody Technique),ELISA or PCR are

under development and where available

4.3
The ttnervoustt final stage is
accompanied by reduced ascites, gill
colour can return to normal and in general the fish show little qr no typical VHS
signs, except that more marked abnormality in swimming behaviour can be
seen.Mortality rate is now low.

l-'' : ',

Mortality: depends on virus

5.
subtype, fish health status and environmental conditions. In the range from 10
to 507o,occasionallyup to 807o.
Diagnosis: is by culture in fish
6.
cell cultures in a laboratory, taking from
two up to twenty one days. Faster methods such as IFAT (Immunofluorescence

Prevention: buy fingerlings

8.
only from VHS free farms. In VHS
endemic zoneswhere no clearancepolicy
is agreed, the practice of buying surviving year classesfrom VHS infected suppliers will select for fish with lower sensitivity in new outbreaks. Disinfect
salmonid eggs using iodophores routinely. If purchasing from abroad insist on a
health cerlificate acceptable to national
veterinary authorities.

Fig.8.4

10
bow trout and salmon species, mainly
Pacific salmon. Coho salmon, brown
trout, pike, coregonids and grayling are
more resistantand may act as carriers

3.

Temperature at outbreak: The

critical temperature is around 10.C in
spring and autumn. Outbreaks are fare
above15'C.

Fig.8.5
9.
What should I do? There is no
treatment for VHS. A reduction of mortality can be achieved by feeding medicated fish feed to control secondarybacterial infections but only after carrying
out bacteriological examination and
antibiotic sensitivity tests.
VHS infected fish should be fattened as
soon as possibleso that the stock can be
slaughteredfor table sale.
Only an immediate identification (laboratory), population control (quarantining)
a n dp r ev ent iv edis jn fe c ti o n
m e a s u recsa n
reduce the spread of VHS. No effective
VHS vaccineyet exists.
10.

Spring Viraemia of Carp (SVC). The

importance of IHN in Canadaand USA is
comparableto that of VHS in Europe.
IHN was introduced into Europe in lg\j
and so far outbreaks have occurred in
France,Italy Germany and Belgium.
2.

Susceptible fish species: rain,

4.
Clinical signs: rainbow trout
and salmon fry show numerous yolk sac
haemorrhages(Figure 9.1), darkening of
the skin, haemorrhageson the abdomen
and in the eye around the pupil (Figure
9.2). Occasionalexophthalmia(pop eyes)
and swollen abdomen (ascites : accumulation of fluid), long white discharges
from the anus (pseudo faeces), bleeding
on the fin base, anaemia of the intemal
organs,petechial (pin prick like) haemorrhages in the visceral fatty tissues and

.1,

VHS is a,Notifiable disease

Ll#':tf,+

Since 1991 this fish virus diseasehas

been on List II of the European Union
9l /61 IEEC "Council Direcriveconcerning animal health conditions governing
the placing on the market of aquaculture
animalsand products".

iffi ;,::;

SO

ob
thr
ril
so
iri,
ob
thr

sp
his

10
rec
mc

old
10
Ge
fisl
we
infr

per
Afl
Eur
los
Aft
dis
ma

6.
lab
Cul
ful
asy
rapi
beir
dete
hou
,7

Section9
Fish Pathogenic
Viruses
Infectious
Haematopoietic
NecrosisVirus, IHN
(of salmonids)

F++;;;
Fis. 9.1

**t**

t.

Pathogen: The IHN Virus

(IHNV), a rhabdovirus of the samegroup
as
the
viruses causing
Viral
Haemorrhagic Septicaemia (VHS) and

wat
cart
inat
infe
bloc
Stre
high
ture
in a1
As r
acid
Fish
time
tion
farm

Fig.9.2

8.
IHN
salm
or e)
IHN

11
sometimes in the muscle can be
observed.The stomach is distended and
the gut is empty of food, instead being
filled with a gelatinous substance.In
someacute caseswith immediate mortalities, these gross signs may not be
observed.The characteristicnecrosis of
the haematopoetic organs (head kidney,
spleen) can only be seen by an
histopathologicalexamination.
Mortality: at a temperature of
5.
l0-12'C maximum mortality occurs in
recentlyhatchedfry after 8-15 days with
mortalitiesup to 80-100Va. In one year
old fish losses normally do not exceed
lj%o.
Generally the highest mortality occurs in
fish weighing less than 1009. Fish,
weighingmore than l00g show a chronic
infectiveprocessand lossesover a longer
periodmay be up to I0-20Vo.
After the introduction of a new virus into
Europe, it is to be expected that initial
losseswill be high, possibly up to 1007o.
After a period of "naturalisation" of the
disease,it is to be hoped that mortalities
m a yb e co m eles ss ev er e.
Diagnosis: by cell culture in the
6.
laboratory, taking fronl 7 to 2l days.
Cultureof the virus can be very successful using roe and milt samples from
asymptomatic carrier, broodstock. More
rapid methods (IFAI, ELISA, PCR) are
being developed which will make the
detectionof IHNV possible in only a few
hours.

9.
What should I do? No treatment of IHN is possible.In infectedpopulations the acute phase can be avoided
by increasing water temperature within
24 hours of a clinical outbreakup to more
than 18"C for 5-7 days,which in practice
is rarely possible.The virus is not killed
and, after returning the water temperature
to normal, new outbreakscan occur.
It is unlikely that a IHN vaccine will be
available in the next few years. Spreadof
IHN can only be restricted by immediate
identification in the laboratory, population control (quarantining, slaughter of
stock) and preventive disinfection measures and of course disinfection of the
farm.
10.
Since 1991 this fish virus diseasehas been in List II of the European
Union 9l/67lEEC "Council Directive
concerning animal health conditions governing the placing on the market of aquaculture animals and products".

Section10
Fish Pathogenic
Viruses: Infectious
PancreaticNecrosis

(rPN)
of Salmonid fry

Tianspission:
through the
water and the gills, from asymptomatic
canier fish, fish predating birds, contaminated and undisinfectedfarm equipment,
infected transport water, eggs and even
blood suckingparasites.
Stresscausedby overfeeding,transport,
high stocking densities,grading temperature changes,etc. may"iqduceoutbreaks
in apparently healthy populations.
As with VHSV. the IHN virus is heat and
acid sensitive.
Fish surviving IHN outbreaks are life
time car:riersof infection. Full disinfection of the farm is in the interest of the
farmer.
Prevention: purchasefish from
8.
IHNV free farms. Routine disinfection of
salmonid eggs with iodophoresin early
or eyed stages.
IHN is a notifiable fish disease

3. Temperature at outbreak: between 6

and 16'C, not a very crucial factor.
Frequency of outbreak: The age
of the fry is critical. For infection the first
to third week after yolk sack absorption
and the starl of feeding is of prime importance. Outbreaks rarely occur after 20
weeks of feeding and fry of that age do
not show any clinical signs but are still a
possiblesourceof infection as asymptomatic virus carriers.
4. Clinical signs: dark colouration,
swelling of the ventral region (as if the
fish swalloweda pea, Figure 10.1 - top:
normal rainbow trout fry, below: diseased
fry). Inflammation - petechial (pin prick
like) haemorrhagesoccur on the pyloric
region (Figure 10.2')as well as occasional bleeding on the intemal organs. The
liveq spleenand kidney are very pale and
bile accumulatesin the gall bladder.Dark
colouration of the lower third of the body
and small swellings on the head can be
observed(Figure 10.3).One of the main
characteristicsis a slack, stretchedintestine free of food and filled with a colourless to yellow milky gelatine like slime.
From the discharging intestine mucoid
"pseudo faeces" can be observed,white
worm like mucus hangs out of the anus.
Infected fry show uncoordinated spiral
torsion swimming behaviour. Some or all
of thesesignsmay be absent.
5. Mortality: fry: 10 to 90Vo.
6. Diagnosis:cell culture(up to 2l days),
immuno fluorescence ELISA or PCR
tests(1-2 days) in the laboratory.

L. Pathogen: the Infectious Pancreatic

Necrosis virus (IPNV). This virus
belongsto the family of Birnaviruses.In
Europe five main IPNV subtypes are
known (IPNV-Sp, Ab, HE (pike), TE
(molluscs)and TV (molluscsand carp).

7. Transmission: from infected adult fish

(vi rus carri ers). i ni ected w ater . bir ds
(minor importance), farm equipment,
blood suckingparasites,infected eggs as
well as sperm (vertical transmission

2. Susceptible fish species: fry and parr

of all salmonids as well as pike fry.
Brook trout fry and rainbow trout fry are
very susceptible.IPNV usually causes
mortality only in fry.
In addition, all cyprinids, coregonids,
adult pike, eel, tilapia, severalmarine fish
species(including Atlantic salmonin sea
cages),some ornamentalfish speciesas
well as molluscs can be asymptomatic
carriers. So far the IPN virus has been
identified in about fifty aquatic animal
species.Eel are suspectedto be an occasional sourceof infection.

Fig. 10.1

tz

warm climates.Unusual in extensive cam

culture.
4. Clinical signs: similar signs to VHS:
separationfrom the shoal, exophthalmia
(pop eyes), swollen abdomen - marked
ascites (fluid in the abdominal cavity),
haemomhageson the skin, gills, abdominal fat tissue, swim bladder, other internal organs and in muscle (petechial pin
point shapedhaemorrhagesin the muscle
tissue) - Figures 11.1, 11.2, 11.3 and

Fig. 10.2

1r.4.
Fis.
5. Mortality: steady mortality, reaching
up to 307odependentupon environmental conditions and generalfish health status. Mortalities less in extensive culture.
6. Diagnosis: by culture in fish tissue
culture or using fluorescencemethods in
the laboratory,2 to 2I days. Some laboratories have developed ELISA methods
for SVC which can give a result in a few
hours.

Fig. 10.3
from the parent stock). Clinical IPN can
'Jump" over a few generations.The time
between infection and the first disease
outbreak can sometimesbe severalyears.
IPNV can survive up to eight months or
longer in water and remain infectious.
8. Prevention: purchaseof eggs, fry and
fish only from IPN free farms. Routine
disinfection measuresare recommended.
Vertical transmission can render external
disinfection of the eggs useless. Recent
experiments tend to show that use of
iodophores. as disinfectants for IPN is
only effective if feftilisation is caried out
in the presenceof iodophores.
9. What should I do? IPN is a virus diseasefor which there is no treatment.
Note: fish which survive IPN infection
may be expected to be carriers for their
whole life time - ahd remain a possible
source of further infection.
No field practicable vaccine likely to
become available in the foreseeable
future.
Only immediate identification (laboratory), population control (quarantining)
andpreventivedisinfectionmeasures
can
reduce the spreadof IPN.
10. Since 1991 this fish virus disease
has been on List III (voluntary control for
the time being) of the European Union
91/61IEF,C Council Directive conceming

animal health conditions governing the

placing on the market of aquacultureanimals and products.

Section11
Fish Pathogenic
liruses : Spring
liraemia of Carp

(svc)
1. Pathogen: Rhabdovirus carpio. This
virus is closely related to the viruses
causing the salmonid diseases Viral
Haemonhagic Septicaemia (VHS) and
Infectious Haematopoietic Necrosis

(rHN).
2. Susceptible fish species: carp (especially one and two summer carp), silver
carp, crucian carp and catfish. Grasscarp,
pike and guppy have also proved susceptible under experimental conditions.
3. Temperature at outbreak: in the
spring at water temperaturesbelow 15oC,
rarely above. No outbreaksat water temperatures above 20oC. For this reason
SVC is not reported from countries with

7. Transmission: can be by water

through the gills from clinically infected
fish or from asymptomatic virus carrier
fish, from contaminatedfarm equipment,
infected transpofi water and undisinfected eggs. Blood sucking parasites like
Argulus or Piscicola can also transmit the
virus from carp to carp. Stresssituations
(temperaturechanges,transport, grading,
high stocking density) can trigger clinical
outbreaks in apparently healthy populations.
8. Prevention: purchase fish only from
SVC free farms.
9. What should I do? no treatment possible. A reduction of morlality can be
achieved by feeding medicated feed to
control secondary bacterial infections,
but only after carrying out a bacteriological examination and antibiotic sensitivity tests. Infected stocks must not be
sold for stocking or breeding purposes.
Only immediate identification (laboratory), population control (quarantining)
and preventivedisinfectionmeasurescan
reducethe spreadof SVC.
Vaccine: In some (non EU) countries
some protection against SVC has been
achieved by using a SVC live vaccine
preparation.A live vaccineis a vaccine in
which the pathogenicity of the live virus
pathogenhas been reduced.

.R
Fig'

10.s

been
time
9U61
ing a
the p
anim
SVC
in th
carrie
scrib
9U6i
to the
into
Com
94t8(

Fig.

tL)

Fig. 11.1

Fig. 11.2

Fig. 11.3

Fig. 11.4

10. Since 1991 this fish virus diseasehas

been on List III (voluntary control for the
time being) of the European Union
9ll6llEEC
Councii Directive concerning animal health conditions governing
the placing on the market of aquaculture
animals and products.
SVC is controlled as a Notifiable disease
in the UK. A programme of control is
caried out by. the UK authorities as prescribed in the EU Council Directive
91161 and special safeguardsin relation
to the import of SVC susceptiblespecies
into the UK are defined in the EU
Commissions Decisions 93/44/EEC and
94t865|EEC.

Fig.12.1

Section12
Fish Pathogenic
Viruses:
SleepingDiseaseof
Salmonids(SD)
1. Pathogen: although not fully confirmed, this is believed to be a virus, taking into account both the infective nature
of the disease and the supposed very

F. Baudin-Laurencin

small size of the agent: electron

microscopy shows 40-50nm virus like
oarticles.
2. Susceptible fish species: on farms,
signs have so far been observed mainly
in trout and occasionally in coho salmon.
In laboratory conditions, the diseasehas
been transmitted experimentally to
Atlantic salmon and brown trout.
3. Temperature at outbreak: The clinical signs are mainly observed in the
spring, when water temperature is 8 to
15' C .
4. Clinical signs: fish of any age (fingerlings to I kg and more) rest on their side
on the bottom of the tanks or raceways
(Figure 12.1).If they are disturbed,they
swim for a time then return down to the
bottom. There are no macroscopiclesions
but occasionally secondary skin ulcerations or petechiae (pin prick haemorrhages)on the pyloric organ.
The characteristicnecrosisof the skeletal
red muscle and the apparently linked
degenerative and inflammatory aspects
of exocrine pancreasand heart can only
be seenin the histopathological examination. It must be noticed that in individual
fish or some populations, the lesions can

-1A

be present without any alteration in

behaviour. This lesions show some similarity to PancreasDisease of sea water
reared salmonids.
5. Mortality: in the absenceof any secondary infection, there is no or low mortality. Nevertheless, fish do not eat for
several weeks (2 to 4), and growth therefore ceasesfor this period.
6. Diagnosis: in the absenceof a method
for isolation of the agent by cell culture
or other techniques,diagnosisis basedon
the very characteristicbehaviour and histology.
The laboratory determination of plasma
enzyme activities (Aspartateamino transferase and Creatine kinase (ASAI and
CK)) which increasein associationto the
lesions can be an useful tool for an
assessmentof the prevalence of the diseasein farms.
7. Transmission: has only been achieved
in experimental conditions:
- by intraperitoneal injection or bath
using kidney extract of diseasedrainbow
trout as contaminant
- by cohabitation of diseasedand healthy
trout.

Section13
Fish Pathogenic
Bacteria : Enteric
Redmouth Disease
(ERrlI) of salmonids
1. Pathogen: Yersinia ruckeri, which
belongs to the bacterial family, the
Enterobacteriaceae.
2. Susceptible fish species: mainly rainbow trout and Atlantic salmon. Almost
all other fish species can be asymptomatic carrier fish as can freshwaterinver,
tebratessuch as crayfish.
3. Temperature at outbreaks: no specific optimal water temperatures,and outbreaks can occur throughout the year,
often in spring and autumn. Outbreaks
ale rare in winter with water temperatures below 5'C, although infected fish
with no clear clinical sisns can be
observed.

5. Mortality:
occur.

ff
Fig.

between 10 and 607o can

6. Diagnosis: culture of the pathogen on

a specific culture medium (bacteriological examinationfollowed by antibiotic
sensitivity tests), 5 - 1 days.

Fig. .

7. Tr t
stood
due t
and
Contr
can L
suryir
has a
mafiu

8. Preyention: identical to that recommended for all yiral diseases.Buy live

eggs and fish only from SD free farms. In
view of, the possibility that transmission
can be on eggs, disinfect the eggs using
iodophores.
9. What should I do? There is no known
treatment ior the disease.In farms where
SD has been recorded, a survey basedon
the research of plasma enzyme activities
and/or histology could allow an early
diagnosisas an aid to the decision:
a) to slaughter the fish if they are large
enough to be table fish.
b) as for PancreasDisease,try to limit the
intensity and the duration of the outbreak
by decreasingthe food ration.
Food supplementation with vitamin E
and/or seleniumhas so far not been found
to be effective with already diseasedfish.
Standard approachesto stress reduction
may be of help.
The eradication of the diseasein contaminated farms would probably need sanitary measuresidentical to those used for
viral diseases:fallowing of the ponds for
a while and disinfection.

4. Clinical signs: the first signs include a

swollen abdomen (stomach filled with
gas and fluid, Figures 13.1 and 13.2),
dark colouration, separation from the
other fish, enlargement of the spleen
(rough surface), small haemorrhageson
the thymus gland (small vault in the gill
cayily aI the base of the gill operculum)
and haemorrhages,mainly on the paired
fins. Later, the "classical" red mouth
colouration follows in which reddening
of mouth corners, gums, palate and
tongue can develop into total mouth reddening. The gill operculae can turn red
and haemorrhagescan be seenin the eyes
(Figures 13.3,13.4 and 13.5).
In fry measuring less than 5 cm in the
hatchery, ERM is mostly without gross
clinical signs, mortality is the only sign.
With repeatedoutbreaksthe frequency of
clinical signs diminishes.

Fig. 13.1

Fig. 13.2

8. Pr
fish, i
sities
(Prot
cessf
out or
imun
Vacci
beforr
time i
up pr
up to
and f
sure,
On si
vacci
recon
turers
Note:
vaccir

tc

Fig. 13.3

Fig. 13.5
7. Tlansmission: much still to be understood, but transmission is believed to be
due to canier fish, (including gold fish
and other cold water ornamentals).
Contaminatedfarm equipment and water
can also be involved. The organism will
survive for several months in water and
has also been found in bird faeces, in
mammals and in man.
8. Prevention: quarantine purchased
fish, avoid stressand high stocking densities.
(Protectivef Vaccination: is very successful. Vaccination should be carried
out on fry weighing more than 3 g (minimum weight, nof aYerage weight).
Vaccinatefingerlings at least twenty days
before moving to infected waters. This
time is neededfor the fingerlings to build
up protective immunity. A protection of
up to 8 - 12 months is generally obtained
and for sites with a low infection pressure,protection can last more than a year.
reOn siteswith a high infectionpressure
may
be
6
months
vaccination after about
manufacvaccine
recommended.Follow
turers instnrctions for use carefully.
Note: basic conditionsfor successfuldip
vaccination are :-

Fig. 13.4

G. Giorgetti

A.
1) do not vaccinate fish weighing less
than 3 g (individual weight, not average
weight!)
2) the fish stock to be vaccinatedmust be
free of pathogens.
3) do not feed for 24 hours before vaccination.
4) during immersion vaccination the fish
must be able to "swim" in the net. The
protective "substances"penetratethe fish
mainlythroughthe gills.
5) corect dilution of vaccine stock and
use in relation to weight of fish per batch
of vaccine.
6) accurateweighing and draining before
and after treatment and exact time measurement means better results (use a
timer).
B. In case of spray vaccination (Figure
13.6):
1) a compressor pressure of 5-6 bar
should be reached
2) for a diameter of the spray valve of 2
mm (2000 mVmin) the pressure should
be 5 bar - 6 bar in caseof using a 3 mm
(3000 mUmin) spray valve
3) spraying time: 30 sec. Not more than
40 - 45 sec.For spraying follow a scheme
such as that shown in Figure 13.7
4) fish should be on monolayer on the
trough - ideal is a ratio such as 10 kg living weight of 10g (averagebody weight)
fingerlings (Figure 13.6)
5) fish should not rest more than 1 min on
the trough
6) follow points 1 to 3 and 6 of para A.
In practice it is often not possible to keep
fingerlings until they reach the minimum
weight of 39 in the hatchery on uninfected water. Therefore in areaswith a high
infective pressure a pre-Yaccination of
fish weighing less than 39 using a lower
vaccine bath concentration may assist.

The bath exposuretime should be at least

two hours and up to six hours and the
water should be aerated.Careful observation of the behaviour of the fish is necessary. After 8 to 12 days the fish can be
transferred to infected water. At this
weight the fingerlings are not yet completely immuno-competent (this means,
able to produce enough protective antibodies) but they are partially protectedby
the pre-vaccination. After reaching a
weight of 3-4 g (at which they become
immuno-competent)the fish should be re
vaccinated using the method recommended by the manufacturer.
Other vaccination tips can be obtained
from the vaccine manufacturers.
9. What should I do? fish not protected by vaccination can be successfully
treated by an appropriate medicated feed
treatment.but only after carrying out a
bacteriological examination and antibiotic sensitivity tests. However, especially in districts with a high infective challenge, new outbreaks can occur only l-2
months after therapy. Therefore revaccination is strongly recommended.
No handling or grading ERM suspector
ERM infected fish should be undertaken.
In virus infected fish stocks (VHS, IPN)
vaccination against ERM is often not
very successful.
Since 1991 this fish virus dis10.
easehas been in List III, (voluntary control for the time being) of the European

Fig. 13.6

to

tive diagnosis can be made in one day,

but no antibiotic sensitivity test is possible with this method.
Increasing drug resistance is being
observedin many furunculosis outbreaks
so that antibiotic sensitivity tests are very
important if therapy is to be adequate.
Under stresssituations, furunculosis outbreaks with high mortality rates can
occur in what were apparently healthy
fish stocks.

Fig. 13.7
Union 9l/61lEEC "Council Directive
concerning animal health conditions governing the placing on the market of aquaculture animals and products". Member
Statesof the European Union are free to
decide wether or not to control ERM
within their borders.

SectionL4
Fish Pathogenic
Bacteria:
Furunculosisof
Salmonids

abscessesare not observedvery frequently and mainly in the acute stage of the
disease (Figures 14.3). In fry asymptomatic infection is common.
5. Mortality: for fry up to 50Eo, generally up to 30Voin older fish.
6. Diagnosis: culture of the pathogen
on a suitableculture medium followed by
antibiotic sensitivity tests which takes
about 5-l days overall. Using an
immunofluorescencemethod a presump-

1. Pathogen: Aeromonassalmonicida
(subsp. salmonicida and subspecies
achromog enes, atypical).
2.
Susceptible fish species: salmonids
of all age groups, brook and brown trout
particularly
are
susceptible.
Furunculosis was originally a diseaseof
freshwater salmonids,but with the intensification of marine salmon farming is
now also a very significant disease of
salmonids in the marine environment.

7. Transmission: infection may be

transmitted by water, eggs, farm equipment, birds, employees, carrier infected
fish and blood sucking parasites
(Argulus, Lepeophtheirus).
8. Prevention: minimiseunnecessary
stressand overcrowding. Improve water
flow. Increasingly effective vaccines are
becoming available, but so far these
require intraperitoneal injection rather
than bath, so that costs of labour for vaccination are high. Where fish are simul-

Fig. )

taneo
such
unlike

9. 1
firmar
mean
result
sible
incluc
oxolir
sulph
ferent
regulr

10. r

Fig.14.1

hasbr
the ti
9U6',
ing a
the pl
anima
the E
wethe
withir

Fig. 14.2

Fig. '

3. Temperature
at
outbreak:
although "traditionally" a summer disease at water tempe{aturesabove 16oC,
outbreaks can occur at lower water temperatures,e.g. 7"C but then often asymptomatic.
4.
Clinical signs: external haemorrhages on the skin and fin bases(mainiy
the paired fins) (Figure 14.1). Internally,
haemorrhagescan be seenon the visceral
organs and in the musculature (Figure
L4.2).Comparedwith VHS thesemuscle
haemorrhagesare diffuse and superficial.
"Classical" signs such as the boil like
"furuncles" which can cause deeo

17
3. Temperature at outbreak: asymptomatic infections above 12'C. Clinical
signs are always observed at temperaturesabove22'C.ED is a tvoical surtmer
disease.

Fig. 14.3
taneously infected with virus diseases
such as VHS or IHN. vaccination is
unlikely to be successful.
9. What should I do? subjectto confirmation of an appropriate drug by
means of antibiotic resistance test
results,then very effective therapy is possible using a range of oral therapeutants
including amoxycillin, oxytetracycline,
oxolinic acid, flumequine or potentiated
sulphonamides. Availability of the different therapeutantswill depend on local
regulations.
10. Since 1991 this fish virus disease
hasbeen in List III, (voluntary control for
the time being) of the European Union
91167|EEC "Council Directiveconcerning animal health conditions governing
the placing on the market of aquaculture
animalsand products". Member Statesof
the European Union are free to decide
wether or not to control furunculosis
within their borders.

Fig. 15.1

Sectiontr5
Fish Pathogenic
Bacteria:
Ery,throdermatitis
(ED) of Carp
and
Other CyprinidsCarp Furunculosis
l.
Pathogen: Aeromonassalmonicida
subsp.rzova,atypical group. Most of the
fiequent casesof summer ulcer diseases
of cyprinids, including "fresh water red
diseaseof eel" have an ED background.
2.
Susceptible fish species: mainly
ornamental (goldfish, koi carp, etc.) but
also other cyprinids,whitefish and eel.

Fig. 15.2

4. Clinical signs: haemomhageson

the skin and fin bases(mainly the paired
fins). Sporadic fingernail sized to 3 cm
diameter ulcers covering the whole fish
can be seen These ulcers can extend
through the muscle into the abdominal
cavity and lead to protrusion of the intestine. The ulcers are observed mainly on
the dorsal side of the lateral line behind
the head or at the base of the tail fin
(Figures 15.1 and 15.2). The white border around the open red ulcers is typical
for ED (Figure 15.3). If this border turns
black the lesions are healing.
After moving fish in springsponlaneous
cases of recovery (without therapy) as
well as unexpected outbreaks can be
observed.
5. Mortality: generally low, rarely
reaching 20Vo. dependingon environmental conditions and fish health status.
6. Diagnosis: identification of the
pathogen by bacteriological examination
and culture followed by antibiotic sensitivity tests, taking five to sevendays, one
day for immunofluorescence (no antibiotic sensitivity test). Culture of the
pathogen is frequently only possible in
the acutestageof infection.
7. Transmission: by water, farm
equipment, birds, employees, infected
carrier fish but mainly by blood sucking
parasites(Argulus).
8. Prevention: quarantine all purchasedfish. Invasions of blood sucking
parasites should be prevented. Reduce

Fig. 15.3

lo

extension(ascites)(Figure 16.1) . Scales

may slough off. In peracute cases,there
may be no external signs, but rapid onset
of mortalities. Acute cases may show
haemorrhagesof the gills and vent, and
chronic casesreveal abscessesand ulcers.
These ulcers may eventually become
moulds
water
co-infected with
(Saprolegnia) (Figure 16.1).
Internally, there are haemorrhagesof the
internal organs, and there is a
blood-tinged fluid in the abdominal cavity. Spleen and kidneys are enlarged.
None of the external and internal signs
are pathognomonic.

stress situations especially at high water

temperatures. Routine bacteriological
examination before moving fish in
autumn and spring.
Protective vaccination with furunculosis
vaccines is established in salmonids
and these also protect against EDi
Furunculosis of carp (cross-protection).
An ED specific vaccine is now available
and vaccination can be used as a preventive especially when moving fish in
spring to sporl angling associations to
reduce the occurrence of unsiehtlv
lesions on the fish.
9. What should I do? subject to the
results of antibiotic sensitivity tests on
the causative organism, medicated feed
therapy can be very successful. At water
below 15'C the successofa
temperatures
medicated feed therapy can not be guaranteed because of lower food consumption which can make it difficult to get
adequatedrug uptake in cyprinids. In this
case, if valuable enough, treatment by
injecting antibiotics into each fish individually. Do not handle or gradeinfected
fish.
In virus infected fish stocks (SVC) vaccination against ED is not very successful.

Section16
Fish Pathogenic
Bacteria: Motile
Aeromonas
Septicaemia;
NIAS; Bacterial
Haemorrhagic
Septicaemia;Red

Pest
1. Pathogen: various motlle Aeromonas
species,especiallyAeromonashydrophila, an example of a facultative fish pathogenic bacterium. There is an unknown
number of serotypes,and the organisms
are also related to the non-motile
Aeromonas salmonicida, causative
agents of furunculosis and Carp
Erythrodermatitis.

5. Mortality: because motile aeromonads occur concurrently with other disease

causingagents,it is not possibleto give
figures for lossessolely due to MAS.

Fig. 16.1
2. Susceptible fish species:all speciesof
fish, freshwaterand salt water, cold water
and warm water. World-wide occurrence,
and typically a disease of pond culture
fishes such as carp, goldfish and catfish.
MAS often concurs with viral infections
such as Spring Viraemia of Carp (SVC,
seeSection 11) or other bacterial diseases
(Carp Erythrodermatitis, see Section 15).
It is also closely related to the Epizootic
Ulcerative Disease Syndrome (EUS) in
Asian rice-field fish culture. In addition,
motile aeromonads cause disease in
frogs, turtles, snakes. Moreover, in
humans,motile aeromonadsare associated with various conditions including gastro-enteritis, wound infections and septicaemia.
3. Temperature at outbreak: above
10'C, typically in spring when pond fish
again become metabolically active.
Outbreaks are usually associated with
poor water quality, especiallylow oxygen
levels, high levels of organic matter, and
pollutants. Almost regularly there is a
precedinghistory ofstress (handling, para s i te i n festati on.poor over-w i nteri ng
conditions). It is questionable whether
MAS is a primary disease,or whether it
only occurs due to secondaryinfections.
4. Clinical signs: not typrcal; the sameas
for any bacterial septicaemia,i.e. haemorrhagic and ulcerative lesions in the skin
and muscle, necrosis of fins and tail (fin
rot, tail rot), exophthalmos, abdominal

6. Diagnosis: isolation of organisms

from hind kidney. A quicker confirmation by ELISA or immunofluorescenceis
very difficult and mostly unreliable
becauseof the numerous serotypes.
7. Transmission: motile aeromonadsare
part of the normal water microflora and
can be found even in tap water. They
occur on the gills and skin as well as in
the gut contentsof perfectly healthy fish.
Only under poor conditions can they
overcome the fish's defence mechanism
and invade tissues - facultative fish
pathogens!
8. Prevention: drain and disinfect ponds
after use. It is unlikely that vaccines will
be developed on a commercial basis
becauseof the ubiquitous presenceof the
organism and because of its numerous
serotypes.Clearly, the only means to prevent MAS is to control the underlying,
predisposingfactors,i.e. generalhygiene,
stresslevels and water quality.

1. 1
um: -R
/,.

ing or
coho
most l
infect
(Arcti
brook
and D
be as
ticula
anime
ly to
water
BKD
lar to

3.

peratl
Occa
rates

4. r
fish s
one e
bubb
cloud
occur
and l

9. What should I do? Because motile

aeromonadsare ubiquitous organisms, it
is usually neither feasible nor sensible to
treat fish with antibiotics. A procedure
frequently performed in European carp
culture, i.e. prophylactically administering drugs without any bacteriological
examination, and certainly without carrying out any antibiotic resistance test, is
not only illegal but also a waste of
money.

Fig.

tv
i

Section 17
Fish Pathogenic
Bacteria : Bacterial
Kidney Disease

(BKD)
Fig. 17.1
1. Pathogen: Gram positive bacterium: Reni bacteri um salmoninarum.
2. Susceptible fish species: in reducing order of susceptibility: salmon (the
coho or silver salmon is world wide the
most important transmitter and source of
infection for BKD), Salvelinus species
(Arctic char are more sensitive than
brook trout), brown and rainbow trout
and Danube salmon. Non salmonids may
be asymptomatic carriers. BKD is a particularly seriousdiseasein salmon,since
animals with infected kidneys are unlikely to achieve a successfultransfer to sea
water.
BKD is a typical chronic infection similar to fish tuberculosisin ornamentalfish.
3. Temperature at outbreak: all temperature ranges, throughout the year.
Occasionally producing high morlality
ratesbetween8 and 14'C in the spring.
4. Clinical. signs: extemally, a few
fish show pop eye or even have a loss of
one eye (compare with sub-clinical gas
bubble disease), the cornea can be
cloudy, small partially bloody blisters
occur along the lateral line (Figure 17.1
and 17.2), bloody pectoral fins, abscess

Fig. 17.2

like opercular damage (furunculosis is

often suspected).
Internally, bloody ascites (fluid accumulation in the abdominal cavity), in some
casestypical kidney signs can be absent
and the skin and eye signspre-dominate.
A slight enlargementof the kidney will
normally be evident in many fish. In
more typical cases, white-greyish nodules (Figure 17.3), filled with a white
fluid are seen in the kidney. Sometimes
theselesionscan also be seenon liver or
spleen(producedby daughtercolonies of
the pathogen). There is often a pale
opaque membrane encapsulating the
spleen or hearl. Massive enlargementof
the spleen (Figure 17.4 and 17.5) can
also occur. In Pacific salmon,holes in the
muscle can be observedmaking the fish
uselessas table fish (Figure 17.6).
5. Mortality: from individual mortalities to total loss of stock, particularly in
infections of salmon on transfer to seawatdr.
6. Diagnosis: where an ELISA test
can be carried out, this is the quickest
identification method taking as little as
forty minutes. Immunofluorescencetakes
about a day. A presumptiveidentification

Fig. 17.3

may also be made by the observation of

non motile, non acid fast, Gram positive
cocobacilli in squash and histological
preparations. Culture of the pathogen is
still necessaryfor unequivocal identification and sometimes for differentiation
from Proliferative Kidney Disease(PKD)
or Nephrocalcinosis (NC). The pathogen
grows very slowly - taking six to eight or
more weeks for confirmation of a presumptivediagnosis.
7. Transmission: horizontal fish to
fish transmission. Apart from this, BKD
is the only bacterial fish infection known
to be transferred vertically within the
eggs. Signs may not appear until fish
reach a size of about 15 cm. The means
of transmissionof this diseaseis still not
well understood.
8. Preyention: purchase eggs only
from BKD-free farms.
After hatching, the fry should be quarantined as should fish up to fingerling size
purchased from BKD endangeredareas
(also for salmon and Arctic char).
Thi s di seasecan remai n i nco nspicuous
for a long time after the introduction of
infected fish.
Egg disinfectionusing iodophoresis use-

20

"a

IAITNS.

Standard approachesto stress reduction

and the optimisation of fish health conditions can be successfulwith BKD, reducing 20-307omortality almost'to zero.
A field practicable vaccine is unlikely to
become available in the foreseeable
future.
Erythromycin, although effective for prevention of vertical transmissionin eggs if
used appropriately is not licensed for that
use in any European Union country.

Section 18
Fish Pathogenic
Bacteria:
Rainbow Trout Fry
Syndrome (RTFS)

Fig. 17.4

Bacterial Cold
Water Disease

(cwD)
Fig. 17.5
less since iodophores will only kill bacteria on the egg surfaceand not thoseinside
it, so this will not prevent vertical transmission.
Researchin Canada(which together with
the north-westernpafi of the USA is most
important region for BKD infections)
shows that injecting the parent stock 6-8
weeks before stripping using a high dose
of erythromycin can ensure BKD-free
eggs.
9. What should I do? BKD is the
most difficult bacterial diseaseof domesti c fis h t o c ont r o l . Al th o u g h e ry thromycin is reported to be able to control the disease, this is not universally
accepted.Most of the bacteria are located
(ust as are viruses)inside the cells of the
fish, mainly the protective cells (for
example macrophagesof the blood) and
therefore are difficult for therapeutantsto
reach.
On infectqd farms repeatedoutbreaksare
to be expected. Infected fish stocks
should be fattened as table fish as soon as
possibleand must not be moved off the
site alive.

10. Since 1991 BKD has been on List

III (voluntary control) of the European
Union 91/61/EEC Council Directive
Concerning animal health conditions
governing the placing on the market of
aquaculture animals and products".
Countries belonging to the European
Union are free to decide whether or not to
attempt to control BKD within their borders. BKD is a notifiable diseasein the
UK. Total disinfection of the farm is recommended, particularly for restocking

1. Pathogen : the Cytophagaceaeare a

group of bacteria associatedwith several
fish diseasesyndromeswith overlapping
signs. In particular Cytophaga psychrophila (or Flexibacter p sychrophilus)
is involved in these conditions. Cold
water disease,sometimesknown as saddleback diseasehas been reported from
salmonids for many years. More recentIy a condition associatedwith high mortalities, rainbow trout fry syndrome
(R[FS), has steadily increased in importancein the last ten years.

Fig.

(sad
a pi(
obse
darkt
18.2
lings
pedu
of tn
RTFi
infec
enlar
abdo

to 5C

6.
on
exan

tEStS

(no e
fish
species:
2. Susceptitrle
salmonids, mainly fry and fingerlings.
RTFS in fry in early cases between the
4th and 7th week from first feeding, but
more recently affecting larger and larger
fish (>50g) on fingerling and ongrowing
sites.Eel and carp can be asymptomatic
carriers.
3. Temperature at outbreak: mainly
during the cold-water periods - end of
winter, beginning of spring. In case of
RTFS.8 - 14'C.

Fig. 17.6

4.
Clinical signs:
CWD : 2 - l0g (3 - 10 cm) fry: white

i:f
;a::':;

Fig.

7. T[ansmission: horizontally by
water, but parlicularly on fish and eggs.
Vertical transmission on eggs seems
probable.
(saddle) spot up to a deep necrosis (as if
a piece has been bitten out) can be
observed in the dorsal fin area as well as
darkening and pop eye (Figures 18.1
18.2 and 18.3). Later stageson fingerlings show skin ulceration from which
peduncle (Figure 18.Q and anterior third
of trunk (Figure 18.7) are primary sites.
RTFS: (0.2 - 29 fish) general septicaemic
infection signs, anaemia, considerable
enlargementof spleen, haemorrhageson
abdominal fat (Figures 18.4 and 18.5).
5. Mortality: in a progressedstage:up
to 507a,50-80Vofor RTFS if not treated.
6. Diagnosis: culture of the pathogen
on culture medium (bacteriological
examination) and antibiotic sensitivity
tests, five to sevendays. IFAI-test 2 - 3 h
(no antibiotic sensitivity test).

8. Prevention: still not well understood, general optimising of environment, reduction in feeding and optimising stocking conditions. Site disinfection
between fry batches. Separationof year
classes.
9. What
should I do?
the
Cytophagaceae
are very resistantorganisms which can hide under scaleetc. on
tanks and pipework which can therefore
be difficult or impossible to fully disinfect. Outbreaks of RTFS can be controlled by appropriateantibacterialtherapy but frequently require higher levels
for effective control than for other bacterial diseases.Drug resistancecan develop
quite quickly so that for example oxytetracycline is becoming increasingly ineffective for control of RTFS. Apart from
measures such as reduction of stocking
density, water and feeding optimisation,

R. Rangdale

Fig. 18.4

the following prophylactic and management measuresare recommended:

- egg disinfection with iodophores (double dosage advised) or glutaraldehyde
(400 mg/l - 10 min = 4009 / mz, 200 mgl
- 20 min)
- separation of yolk sac fry from egg
shellsas soon as possible
- l7o sah bath for yolk sac fry every 2nd
day
- formalin bath for fry after yolk sac
resorption (ectoparasite prevention)
1:6000 (1 ml fresh formalin I 6 | water,
bath 30 min.
- salt baths | - 1,57o/ 30 min as many
times as seento have positive effects.
- extra feed supply with vitamin C and Bcomplex.
- frequently gill inflammation, ERM and
hexamitiasis (also IPN) may accompany
to RTFS and should be controlled as to
enhancetreatment of RTFS.
If these does not succeed- further therapies may be recommended:
- Oxytetracycline (OTC) 3 g/kg feed,

N. Kayer

ZZ

l,5%oliving weightiday,8 - 10 d
- Amoxycillin200 glt living weight/day,
8 -1 0d
- Enrofloxacin (Baytril@) 10 m1 of the
commercial l07o-dlhttionlkg feed, lvo
body weight/day,7 d
No vaccine is yet available.

This group of diseasesis of increasing

importance and is the subject of research
into disinfection and control, so that the
present limited state of knowledge will
hopefully soonimprove.

Section 19
Fish Pathogenic
Bacteria:
Edwardsiellosis;
Edwardsiella
Septicaemia
L. Pathogen: Edwardsiella tarda. Abacterium belonging to the family
Enterobacteriaceae,but serologically not
related to Edwardsiella ictaluri. There
are four serotypes,with serotypeA being
the most virulent and responsible for the
majority of diseaseoutbreaks.
2. Susceptible fish species: all warrn
water fish, especially channel catfish and
eel, but also carp, goldfish and tilapia,
with disease mainly occurring in large
fish. Edwardsiellosis is a major problem
in the Southern United States and in
Southeast Asia (particularly Japan and
Taiwan).
In addition, the organism causesdisease
in seals,sealions, porpoises,turtles, alligators, snakes,cattle, pigs and birds, and
can cause gastro-enteritisand meningitis
in humans.

Fig. 18.5

3. Temperature at outbreak: typically

above 30'C. Furthermore, poor water
quality, especially a high level of organic
matter, precipitates disease.

Fig. 18.6

Fig. 18.7

Fig. t

R. Rangdale

R. Rangdale

4. Clinical signs: small cutaneouslesions

(Figure 19.1) that can develop into large
abscessesin the muscle (Figure 19.2).
These abscessesare filled with necrotic
tissue and cause a very striking foul
odour. Small white nodules can be found
on the gills. In scale-lessfish such as catfish, infected skin becomes depigmented
(Figure 19.3). General signs of septicaemia are ascites,prolapse of the anus,
exophthalmus,opaque eyes.
Internally, there are white nodules on the
liver, kidney and spleen. The typical
signs of septicaemia are displayed.
Kidneys are enlarged. Eels can develop
either nephritis, i.e. inflammation of and
in the kidneys, or hepatitis,i.e.
abscesses
ulcers and abscessesin the liver.
5. Mortality:

usually not very high

(arou
unde
losse
and
beco
enter

6. Di
tion r

'+i;

r
Fig.

7. TFansmission: the mode of transmission is not clear, but the organism is obviously wide-spread and occurs in a freeliving form in mud and water from
ponds. Covertly infected fish are a reservoir of the organism; they cany the bacterium in the gut. Also, Edwardsiellct
tardamay be part of the normal microflora of fishes' surfaces, and only predisposedfish becomeseriouslyill.

Fig. 19.1

re

Auburn Univ

''''-.,

9. What should I do? acute outbreaks

can be controlled via medicated feed.
Oxytetracycline is reported as being
effective when fed for ten days, but resistant isolates have been described.
Mortalities usually stop after two to three
days of treatment,but lesions heal slowly
and leave scartissue.

Fig. 19.2

Auburn Univ

(around 5Vo), but can increase to 507o

under adverseconditions. Other financial
lossesoccur due to extensivedisinfection
and deodorisation procedures that
become necessary when infected fish
enterprocessingsites.
6. Diagnosis: clinical picture and isolation of organismsfrom kidneys and mus-

cle. Identification and antibiotic resistance tests take about one week. Quicker
confirmation, but no resistancetest, can
be done in one day by immunofluorescence or ELISA. An antibiotic resistance
test is absolutely essential, as there a"re
increasingproblems with drug resistance
amons Edwardsiella tarda isolaIes.

Section20
Fish Pathogenic
Bacteria:Enteric
Septicaemiaof
Catfish;BSC;
"Hole-In-The-Head"
Disease
1. Pathogen: Edwardsiella ictaluri. A
bacterium belonging to the family
Enterobacteriaceae,but serologically not
related
to
Edwardsiella
tarda.
Serologicallyhomogeneous.

,,.:t

2. Susceptiblefish species:naturalhosts
are various catfish species, particularly
the channel catfish. European catfish as
well as rainbow trout are susceptible
under experimental conditions. Disease
occursin fish of any age.ESC is the main
scourge of the catfish industry in the
United States. but it also occurs in
Thailand.

Fig. 19.3

8. Prevention: minimise stress, avoid

high stocking densities. Optimise water
quality. At present.thereis no commercial interestin developinga vaccine.In
carp, injection of glucan provides some
level of resistance.

e
Auburn Univ

3. Temperature at outbreak: typically

between20'C and 30'C. althoush infec-

a+

5. Mortality: ranging from l07o to 50Vo.

6. Diagnosis: clinical picture and isolation of organismsfrom kidneys and brain
or other internal organs, skin or muscle.
Identification and antibiotic resistance
test take about one week. Quicker confirmation, but without any antibiotic resistance test, can be made in one daY bY
immunofluorescence or ELISA. An
antibiotic resistance test is absolutely
necessary,as there are increasing problems with drug resistance among
Edwardsiella ictaluri isolates.

i' l'j; 1 . ; ;, ,1,

l,'.:';".'.' ; ''".""r

Fig.20.1
tions at lower temperatures have been
reported. The disease occurs mainly in
late spring and again in autumn, but not
at very high summer temperatures.
Fluctuating temperatures may be more
important than the absolutetemperature.
4. Clinical signs: infected fish refuse
food and swim listlessly at the water surface. Sometimes they appear "hanging"
a
in
wat er
a lm o s t
in
the
"head-up-tail-dowri" position. Spiral
movements and erratic swimming bursts
can occur. Haemorrhagesappear around
the mouth, on tho lateral and ventral portions of the body and the fins, and can
eventually cover most of the fish's surface. Infected areasbecome depigmented
(Figure 20.1). In typical cases, there
appears a longitudinal, ulcerative lesion
between the eyes, eventually exposing

7. Tlansmission: Edwardsiella ictaluri

survives well in pond bottom mud (up to
ninety days) but not in the water column.
Auburn Univ
The organism can be taken up with food,
the skull bones ("hole in the head") then enter the gut and thence the blood
stream. This infection rapidly leads to a
(Figure 20.2i).The above signs are typical for fingerlings, whereas fish over 15 septicaemic form of the diseasewithout
cm sometimes do not exhibit extemal typical external signs, but with high mortal i ti es.A l temati vel y.the or ganismm ay
signs, and smaller fish show anal proenter the nose and barbels,and from there
lapse as the only sign of an enteric infecascend into the olfactory stem and into
tion.
Internally, the spleen is dark red and the the brain, eventually causing the longituliver pale or mottled. Haemorrhages dinal lesionsbetweenthe eyes,i.e. at the
site of the olfactory lobe in the front
occur throughout the viscera and the peritoneum as well as the musculature. skull.
Kidneys, liver and spleen are enlarged, Fish surviving the diseasebecome carriers of the organism and probably harbour
and often the abdominal cavity is filled
the bacterium in the forebrain or in the
with fluid.
gut. They may represent only l7o of a
In over-wintering fish, small white nodules often can be seen on the body sur- population, but this level is high enough
face, indicating healed, scarred lesions. to cause clinical diseasein the next seaThose fish have survived the diseaseand son.
Also, Edwardsiella ictaluri may be part
must be regardedas carriers ofthe organof the normal microflora of fishes' gut,
ism.
and only predisposedfish become seriously ill.

?1lJi];{ffi

8. Prevention: minimise stress, avoid

high stocking densities. Optimise water
quality. Drain and disinfect ponds after
use. Do not mix different year classesof
fish.
At present,a vaccine is not commercially
available in Europe. In carp, injection of
glucan provides some level of resistance.
9. What should I do? acute outbreaks
can be controlled via medicated feed.
and
Oxytetracycline
Potentiated
reported as being
are
sulphonamides
effective when fed for five days, Lrut
resistantisolates have been described.

Fig.20.2

Fig. '

Auburn Univ

In all
wate
sourc
frequ
and
Sapr

1.
para,
)

spec
3.
cific
high

4.
mari
plies
duce
tilise
of th
Spor
othe
If th
al, v
incrr
stoc
also
Notr
ond
Sap
thin
icall
infe
itg)

kol

':#.

Fig.21.1

Section21
Fungi : Saprolegnia
z Saprolegniasis
In all aquatic systems,in river water, well
water, ground water and spring water,
sourcesof fungal sporesexist. The most
frequent in water are the aquatic fungi
and particularly members of the genus
Saprolegnia:

Fiq.21.2
Previous damage to the mucus membranes of the fish predisposesthe animal
to fungal infection. An example is shown
in Figure 21.3 with Saprolegniagrowing
on ED lesions. In practice mainly male
salmonids are very susceptible to
Saprolegnia infection induced by certain
hormonal causedskin sfiucture changes.
In casesof massiveinvasion mortalities
c a no c c u rtFi gure 21.4t.

of such makes them unsaleable.

6. Diagnosis: a simple skin scrape
preparation examined microscopically at
a 25x magnification clearly shows the
fungal hyphae and spores(Figure 21.5).
7.
Tfansmission: by water, fish to
fish, equipment, etc. - horizontal transmission, insufficient health condition.

5. Mortality:
generally
low,
8. Prevention: optimise health condiSaprolegnia is rarely the primary cause tions - improve water quality, reduce of
of diseasebut the unpleasantappearance the stocking density, optimise feeding,

llii:i

i;

1. Causative organism: Sctprolegnia

parasitica is ubiquitous.
2.
Susceptible fish species: all fish
specles.
Temperature at outbreak: no spe3.
cific range, development is quicker at
higher temperatures.
4.
Clinical signs: Saprolegnia is primarily found on dead tissue and multiplies quickly. The fungus typically produces a fluffy mass, parlicular on unfertilised eggs (Figure 21.1). The sporangia
of the fungus contain hundreds of motile
spores,which aid rapid fungal spread to
other susceptiblehosts(Figure 21.2).
If the susceptibility (also againstbacterial, viral and parasitic infections) of fish
increases, due to poor water quality, high
stocking density, etc. Saprolegnia can
also invade muscle tissue.
Note: Saprolegnia is primarily a secondary parasite. An infection with
Saprolegnia is usually a sign that something elseis wrong (exceptfor physiologically compromised animals, e.g. fungal
infection of male salmonids after soawning).

Fig.21.4

D J Alderman

26
carp in regions with (higher) water temperatureswhere grass carp really eat the
weed and not commercial carp pellets,
optimising pond hygiene.

.!,:,,;i;,1:,.:

tit,

:t;ffi;,

9. What should I do? effective treatment is not practicablein (mostiy large)

cyprinid ponds. Preventionis the effective ootion.

D J Alderman

Fig.21.5
control other possiblediseases(examination and diagnosis) which cause secondary fungus infections.
9. What should I do?
Remove dead eggs or fish immediately.
(e.g.
The most activechemotherapeutants
malachite green) which have been used
for many years for fish disease controi
pulposesare not approvedfor use.These
are chemicals which are free available
but from the moment they are usedas fish
therapeutantsthey change to medicines
and their use becomes illegal in some
countries. In Germany malachite-green
oxalate is licensedfor the preventionof
Saprolegniasisin salmonid eggs during
incubation. The license applies only for
egg-treatment.

Section22
Fungi : Gill Rot :
Branchiomycosis
1. Causative organism: the fungus
Branchiomycessp. There are two types,
one grows all over the gill, the other one

is to be found in the central blood capillaries of the primary lamellae.

2. Susceptible fish species: mainly
cyprinids, especially carp of all age
groups.
3. Temperature at outbreak: towards
the end of summer in warmed water and
over weed covered ponds.
4. Clinical signs: red-brown colouration of the gills developing to a high
degreeof gill necrosis,producing"holes"
in the gill arches(Figure 22.I).
5. Mortality: in casesof advancedgill
necrosismassive lossesup to 507o and
mo re i n 3 -4days.
6. Diagnosis: as for SaproLegnia,gr11
scrape preparation. The red-brown
colouration of the B ranchi omyces hyphae
and the typical round shape of the big
sporescannotbe confused(Figure22.2).
7.

Transmission: as for Saprolegnia.

8. Prevention: if possible (for large

carp ponds) increasethe flow of fresh
water tempwater (decreasing
eratureand reducingalgal bloom), reduction of weed,for exampleby using grass

Section23
Fungi :
Crayfish
plague
(Aphanomyces
astaci)

the
organism:
1. Causative
OomycetefungusAphanomycesastaci
2. Diagnosis: Between 1870 and 1940
the European freshwater crayfish
(Astacus astctcus,Astacus leptodactylus
and Austropotttmobiwspallipes) were
almost completely destroyed. These
speciesonly survived in small isolated
water systems (mostly above 600 m
height) on the European continent and
Spain, the British Isles Norway and
Greece. In the period from 1960 to 1990
nativecrayfishpopulationsin thesecountries have also largely been destroyed.
North American crayfish (e.g. the signal
crayfish - PaciJastacusleniusculus) are

w
4

*,:a'

i.-...
.
l,..

w
Fis'

large
there
envi
large
be ki
?

mort
plag

4.
shoi
the 1
infec
of a
t1t'

almc
hund
hasi

6.
tion
mad

T-.-3

z.'#

'' '
''.:r.
'.::*+4

"r'

Fig. 22.1

Fis.

27

Fig.23.1
largely resistant to crayfish plague and
therefore can act as carriers. In poor
environmental conditions even these
largely resistant American crayfish can
be killed by crayfish plague.
3. Temperature at outbreak : major
mortalities tend to occur in summer, but
plague can occur at all times of the year
4.
Clinical signs: Infected crayfish
show whitened necrotic musculature in
the tail, often accompanied in chronic
infections by melanisation (blackening)
of affected exoskeleton (Figure 23.1,
) 7't\
5.
Mortality: in European crayfish is
almost always l00%o,and in over one
hundred years no evidence of resistance
has developed.
6. Diagnosis: Presumptive identification of the causative organism can be
made from a fresh microscopic mount of

Fig.23.3

D J Alderman

Fig.23.2

D J Alderman

a piece of infected exoskeleton (Figure

23.3). Isolation and culture of the
pathogen is required for absolute confirmation.

eliminate the pathogen. There is no reliable method yet established to confirm

absence of infection in N. American
crayfish.

7. Transmission:
principally on
infected crayfish, both susceptible and
resistant. The latter readily act as infected carriers. Contaminatedtraps, fishing
gear, boots and other equipment can also
carry infection. Parlicularly with large
outbreaks, fish transport and birds and
other wildlife may act as vectors.

10. Since 1991this diseasehas been on

List III (voluntary control) of the
European Union 91167/EEC Council
Directive concerning animal health conditions governing the placing on the market of aquacultureanimals and products.
Countries belonging to the European
Union are free to decide whether or not
to attempt to control this diseasewithin
their borders.

8. Prevention : Do not introduce crayfish from infected sources. Buv onlv

from diseasefree farms.
9. What should I do? : No treatment
is possible and once natural waters are
infected furlher spread of infection is
normally inevitable. In farmed stocks in
completely enclosed waters, total
destruction of al1 crayfish and thorough
disinfection followed by restocking may

D J Alderman

Section 24
Nlajor Ecto- and
Endoparasitesof
Farmed Fish
Introduction:
Sections24 to 4l describethe major ecto
and endoparasitesof farmed fish.
Under good environmental and health
conditions fish can survive quite well
whilst infected with many of these parasites.
Note: Treatments to control such parasites is only to be recommended in
cases of massiye invasion, which often
cannot be observedby the naked eye.
Heavy parasiteinfestation is often a sign
of adverse environmental conditions
which have to be identified and
improved. Any therapeulictreatments
(immersion baths) produce additional
stressfor the fish and in some circumstancesmay be worse than the presence
of the parasites.
One example is shown in Figure 24.1, a

28

r:i'..

9. What should I do? immersion

bath treatment with formaldehyde :
1:4000 or 1:6000 (this means 1 ml formaTin/ 4 or 6 | water) of the commercially available formalin (37 - 40Vo)for one
hour, depending on condition and vitality
of fry; or salt2-37o/Ihfortrout, I,57ol7
h for cyprinids. Salt does not kill the parasite as effectively as formalin does, but
is better tolerated especially by weakened
fry.
More impofiant than direct morlalities is
the indirect damage due to decreasing
health condition and sill lesions.

Section26
Flagellates :
Hexamita

Fig. 24.1
so called "palisade"gill causedby a massive invasion of the funnel shapedciliate
Glossatella sp. Crowded on the gill. In
case of massive invasion a ffeatment
should be underlaken and water quality
should be checked (these parasitesoften
occur becausethe water is over contaminated with organic matter) and improved.
For thesereasonsthis guide only reviews
those parasiteswhiih are of real significance to fish farming practice.
Widespread parasites of low pathogenic
significance and,for which there is no
practical treatment are not considered.
The photographs shown are all "fresh
squash" preparations - unstained and
seenwith a simple microscope.

ornamental fish with moderate to severe

infections. Costia is a typical hatchery
flagellate.
6. Diagnosis: microscopically, gill or
skin scrapepreparationat 25x magnification or greater.The flagellate is about the
same size as skin cells. The parasite is
bean shapedand swims with a staggering
movement.
In the centre of Figure 25.1 two Costia
cells attachedto skin cells are seen.
7. Transmission: by infected fish,
water, farm equipment or employees.
8. Prevention: improved hygiene,
especially in the hatchery.

Section25
Flagellatesz Costia
1. Causative organism: Costia (now
scientifically known as Ichthyobodo
necatorl- in practiie still betterknownas
Costia.

1. Causative organism: Hexamita

(scientifically now correctly Octomitus
salmonis,bt;j.Hexamita is still more common).
Hexamita is a parasite typical of weak
fish, i.e. heavy infections are commonly
observed as secondary infections in fish
in poor health conditions. Hexamita has
often been observedin fish infected with
VHS and it has been speculatedthat the
parasitemay even be able to act as a carrier of VHSV (and therefore perhaps of
other viral pathogens)although scientific
confirmation is lacking. The more likely
explanation for the frequency of concurrent infections is that Hexamita is a sec-

Fis.

ond
fish.
)

saln
men
gfas

3.
asis

4.
rate
beh
Inte
ofte

and

6.
natir
pafi
200t
that
diag
Figr
scra
160
oval
flagr
tion.
pho
1

tion,
prot
equ

2.
Susceptible fish species: ali fish
species,especially salmonid (trout) fry.
3. Temperature at outbreak:
hatchery temperatures.

all

8.
cial

4.
Clinical signs: a slight white-blue
cloudy layer on the skin accompaniedby
an increasing mortality rate.
5.

Mortality:

mortality only in fry or

9.

Fig.25.1

feed
pha
iden

ZY

Fig.26.1
ondary invader of VHS compromised
fish.
2. Susceptible fish species: mainly
salmonids of all age groups, but ornamental fish are susceptible as well as
grassca4).
3. Temperature at outbreak: as far
as is known all temperatureranges.
4. Clinical signs: lingering mortality
rates. In ponds an extremely nervous
behaviour of the fish can be observed.
Internally the hind part of the intestine is
often paler than normal.
5. Mortality: direct mortalities in fry
and ornamental fish.
6. Diagnosis:by microscopicexamination on a scrapepreparation ofthe hind
part of the intestine at a magnification of
200x. The parasite cells swim rapidly so
that some experiengeis neededfor exact
diagnosis.
Figure 26.L shows an unstainedintestine
scrapeprepa.rationat a magnification of
760x. Hexamita cells can be observedas
oval shapedspots.Figure 26.2 showsthe
flagellate parasite at a 320 x magnification, the rapid movement is difficult to
photograph.

Fig.26.2
scription by a veterinary practitioner or
fish health service.

Section27
Ciliates :
Ichthyophthirius,
White spot
1. Causative
organism
:
Ichthyophthirius multifilils, cause of
white spot diseaseor Ich.
Ichthyophthirlzs gets under the upper
layer of fish skin and can be controlled
most easily when leaving the host for
reproduction (cell division and formation
of tomites). Parasite tomites are only
viable for three days even under
favourable conditions which means that
within that time the tomites must find a
new ho'st or die. Fish surviving
Ichthyophthirizs infections show clear
evidence of resistanceto reinfection.

7. Tfansmission: little clear information, but the parasite is easily transferable

probably by infected fish, water, farm
equipmentand employees.
8. Prevention: good hygiene, especially in the hatchery.
9. What should I do? use medicated
feed e.g. Dimetridazol or magnesium sulphate (200 - 300 mg/kg feed, 5 d), after
identilicationof the parasite and pre-

Fig.27.1

2. Susceptible fish species : ail

species and age groups. An important
problem in ornamentalfish and eel farming.
3. Temperature at outbreak: from 3
- 28'C. In temperature ranges, above
20"C a very rapid multiplication of
Ichthyophthirias can occur.
4.
Clinical signs : fish "rub or flash
and show evidence of breathing problems. In heavy infections the adult parasitic white spots (0.5 - 1 mm sized) are
visibleto the nakedeye.
5. Mortality : dependenton fish size
and infection intensity.
6, Diagnosis: can be made macroscopically (i.e. by the naked eye) for
adult parasitesin heavy infections (presence of white spots) as well as microscopically from a skin or gill scrape
preparation(25 x), Figure 27.1,27.2 and
27.3.

30
chite green / I fresh forrnalin, from this
basic solution take 25 mV m3 bath - th)
may be used.
The legal status of malachite green treatments of food fish are however unclear
and residueswill remain in the muscle of
treated animals for very long periods.

Section28
Ciliates:
Chilodonella

Fig.27.2

Fig.27.3

9. What should I do? infected fish

should be held at a reduced stocking density. Ornamental fish should be transferred every twelve hours into clean
8. Prevention : for aquarium and tanks.
pond fish use quarantineor immersion The best treatment for Ichthyophthiriasis
(as well as for all the other ectoparasitic
bath treatment before stocking. It is betCiliates), is still a Malachite green
ter if this is done at the site where the fish
originate. Lower stocking densities, immersionbath, e.g. 2 - 3 g / 10 m3 long
term bath (stop water flow as long as tolincreased water flow for holding facilierated,aerate). Repeatbath at least three
ties, only put "clean" carp spawners in
times with time intervals of 24h is
spawning ponds, immediate transfer of
carp fry after hatching to "large surface" unavoidable for the control of continuponds, frequent routine examination of
ously emerging tomites.
Alternatively a malachite green I
high density stocked fish.
formaldehyde combination (4 g mala7.
Thansmission : infected fish and
water, plants (aquaria), snails and live
food (for ornamental fish).

Fig.

:
organism
1. Causative
Chilodonella sp. which causes gill damage. Infection produces extensive dischargesof mucus. It is primarily a parusite of weakenedfish, but it can also easily infect healthy fish. As well as treatment an improvement of environmental
quality and general health conditions
should be ensured.
2. Susceptible fish species : all
speciesand age groups.
3. Temperature at outbreak
temperaure ranges.

: all

a lor
form
600
form
gree
mala
this I
th)
shov
salt
I.5E
succ
not
para

4. Clinical signs : a white cloudy

layer on the mucus, mainly on the back
between dorsal fin and head resion Figure 28.1.
5. Mortality : depending on fish size
and infection rate. It can be a problem for
carp in winter ponds.
6. Diagnosis : microscopically on a
gill or skin scrape preparation (60 - 160
x), Figures 28.2 and28.3.

1.
spec
uine

7. Transmission : infected fish, water,

undisinfectedfarm equipment, plants and
live food for ornamental fish.
8. Prevention: low stockingdensities
and, if possible, an increased water flow
rate. Only stock clean fish. Frequent routine examination especially when fish
stocks held at high density. Chilodonella
is a parasite of fish in poor condition
thereforeoptimise environmental quality.
Examination of carp before stocking in
winterponds.Generalhygiene.

Fig.28.1

9. What should I do? : for non-food

fish, malachite green (2-3 e / 19 rn3) as

Fig.

JI

Fig.28.2
a long term immersionbath, short term
formaldehyde bath treatment (1:40006000/I-2 h, that means one mililitre of
formalin / 4 | or 6 I water), malachite
green / formaldehyde combinatiorl (4 C
malachite green / I fresh formalin, from
this basic solution take 25 mV m3 bath lh) and chloride liming for big ponds
show good results. For ornamental fish
salt baths (2.5 - 37o for salmonids, 1 1.57ofor cyprinids - bath th) can also be
successful,but using sodium chloride is
not often very efficient, only reducing
parasitenumbers, not eradicating them.

Section29
Ciliates
Trichodina sp
1. Causative organism : Trichodina
species- more a commensal than a genuine ectoparasite.

Fig.29.1

Fig.28.3
2. Susceptible fish species : all
speciesand age groups.

undisinfectedfarm equipment, plants and

live food for ornamental fish.

3.
Temperature at outbreak
temperatureranges.

8. Prevention : Trichodina often

occursin combination with poor environmental quality producing a decreaseof
general health conditions. Therefore
hygiene in hatcheries and quarantine for
ornamentalfish js most important.

: all

4.
Clinical signs : the fish show a
grey-blue turbid layer on the skin.
5. Mortality : depends on infection
rate and fish size. In practice high mortality rates only occur in cases of massive invasion, mainly affecting rainbow
trout fry and fingerlings.
6. Diagnosis : examination at 60 - 160
x magnification of a gill or skin scrape
preparation. Figure
29.1 shows
Trichodina (160 x) in a skin scrape
preparation. In a 500 x anterior view of
Trichodina (Figure 29.2) the hooks and
cilia can be seen clearly. Figure 29.3
shows a side view of Trichodina, much
differerit compared to the well known
front view (Figure 29.2).
7.

Transmission : infected fish. water.

Fig.29.2

9. What should I do? after microscopical identification of the parasites,

which can be done by experienced fish
farmersthemselves(Figure 29.1). long
term baths (2-3 g / 10 m3) with malachite
green (for non-food fish species)or combination of malachite green and
Formaldehyde (see Section 28), short
term baths using formaldehyde (see
Section 28), chloride liming for big
ponds can be used as well as sodium
chloride for ornamentalfish and sensitive
domestic fish fry as shorl term baths: 1 l.5%o,20-30 min or as a long term bath :
0.2 - 0.3 7o for at least 10 - 12 hours.
Note: Treatment with salt is generally
noI I00Vosuccessful.

32
tion (160 x) - massiveinfection.
Figure 30.3 shows 3 parasitesat a magnification of 500x in a skin scrapepreparation. The ring of cilia at the wide end
(mouth) is seenclearly.
6. Diagnosis: by microscopicexamination of a gill or skin scrapepreparation
(60-160x).
7. Tlansmission : by infected fish,
water (especially with highly organically
contaminated water) and undisinfected
farm equipment.

Fis
;F.
,

.,:l',tj.:,:

6i*ff: '.i:,;'r

Fig.29.3
Trichodina, Trichodinella, Tripartiella,
Foliella and others related ciliates differ
only in shape,size and hooks. The damage causedis comparable:mucus and gill
injuries up to gill swelling or even gill
necrosis as well as fin damase in frv and
small ornamental fish.

8. Prevention : quarantineor immersion bath treatment before stocking. It

would be best if this could be done on the
supplying site.
Improve the environmental quality,
reduce the loading of organic matter.
Hygiene in the hatchery, routine exami2, Susceptiblefish species:all species nation of the fry.
and age groups.
9. What should I do? after micro3. Temperature at outbreak: almost scopical identification of the parasites,
all temperature ranges. Apiosoma/ which can be done by experienced fish
Glossatellainfection is a clear sign of the farmers, long term baths with malachite
green (2 - 39 / 10m: for non food fish
excessive contamination of the water
species or combination of malachite
with organic matter.
green and formaldehyde (see section 28),
shorl term baths using Formaldehyde
4.
Clinical signs : not very clearly
(see section 28), chloride liming for big
defined, sometimes a slight grey-white
layer on the skin and problems with res- pondscan be used.
piration can be observed.
Glossatella attacheswith a foot disk onto
the gills (Figure 30.4,400 x magnification) or/and onto the cells ofthe skin and
5. Mortality : acute mortality only
occurs with fry with massive infections therefore gaseous exchange is affected.
This can lead to a kind of "allergic" reacas shown in Figure 30.1 (25 x magnification) which shows a palisadegill with a tion causing decreasinghealth and morrow of parasitesalong the primary lamel- tality. This figure also shows an acute
massiveinvasion (which should be treatlae of the gills.
Figure 30.2 shows a skin scrapeprepara- ed) - palisade gills. Glossatella eats

mic
mat
isv
with

Section30
Ciliates.'
GlossatellnlApiosoma
sp
1. Causative organism: Glossatella/
Apiosomaspecies.

l.
zoa
spo
stag
is a
para
sco[
t oi
Kidr
,,

clini

d
*

E
ffi

Fig.30.1

Fig.

Fig. 30.2

Fig. 30.3
microorganisms and "detritus" (organic
matter of diverse origin in water) which
is whirled towards the mouth opening
with help of the cilia.

Section31
Myxozoa :
Proliferative
Kidne.vDisease
(PKD)
1. Causative organism: to give protozoan parasites a scientific name, the
spore must be identified, since the spore
stageof the parasiteresponsiblefor PKD
is as yet unknown, in the meantime the
parasite cell which can be seen microscopically in inflamed kidneys is referred
to as the PKX cell (= Proliferative
Kidney X (unknown) cell).
2. Susceptible fish species: severe
clinical disease in rainbow trout. The

Fig. 31.1

Fig. 30.4
same or closely similar parasites are
known to occur in brown trout, Arctic
char, brook trout, grayling, salmon and
pike. PKD is water systemlinked, i.e. it
only appearsin fish in infected water systems not in fish in well or spring water.
3.
Temperature at outbreak: PKD is
extremely temperature dependent, the
earlier and wanner the spring, the higher
the lossesdue to PKD in table size (300 500 g) fish in autumn. Clinical disease
(as opposed to infection) occurs at water
temperaturesabove 16"C.
4.
Clinical signs: externally, swelling
of the belly: darkening of skin colour,
exophthalmos(pop eye) (Figure 31.1).
These external signs only appear some
weeks after the first internal clinical signs
of PKD.
Intemally, a slight enlargement of the
kidney increasing over several weeks to
gross enlargementwith a marbled white
to grey colouration (Figures 31.2 and
31.3). In advancedcasesascites(accumulation of fluid in the abdominal cavity) occurs resulting from failure of normal kidney function. The inflammation
of the kidney seenin PKD resultsfrom an

Fig. 31.2

excessive response to the presence of

the PKX parasite.
5. Mortality : dependenton the water
temperaturethrough the summer season.
In southern England infection of naiVe
fish normally first occurs in early May.
Parasite numbers increase and kidney
inflammation norrnally first becomesevident in late June to early July, severity
increasing through August. In south
western France with warmer water temperatures, clinical disease is frequently
evident from February to November,
whilst in Scotlandclinical diseaseis normally found only in exceptionally warm
summers.
6. Diagnosis : clinical diseaseoccurs
routinely in fish farms on infected waters
so that diagnosison such siteswill be by
gross obserwationof kidney enlargement.
Histological examination of tissue (kidney) samples will provide confirmation
that the kidney swelling is related to the
occurrenceof PKX. The parasitecan also
be observed by the experienced eye in
kidney squash preparations at a 1000 x
magnification using immersion oil.

34

ti'#

Transmission: the mode of trans7.

mission is not yet understood.Myxozoa
have complicated life cycles with several
intermediatehosts.The study of theselife
cycles under laboratory conditions is difficult but essentialfor understanding.For
PKD neither the complete life cycle is
known nor are the presumedintermediate
hosts, the route of infection or all developmental stagesin fish.
8. Prevention: on farms on infected
waters which have accessto bore hole or
well water, young fish should be kept in
this uninfected water for as long as possible. Stocking of naive fish into PKD
infected waters should be carried out as
late in the seasonas possible.
Because the life cycle and intermediate
hosts are not known, prevention by controlling intermediate host(s) is not possible.
What should I do? although PKD
9.
can be controlled by use of Malachite
green therapy, this method is not acceptable for use in fish food species.
As water temperaturesfall in the autumn
the severity of kidney inflammation
rapidly reduces and the normal appea.rance of the kidney is regained. Fish
which have been exposed to PKD and
recovered in this way are then largely
immune and do not react to reinfection in
the following spring with seriousinflammation of the kidney.

Section32
Nlyxozoa : Whirling
Disease/WD

ry

&
#

,i

Fis

Fig.31.3
32.1. Animals swim with a spiral motion
around the transversal body axis, with
abnormal nervous reactions to disturbance producingfast swimming movements until the animals are exhausted.
About 3 - 4 months after first infection,
skull deformations, shortenedgill plates
spinal curvature (Figure 32.2) and shortening of the lower or upper maxilla are
increasingly observed.
Thesesigns occur separatelyor in combination. Brown trout generally do not
show these signs when infected by WD.
The reasonfor this is not known.
6. Diagnosis: In the laboratory by histological examination of skull cartilage
shmples.Enzymatic digests of macerated
skull samples are also used for micro-

1. Causative organism: the myxozoan

Myxoboluscerebralis.

scopic diagnosis. With experience the

parasitecan also be seenmicroscopically
in a unstained squashpreparation (400 1000 x, using immersion oil).The presence of the parasite in the skull causesit
to develop abnormally and particularly
affects the developmentof the ear and the
organs of balance, hence the behavioural
abnormalitiesand easy loss of balance in
infected fish.
7. Ttansmission: in the last few years it
has been demonstrated that water and
mud worms (Tubfex genus) are the
source of infection. In practice this does
not mean that WD can be controlled by
eradicatingthe worms (sterilisation of the
interior pond bottom is of course almost
imoossible).

8. 1
fish
(or I
are l
fica
6-7
ferrr

9. r
pos
free
plas
fish
The
for r
afu

a::i-

2. Susceptible fish species: almost all

salmonid speciesare susceptibleto infection as fry and young fingerlings, but
show no gross signs of that infection
immediately. Gross lesions appear at a
size of about 6 - 7 cm. Brown trout a"re
very resistant to WD.
3. Temperature at outbreak: no specific temperaturerange.
4. Clinical signs: dark colouration of
the posterior third of the body, Figure

,,'

L-

Fig. 32.1

Fis

35
sometimesthe operculaeare open, which
gives evidence of respiratory problems.
5. Mortality: mainly juvenile fish (carp
and rainbow trout) in casesof moderate
infections. Higher mortality rates occur
with heavy infections of juvenile carp eel
and catfish frylfingerlings and juvenile
fish in recirculation systems (Figure
33.1). Mofialities increase with water
temperature.
6. Diagnosis: microscopically on the
gill arches (Figures 33.1 and 33.2) and
on gill scrapeprepa.rations,rarely on the
skin, at a magnification of 25 x and more.
The parasite is worm shaped, has an
attachmentorgan with 2 big hooks and a
sucker surrounded by a ring of smaller
hooks (Figure 33.3).
Dactylogyrus is oviparous, the small
brown eggs can often be observedmicroscopicallytFigure 33.4).

Fig. 32.2
8. Prevention: on infected farms young
fish should be kept in concrete or plastic
(or plastic lined) ponds or tanks until they
are large enough to resist infection (ossification of cartilage). When fish exceed
6-7 cm in length, then they can be transferred to earth ponds.
9. What should I do? ho therapy is
possible. Purchase fish only from WD
free farms. lnstall sufficient concreteor
plastic lined ponds for ,use with young
Iish.
The spore (resistanceform) can survive
for several decadesso that once infected
a farm will remain so.

Section33
Nletazoa z
Ilonogeneans,
Dactylogyrus
1. Causative organism: Dactylogyrus
sp.
2. Susceptible fish species: all fish
speciesbut mainly juvenile and one summer carp"in warm water temperatures,eel
and catfish in recirculation svstems.
3. Temperature at outbreak: no specific temperaturerange.
4. Clinical signs: no specific signs,

Fis. 33.1

Fig. 33.2

7. Transmission: by infected fish,

water, farm equipment or employees.
8. Prevention: stringent hygiene, mainly for fry as well as quarantinefor eel and
catfish for intensive/recirculation systems. Quarantinefor ornamental fish.
9. What should I do? long term
immersion bath using:
An organophosphateinsecticide such as
trichlorfon: lg /3mz water for cyprinids
or 1gl6m3water to allow survival of food
where fish are dependenton natural food.
Igl4mz water for salmonids. Products
such as trichlorfon should only be used
where permission from the appropriate
authoritieshas been obtained.Do not use
trichlorfon in:
1) areasused for water supplies
2) drinking places for animals

36
5. Mortality: acute mortality only for
fry and ornamentalfish with heavy infections (Figure 34.1).
6. Diagnosis: microscopically in skin
scrapepreparations (Figure 34.L), rarely
observedon gill scrapepreparations(25x
magnification). The parasite is worm
shaped,has an attachment unit with two
big hooks and a sucking organ surrounded by a ring of smaller hooks. The parasite is viviparous,the "larva" can be seen
microscopically (the pair of attachment
hooks are recognisable inside the parent
parasite,Figure 34.2).

150 mg/m3 in the recirculation water has

given good results as a long term bath.
Note: mortality is mainly causedby massive gill inflammation so that a check
examination after treatment is recommended.

Section3{
Nletazoa :
Nlonogeneans,
Gyrodactylus
1. Causative organism: Gyrodactylus.
2. Susceptible fish species: all species,
but only presentsa significant problem in
casesof massive infection.
Fig. 33.4
Formaldehyde has only limited effect.

3. Temperature at outbreak: all temperature ranges.

In recirculation systems (eel or catfish)

dactylogyrosis can become a major problem. Use of mebendazole solution, 75 -

4. Clinical signs: no specific signs,

scrubbing and fast swimming movements
can be observed.

Fig. 31.1

Fig. 31.2

Fis'

7. Tfansmission: by infected fish,

water, farm equipment or employees.
8. Prevention: stringent hygiene mainly
for fry as well as quarantinefor ornamental fish, finally, routine bath treatment.
Treatment only should be used in cases
of massive infections.
9. What should I do? long term
immersionbath using:
trichlorfon.lg /3m3 water for cyprinids or
I g I 6 mz water to allow survival of food
where fish are dependenton natural food.
lgl4mz water for salmonids. Products
such as trichlorfon should only be used
where permission from appropriate
authoritieshas been obtained. Do not use
trichlorfon in:
l) areasused for water supplies
2) drinking places for animals.
Salmonids can be treated by immersion
bath with formalin (see Section 25);
baths may be extended to more than one
hour.

1. (
larvr
spec
ts

fish
the p

3. 1

cific

4.(
infec
35-1
one(
dark

5. I
rare.
and r

Fig.

37

Fig. 35.1

Section35
Metazoa z
Thematode
metacercaria :
Eye Fluke
1. Causative organism: endoparasitic
larvae of different Diplostomidae
species,mainly the genusDiplostomum.
2. Susceptible fish species: almost all
fish species depending on the speciesof
the parasite.
3. Temperature at outbreak: no specific temperaturerange.
4. Clinical signs: the eye lenses of
infected fish become cloudy (Figure
35,1) and in the final stage blindness of
one or both eyescan occur.The fish show
dark body cclouration.
5. Mortality: acute mortality is very
rare. Infected fish show poor growth rates
and poor health probably due to the fact

Fig. 35.3

Fig. 35.2
that they have problems with locating
feed.
6. Diagnosis: microscopically on a
squashpreparationof the eye Tensat a25
- 60 x magnification the larvae (metacercaria) can be easily observed (Figures
35.2 and 35.3).
7. Transmission: seeprevention.
8. Prevention: the fish is the second
intermediate host. The primary hosts are
snail speciesand the final hosts are water
birds. An outbreak of eye fluke can only
be avoided by breaking this chain, for
example by netting over the farm and/or
eradicating the snails. The best way is to
carry out both measures.Regular fallowing of pondswill also assist.
9.
What should I do? no effective
treatment of infected fish is possible prevention is the onlv route!

Section36
Metazoa:
Nematolles.
Swimbladder Worm
of Eel,
ttAnguillicosistt

1. Causative organism: the nematode

Anguillicola crassus(or "crassa").A relatively harmlessparasiteof the Japanese
eel (Anguilla japonica), which lives in
"harmony" with this parasite. It was
introduced to Europe in about 1980 pre-

sumably by trade and transport of eel and

is multiplying rapidly among populations
of the European eel (Anguilla anguilla).
First identification in Europe was in Italy
1982,then Holland in 1984, Germanyin
1985, Belgium and Denmark in 1987,
and France and England in 1989. It is still
spreadingto the east- first identifications
in Poland and Sweden were in 1990.
These first identifications follow the
main routes of eel transport lorries. This
parasite has four larual stages, two of
them in the swim bladder.
An invasion with Anguillicola has no
influence on the edibility of the eel, the
edible part is not dapaged.
2. Susceptible fish species: In Europe,
only the European ee1(Anguilla anguilla).
3. Temperature at outbreak: no specific, normal life temperaturerange of eel.
4. Clinical signs: in general, no extemal
signs of infection
are evident.
Occasionally there is a general impairment of health and an increasedsusceptibility to other diseases.After dissection a
swollen swim bladder (Figure 36.1) and
occasionally (dependentupon the severity and length of time of infection) a thickening of the swim bladder membranecan
be seen.When opened,the swim bladder
shows the presenceof different developing or age stagesof the nematode parasite (Figures 36.2 and 36.3).
Onl y i n cases ol massi ve i n vasion
changesin behaviourcausedby the swim
bladder membrane thickenins can be
observed.
5. Mortality: low mortality. Recent
observationssuggesta stabilising of the
spread of anguillicosis. In recirculation
systemsAnguillicola does not seem to

3B
lead to the type of damageexpecteda few
yearsago, but the risk of secondaryinfections is increasing.
It may take 10 - 15 years to determine the
effect that this parasite has had on the
migration and reproduction of eel - will
there still be glass eels returning from the
CaribbeanSargassosea?
6. Diagnosis: dissection of the swim
bladder after opening the abdomen. The
larval stages 3 and 4 can be observed
microscopically in the swim bladder
membrane.
7. Transmission: the main intermediate
hosts are small crustaceans(Copepods).
Recent experiments show that numerous
fish speciesmay play a role in transmission becausethey can carry larval stages
of Anguillicola. The copepods often
observedin sedimentation parts of recirculation systemshave an important carrier function particularly if the system is
stocked with infected eel from natural
watersystems.
Briefly the life cycle of Anguillicola can
be explainedas follows : the viviparous
adult female growing in the swim bladder
ofinfected eel deposit larvae which, after
sheddingtheir first skin (larva 1) get into
the water by passing into the intestine by
the Ductus pneumaticus.There the shedding of the second skin takes place producing larval stage 2 which infects to
copepodsand develops there into larva 3.
If an eel eatsand digests these small crustaceansthe larvae penetrate through the
intestinal wall and get into the swim
bladder membrane.where they stay 4
months until larval stage 4 which then
develops into to an adult and fertile
worm. The whole cycle takes about a
year.

Fig. 36.1

Fig. 36.2

8. Prevention: do not purchase infected

eel for stocking if possible.Avoid sedimentation of sludge in recirculation systems and thus the presenceof copepods.
Optimisehygiene.
z--.

l,lu1t424:t442
t
*
Fig. 36.3

9. What should I do? in recirculation

systems and intensive culture systems
both bath and feed treatment with
Levamisole@is possible.This substance
kills the adult, sub adult and larval stages
3 and4. Apparently larval stagesI and2
are not affected. Because in practice all
stagesof the parasite are present simultaneously, repeated treatments are necessary. This means more stressand higher

Fig.

costs
this r
Euro
nary
Cont
diflur
used
poss

l.
diffe
,,.

and c
The
founr
-(
salm
^r
salm

39

Fig. 37.1
costs.Levamisole@is not licensedin for
this use in every Member State of the
European Union, but use under a veterinary prescription may be possible.
Control of carrier copepods using
diflurbenzuron (up to 0.015 mg/l can be
used without damaging the bio filter) is
oossible.

Section37
Vletazoa : Tape
llbrms, Cestodes
1. Causative organism: a range of
differenttapeworm species.
2.
Susceptiblefish species:salmonids
and cyprinids of all age groups.
The following tape worm speciesare
found in the intestine:
- Caryophyllaeus, Figure 37.1, in
salmonids and cyprinids.
- Proteocephalus and Eubothrium in
salmonids (the latter mainly in the first

Fig. 37.2
part of the intestine and in the pyloric
caecae).
- Triaenophorzs in pike.
the grass carp tape worm
(Bothriocephalus), introduced by the
grasscalp, now found in all carp species,
Figure 37.2.
Ligula is found outside the intestine
mainly in carp and coregonid.
3. Temperature at outbreak: outbreaks of tape worm invasions usually
begin with rising water temperaturesin
spring.
4.
Clinical signs: a swollen abdomen
is seen only in small cyprinids with
heavy infections. In general, fish with
heavy infections are in poor condition.
After dissection of the fish the cestodes
can be seenby naked eye in the intestine
(Figure 37.3).
5. Mortality: acute mortality is very
rare, only in casesof massive invasion,
which in practiceis uncommon.
6.

Diagnosis: macroscopically after

dissection of the intestine. The different

cestodespeciescan be identified microscopically (25 x) by the scolex (head)
shape.It is not easy to extract a complete
cestodeout of the intestinecomplete.
7. Ttansmission: by several intermediate hosts (small crustaceanssuch as
Gammarus),fish, if they are intermediate
hosts (for example pike tape worm Trianophorus: the pike is the final host),
birds and other animals.
8. Prevention: control intermediate
hostsby pond liming every year.Net over
the farm if possible. Purchase fish only
from farms with good hygiene control.
Infection levels may vary year upon year.
9. What should I do? in some areas
medicatedfeeds may be available on pre(Di-n-butyl-tin-oxide or
scription
niclosamide(e.g.Mansonil@).

Section38
Metazoa:
Acanthocephalans
1. Causative organism:
Acanthocephalan
species.

different

2. Susceptible fish species: all fish

speciesand age groups depending on the
Acanthocephalan
species.
3. Temperature at outbreak: massive invasionsare only seenin winter and
early spring.

Fig. 37.3

4. Clinical signs: clear external signs

are not evident in live fish. On opening
the visceral cavity parasitesup to 2 cm

40
quences if consumers see heavily
Acanthocephalan-infestedguts.

Section39
Nletazoa : Fish
Parasitic
Crustaceans,Fish
Louse,Argulus,
1. Causative organism: small fish
parasitic crustaceans,Argulus spp.

f
Fig.

2. Susceptible fish species:

speciesand age groups.

all

8.

exail

Fig. 38.2
long can be seen macroscopically on the
intestinal wall.
5. Mortality:
dependent on the
species of Acanthocephalan,usually not
heavy.
6.
Diagnosis: with naked eye after dissection of the intestine, different species
can be identified by the head (proboscis)shape(Figures 38.1 and 38.2)
when observedmicroscopically (25 x).
7. Tfansmission: by intermediate
hosts, amphipods,essentially Gammarus.
8.

Prevention: random sampling and

Fig. 38.3

examination by the fish farmer, mainly

during the winter seasonand when purchasing new fish. General pond hygiene
and yearly liming.
9, What should I do? in some areasa
(Concurat@ or
medicated feed
Mansonil@) may be available on prescription after identification of the parai nvasi ons
In
heavy
s i te .
Acanthocephalansmay perforate the gut
wall with their proboscis (Figures 38.3
and 38.4) and cause considerable damage with severe local inflammatory
response- therefor massive invasions
should be controlled. Such invasionsmay
have also commercially adverse conse-

D. J. Alderman

Fig. 38.4

3. Temperature at outbreak: all temperature ranges but mainly in the summer.

sub
forn
inati

4.
Clinical signs: apart from occasional rubbing the fish do not show abnormal
behaviour.Argulus bites can lead to small
often reddish inflamed wounds which are
indicative of the presence of these parasites.

9. \
phat
l3m
to a
dep
for s
fon
sion
beer
l

5. Mortality: acute mortality only

with young fish in case of heavy infections. However Argulus can act as a carrier for viral (Spring Viraemia of Carp) or
bacterial pathogens(CE).
6. Diagnosis: with naked eye the creeping, almost transparent parasitic
Crustaceaor the bite wounds can be seen
on the fish skin (Figure 39.1).
7. Tfansmission: by water or infected
fish, live feed for ornamental fish from
infected waters.

Argt
able
with
Nott
and
eas
tant

Fis

A1

if-ji.!,i
il+r.g:.,r;
t

Fig. 39.2
ovary of the females) on the gills (Figure
40.1.1.In case of a severe invasion a
decreaseof condition (Figure 40.2) and
gill problems (and thus of respiration
problems)can be observed.

Fig. 39.1
Prevention: random sampling and
8.
examination by the farmer himself or by
gill samples (fixed in
submitting
formaldehyde or J07o alcohol) for examination.
9. What should I do? an organophosphate insecticide such as trichlorfon 19
l3m3 water for cyprinids or 1gl6m3water
to allow survival of food where fish are
dependenton natural food. 1gl4m3water
for salmonids. Products such as trichlorfon should only be used where perrnission from appropriate authorities has
been obtained. Do not use trichlorfon in:
1) areasused for water supplies
2) drinking places for animals
Argulus is not an "obligate" parasite,it is
able to move and survive just in water
without a host (Figure 39.2,25 x).
Note: Argulus is a blood sucking parasite
and can actively transmit infectious diseasessuch as SVC, therefore it is important to controTArgulus.

Fig.40.1

Section-10
MetazoaFish
ParasiticSmall
Crustaceans: '
n.t

Ergasuus
1. Causativeorganism: Ergasilussp.,
a small fish parasitic crustacean.
2.
Susceptible fish species:all species
and age groups, but especially tench.
Also frequently found on brown trout
from extensivewater systems.
3. Temperature at outbreak: June to
the end of September.
4.
Clinical signs: fish behaviour is
normal. The parasitescan be seenby the
naked eye as small white points (the

Fig.40.2

5. Mortality: variable, dependent on

fish species and degree of invasion.
Becauseof the resultant poor condition a
reduction in growth rate (up to 50Vo)can
be seen.Also the fish are more susceptible to other diseases.
macroscopically
6. Diagnosis:
(Figure 40.f ) or microscopically
(Figures 40.3 and 40.4) (25 x magnification).
7. Tfansmission: water and infected
fish.
8. P reventi on: roul i ne examinalion,
mainly in June and after purchasing by
the experiencedfarmer.
9. What should I do? an organophosphate insecticide such as trichlorfon : 19
/3m3 water for cyprinids or 1gl6m3water
to allow survival of food where fish are
dependenton natural food. 1gl4m3 water
Products such as
for salmonids.

*#

Fig.40.3
trichlorfon should only be used where
permission from appropriate authorities
hasbeen obtained. Do not use trichlorfon
in: 1) areasused for water supplies
2) drinking places for animals
Only fertilised females live in a parasitic
mode of life (Figure 40.4),bil an overwintered female can produce about 8 million offspring between June and October.
Therefore light infections invasions with
Ergasilus should be controlled and
infected fish should not be stocked in
untreatable water systems (e.g. gravel
pits). Ergasilas damages fish with its
hooks and by grazing the epithelia and
mucus cells causesgill swelling and gill
necrosis. Also a higher susceptibility
to other (parasitic) diseases can be
exoected.

Fig.4

Fig.40.4

Section41
Metazoa: Piscicola,
Leeches
1. Causative organism: Piscicola
leech.

5. Mortality: acute mortality can

occur in fry or fingerlings, during major
outbreaks. High mortality mainly in
tench or pike (Figure 41.1) as well as
other species living in open water systems.
6. Diagnosis:leechescan be seenwith
the naked eye, they are up to 50 mm
length (Figure 41.2), and produce red
inflamed bite wounds.

2. Susceptiblefish species:all species

7. Tfansmission: by water, fish as
and age groups.
well as plants or stones from infected
watersystems(aquaria).
3. Temperature at outbreak: all temperatureranges,a high multiplication rate
between late spring and autumn.
4.
Clinical signs: no specific behaviour will be observed. occasional rubbing, rapid swim movementsand wounds
from bites may be noticeable.

8. Prevention: routine examination

after purchase,pond hygiene, liming.
9. What should I do? an organophosphate insecticide such as trichlorfon :
1g l3mz water for cyprinids or Ig/6m3
water to allow survival of food where
fish are dependent on natural food.
Igl4mz water for salmonids. Products
such as trichlorfon should only be used
where permission from appropriate
authoritieshas been obtained. Do not use
trichlorfon in:
1) areasused for water supplies
2) drinking places for animals
Quicklime dip bath (pH 10 bath): 1g in 2l
water for 5 seconds(not for pike, danger
of eye damage). Return fish to clean
water immediately.

Fig. 41.1

Some
subjec
treatm
tems d
Part
and h1
tems:

Main r
recirct
the na
nation
This ir
heated
logica

Advar
- high
er mel
- higt
fish tr
year c
one s
produ
calp o

43

'",'i.
,?'

,': -:

,12:l:;:

1 ..:

Fig. 41.2

Section42
Eel and Catfish
Warm Water
Aquaculture
Mainly
Recirculation
Systems,A new
Area with its own
Problems.

- no hazardousover-wintering of fingerlings necessary.

- becauseof the heatedwater successful
production of specieslike eel or catfish
(Clarias sp.)in colderregionsis possible.
- low needsfor make up water (about 2 l}Vo of the systemcapacitya day).
oflocation and area,only
- independence
energy must be supplied.
- a high productivity for big systems.

either for a continuous presenceof staff

and/or the use of expensive alarm systems.
- a backup electricity generator is also
necessary
- economics force high stocking densities, therefore there is a high hygienic
risk.
- biological filters clean the water of
unwanted metabolitesbut not necessarily
of pathogenic organismsand parasites.
- in recirculation systems full control of
antibiotic treatment is difficult. Active
antibiotics can accumulate in the bio filter. Resistantbacterial strains can remain
here and therefore increasing antibiotic
resistancecan be observedin these systems.

Production under controlled conditions?

With recirculation technology, closely
controlled environmental conditions are
required so that an operation of this type
can be compared to an industrial plant.
Theoretically this is possible: the fish can
be examined,the water can be monitored
analytically and treated at any time.
Disadvantages:
- high costs for investment - tanks and Therefore it should be possible to create
optimal conditions for fish in recirculatechnical plant, measures for isolation
tion systems.
(for new or rebuilt farms).
Experience however shows that trouble
- power demandsfor:
x keeping water temperatureconstant free and continuous operation of such
(22-26'C\
systems is rarely possible. Numerous
* c o n ti n u o us
biological and chemical factors affect the
pumprunni ng
* operation of aerating systemsor use recirculation process. Oxygen, PH,
ammonia,nitrite and nitrate values can be
of (expensive)oxygen supply units.
Some overlap with previously discussed
but rapid changes will occur
monitored,
proper
operation
upon
the
dependency
subjects is unavoidable. Techniquesand
Oxygen levels fall
little
warning.
is
a
with
There
above.
plant
mentioned
the
treatment of diseasesin recirculation sys- of
pH
will also change
feeding,
after
a
need
and
thus
failure
risk
of
technical
tems differ from those used in ponds.
production
Part 1: characteristics of
and hygienic needs of recirculation sysFattening Range
Fattening Period
Species
tems:
Main characteristic of fish production in
recirculation systems is the reduction of
the natural grow out period by the elimination of climatic factors (cold season).
This is made possibleby multiple use of
heated water after mechanical and biological water treatment.
Advantages:
- higher water temperaturemeansa higher metabolic rate, hence faster growth.
- high intensity: from a one cubic meter
fish tank for example 40-60 kg calp a
year can be produced (starting with 50g
one summer carp). Conventional farms
produce this amount from two summer
carp on about 500 62 pond surface.

Eel

l4

l7 months

t\-/'ilto

EuropeanCatfish

15 - 18 months

15- 1500g

cary

12 months

50 - 1300g

Catfish I Clarias sp.

t 0 t2 months

5 - 1 O O Oo

Poultry

1.75months

5-1600g

Pigs

4 months

20 100kg

Veal

3.25 months

60 160kg

Thble 42.1: Comparison of fattening periods of dffirent domestic animuls

44
producing changesof the NH3/NHa ratio
or nitrite "shocks" lead to stress in fish
and may cause toxicity and increased
susceptibilities to disease. In principle
changesof this kind can be controlled by
the farmer, but often too late.
Fattening periods - compared with
warm-blooded domestic animals
Compared to chicken or pig farming the
fattening periods for fresh water fish are
relatively long (also for intensive culture). Table 42.1 gives some examplesin
which the mean fattening period for
fish is shown to be 4 times longer than
for warm-blooded animals. From the
hygienic point of view this means that
parasitesand other pathogenic agentscan
infect the fish over a much longer period.
Disinfection
All in - all out systems have definite
advantages from the hygienic point of
view, as they mean simultaneous stocking and emptying of production units
with animals. In recirculation systemsfor
fish this is not really possible. The disinfection of the whole system,pipes, tanks
and biological filter units (for example a
trickle filter) is not possible without stopping the biological filter system. It takes
several weeks to run up (colonise with
bacleia and protozoa) a filter system
which has been stopped and disinfected
and during this time the system is out of
production unless a duplicate system is
available at extra cost.
Emptying the whole system means a
break down of the biological filtration
process. Therefore this part of a recirculation system is a permanent reservoir
of pathogenic organismsand protozoa.
Fingerlings for intensive culture
Obtaining good stocking material (glass
eel, eel fingerlings, one summer carp or
catfish fry) is a problem for recirculation
systemfarmers. It is difficult to obtain an
homogeneous group of fish from a single producer and the parasitological /
bacteriological health statusis often inadequate.
It is very important to stock the system
with parasite free fingerlings and therefore a prestocking examination is really
needed.
Genetic suitability of fish for intensive
culture
In land animal production, the animal
"material" has been adapted to produc-

tion conditions by intensive selection

over severalgenerations.
In intensive fish culture there are high
requirements upon the metabolism and
immune system of the fish. Selection for
recirculation system adaptedfish has not
occurred. European catfish fry for recirculation systemsare mainly derived from
pond farms in easternEurope. Glass eel
are caught in contaminated coastal
regions of Europe and one summer ca4)
are purchasedfrom pond farms selected
only for pond conditions.
Therefore it is not surprising that eel and
European catfish grow out unevenly and
some mortality is to be expected.
Farm managers are strongly advised to
purchaseonly best quality stock (despite
the greater cost) or produce fry themselvesfrom recirculation system adapted
broodstock. Slow growers should be
graded out and discardedbecauseuse of
suchfish is not economic.
Causes of disease in recirculation svstems
The rangeof diseasesin intensiverecirculated culture systemsis much the same
as in more extensive systems, but the
effect of water quality is more immediate.
1. Diseases caused by poor water
conditions
1.1 The role of pH
The pH value indicates if the water is
acid (pH <7) or alkaline (pH >7). For
recirculation systems a pH value around
7 is recommended.To accommodatethe
needsof the bio-filter a slight tendencyto
the alkaline range is acceptable.
If the pH increasesto pH8.0 then:
- Excretion of nitrogen from fish via the
gills is blocked, the bicarbonatebuffer in
fish blood exhausts producing alkalosis
(harmful increaseof the blood pH value)
followed by ammonium autointoxication
(self poisoning). If this situation persists
it will causegill necrosis.
- The total nitrogen content in water at
pH8.0 is dissociated:96 Voas NHa+ and
about 4 % as NH3 (NH3 is highly fish
toxic). At pH9.0 the dissociationis l07o
as NHa+ ard 30Voas NH3. Considering
that the NH3 content should not exceed
0.01 mg/l the importance and danger of
increasingpH values in recirculation systems is obvious.
Therefore sufficient acid binding is
important. Togetherwith.carbon dioxide,

calcium bicarbonate forms a buffer system stabilising the pH value.

- The pH should never fall below 6.0
becausenitrification can break down.
1.2 Ammonium/ammonia and nitrification
Almost all protein metabolites in fish are
excreted as ammonium (NH4+) through
the gills.
Under aerobicconditionsammonium is
oxidised in two steps by bacteria in the
bio filter systems (Nitrosomonas and
Nitrobacter).
The bacterial breakdown of ammonium
to nitrite and then nitrate can only take
place under completely aerobic, oxygen
enriched conditions. Reduced oxygen
levels e.g. after feeding can result in
incomplete breakdown of ammonia e.g.
only to nitrite, which is toxic and should
not exceed 0.1mg/1. Some cases have
been reported in eel farms where a continuous nitrite content of 6 mg/l occuned,
which is almost in the range of acute toxicity. On such farms, of course, the productivity is zero due to toxicity leading to
low growth rates.
Therefore low oxygen should be prevented in order to achieve a continuous breakdown of metabolites. If possible (technically and economically) it is recommended to feed the fish their daily food
ration oyer a longer period to avoid
oxygen demand peaks (use automatic
feeders).
1.3 Oxygen supply and Total Gas
Pressure
The fact that the stocking density of tanks
and the capacity of bio filters are closely
related to oxygen supply often lead the
fish farmer to use oxygen from pressure
tanks or so called oxygen generators.
Using good distribution systems, high
dissolved oxygen values in the water are
possible,but these conditions can favour
the development of gas bubble disease
(chronic or acute).
As an example, in a new eel fattening
systemoxygen saturation values of2TOVo
were registered (22 mg O2l24"C), but
with a Total Gas Pressure(TGP) of only
1067o. In this case supersaturationwas
causedby the unregulatedinflow from an
oxygen generator, low saturation of
nitrogen (65Vo)lead to a TGP of 1067o.
The influence of feeding and resting
times on the Total Gas Pressure is also
very high. Peak values of TGP > I20Vo

are I
t y. R
after
avoi
Gas
whic
100
fish
achi
fish,
recir
minr
Ever
oxyf
men
18r
nitn
100
1.4

Une
diss<
men
befo

Usin
- sed
- wh
- bel
- tric
- dru

Eact
vanti
ually
shou
the t
for f
tion
abou
(BO
inclu
The
unit
faeci
very
)

The
for I
feed
1) cc
ents
minc
2) hi
utilir
uct (
3) k
powl

ile,&\se sluerr1nupelse8rpunpue ;epmod

'luelsrsoreruoceq01I'ueesqcrql\ urc aI <
:peJeprsuoceq pFoqs splorJ pJeJ ulo{ uol}sulluBluoJJelB,{\,,rrol(g
'(r{srJ)lcn
Jo qsIJ re8rel Suoure,(llurcedse'pe^resqo 3urmo11o;eql ur serouerJrJeq 'esnec
eq uuc .{relocer snoeueluodsJo sesuJ cr;rceds ouo uo peseq srsou8erpB .4d,olls -po.rdleurg ,fiqenb qBH e pue uor]sqrln
'ezlS rlsU pue uollelseJur.;o ,{1rsue1ur re^teu.(11ecr1cerd
qclq.Lrelru eql sr su8rs poo; pru4do 8ur,r.r8.,(lqrqqse8rpq81q (Z
'secrrBlsqns,lNereql Jo slsoc eql pur-ur
;o Surpuedep'ob1;otdn :f1qe1rotr41 'S egpadsun;o eruer; eloq,4d,
V 'eseoJcurse
-ssol - oJezuele Jo q8noue 1ou sr qltro.r8 ur Suueeq sleJeurrupu suTurelrl 'slue
'suo4ceJurIeuelcsq
snqJ 'II le lou ro q8noue peeJ tou op
-u1nufrusseceuII Jo flddns elelduroc (1
,t-repuocespue lq8reurrJo ssol '8uq1e,trs (drec 'qsrpec ueedo.rng'qsrJlec'1ee)qsrg
:peeJ
:SA\olloJ
se st uals,(suotl qsIJ Jo uorlcnpo"rdpue lueluoJ eql roJ
1pB 'e1r1edde
Jo ssol leluT 'slee pelceJJ
ur speequollo^\s'uoDslDue^Jed,(q'sure1 -lncJrceJe;o ,fto1srqsesesrppc1d,$ y
eql
luegodurr ere se,r.rlcefqo3ur.Lro11o;
-qoJduorlerrdseg '(selcsnfuocye,r.o,{urqs
'>IueJqlno
'Z
8u;paaypue dlgenb poog
lueJedsuu4rruesse uees eq uec s1s.,(3
'1'97 arnftg) qfuel urur 0I - S 's11F eql JoJe^rsrcopsr lueruuoJr^ue1o ,fiqunb
'(.(ruqs ,{re,l
Jo eeilew?l frepuoces Suoure s1s.(c1e,,lo eql - ereq ure8e 1ng 'suorselur crlrsered
alrq,Lr e8rul reqpr :su8gs:1ec;uIIJ
'V pue seseesrpsnorlceJuresnucel8urs eurn ers qsqlec;o secee;) fcuelsrsuoc leceug
-ue3;o esecur sosrJeuonenlrslueJeJJrpV
pue .{1qenbpooJ eql uo spuedeposIEtrun
'u,roll)l
'alru
eJu
>IeeJqlno
poulqruoJ
eql
eJ?
speJJe
JallrJ
3
sseue^IlceJ$e
eqJ
lou
IBruJou
lcruqceu
Jo
'e1s31v\
pooJ Supnlcur
ICrurIceq] JoJ suorlrpu9c pue uorse^ur - surels.{s uorlelncJrceJ ur eseosrp JoJ
yo ,(ezlrqledeqJ 'roloruBrp eJoru pu uru
sesneceldurrs ees ol e.rer^{re,r.sr lr snrlJ
'(pueureq ue8fxg pcrSoyorg 'sCOg)
,(ep red else.tr crrreSro 3 V - Z lttogu
E ;o s1s.{ce8rel ur pourluoc eJ qcrr{.r
,$uryens p3;o seer8epge 'r{srJlecpuq Iee ezrs qsrJe1qe1ur ,(Fe1n secnpordqslJ 3{
seJods q8norqt :uollcnpordeg
'g
1) elsum crue8roJo uorl
-crued 'uorluJnoloJJelrl elrq.r o1 ,lo.o11e.{ -cnpord q8rq u qlurr surels.{sSuluelp; ro;
'ecuBlsISeJ ,(q pecuepr,rare^rl eql;o uorlereue8eplueUodurr f.re,r sr srqJ 'lrun JelllJ orq eql
o1 dn sesee.rcep
,fiqrq4decsnsspJe.,raJeuv
:sursruu8roelrlssnuc lcelord o1 ,(1e1e1duroc
peloruer oq pFoqs
'sSuqre8ur;
3
o1
sse13
ruor;
JeIIlo
ro
selrsered
yo
ocuosqu
er{l
selcrged
elsem
crue8ro
eq; 'ereq ^,(gen
1ee
E1
1ee
1ueql Jo IIe '.leo - serceds qsrJ peurreJ ur surelqord.{11pnbrel,r ro pee; o1lurod
-pl^lpul passnJSrp
lou oJuqrrqm se8elue,t
Irro4 :selJeds qsg e1q;ldaesng 'Z
seSueqcpcrSoloryud cr;rceds om1 ^,(p6
-pslp pue se8eluu.tpuseq ure1s,{sqceg
JJeISu,!\O SrrrJeJaql
'ueozorods
ao1pn7uo
umtpt4st(c
e'
uodn
flqelu,eur
qcrqt\
suoqeuruexe
JelIrJ
urrup 1e;
.I
-owra(I .'rusruBSJo aallBsnBJ
o^rsuelur
rellrJ
eplcul Jo 1ol s eAIoAur sJolceJeseql
relllJ llaq Jo uorlecrJrluepl 'sJolJBJ IBJeaes Jo
'eseesrpIee crJrc uollBulqruoJ e ol enp s,,(e,tr1e
ere 8upeo1
roleredes IrIqrK -eds e ;o elduruxe u sr runrprls,(corureq ellsered .rol Jo sesecur ,$qugour lq8qs
s>IrrBluorllueurpes puu seler r{laor8 ,ttol 'e1r1eddeJo ssol
:3urs;1
'ds urnqpasttouta1
se IIJns pegoder su8r5 'sercuercrJep
prce
'JellrJorq eq1q8norqt SurssedeJoJeq
,$pg ro g urruetrl 'Suruosrodrunruoturue
'(syesueururoc
cgrceds
urels^{s
uor}Inc
su8rs
ou
ere
eJeqJ
fyeleldruoc lno peJellrJ eq pForIS lueu
lsorule
;o
.,lucrssulc,,
'eyqeredesur
-rrrerJo dnor8 eqt o1 Sur8uoleq)sellntrere
.,$qenb
re1e,r
-rpos urroJ pelsur lnq Jele^\ ur eAlossrp
(setcedsluere;;rp) 'ds untprys,bolura(I pue uorlrlnu surels,{s uorlelncnceJ uI
lou op qcrl^\ saceBJpu? pooJ uel?eufl
(gg uoqcesees'serceds 'ecuegodurg leer8;o sr sure1s,ftuopel
lueregp)'ds (urom 1yB)sru{.7o1&coq -nJrlJar a8rel u1 poal pa$updo go as11
lueulaeJl JelE.tr IBJluErIJeI,{ n'l
(67 uo4ces ees) 'ds outpoq)lq .,(11pnbrepurq eql 'obajr
(lZ uoqcesees 'esuesrp
'(obt uurIl sseleq ppoqs) Jo dCI e ot speel uolleJnlus ueSorlp
lods elrqrr) sutl4lnut snutqlqdo{qryc1:srue1s.(s
qcns Jo lueure8eueureql uo
Suuopnodsselpue ,(trpqetsJslB,^Jeileq lrrol y 'obO1ZJo uorlemtes e 'y8ur 91
ueeru plno.{\ sql eldurexe Iee peuo4ueur
lceggee,rrle8eue eABqpue pelresqo ueeq sueeurlueluoc leg;eq8rq e '1ue1uoc1ey'Jolleqeqt relletuseq1 'sluauod e^oqu eql u1 'eyqrssodeJBsenlul ue8fxo
,{1luenber;eleq solrsered8uu,ro11og
eq;
'surels.{s
uorlelncJrceJ
pecnpolur
ur
eq
-ruoc
pnp1,rl.1pq
er{l
qBW 'ob1OI Jo senle^ dCJ qtr.4Aue^g
Jo ezrs elcqmd ^\eJ
'peuIIu
uec selrseredqsrJ ..eprslno,,1e ,ftoeq1u1
poogeq1lo ,{1ggq
:uu s1e11ed
-Bls Jalu,r{ol lue^olor srotreJluepodtul -re1ep1ef lou eJBsuralsds uorlelnJrrJeJ
s uoll E ls aJul Jrll sB Jud' g
JoJ senls^ runrurldo eql Je^e.&\oq'qsrJ
.SI
roJ
soterquror8 lseq ot Surpeel'pa^erqce
-reurru pu suilulr^ 1o ,(1ddnselenbepueq pFoqs senlel runrurldo 'Suruuegqsry
'sprce e^rsuelw q 'popro^ oq plnoqs o/00I
,{pe; peprnpsun Jo ,(yddns elenbepe ueql eroru Jo senle^ dcJ ol speol qcrqa
'sprce
ue8,{xo
Surpnycur
uorlernlesredns
s?C
'urelqo.rdsql pro^s
ourrue Jo uorlrsodruoc ,(lr1enburelord :eJsJolceJlueilodur lsour eql
,(eur (poued.,(epeuo rolo roqloue reg?
urseq euo Surpeeg)SurpeegSur,rlorrea',$
-lluotu elnJe esneJr.reJpue elqrssodere
suortJaJurIBJT^(8
suo4ceJurleuelcuq (1
suolsu^uretrsered(9
syesueururoc
(g
senbruqcelSurpee;pue
peeJ(?
'$rrcnb
,{lrrcnb re1e.u.(E
lueureSeueur(7
ecrlep uorlelncrroergo ldecuoc (1

'..ernlJruts..leJoeJprlos puu poo8 se

o
e.,
ou
'i

J
IM
S

.{
1
o
a,nu

as
m
ET

q3
's
eq

{r
s{

su

CI

pl
po
-p
-lu
-{si
-lu

ol
-oJ
-x
'po
-u
eA?

pIn
'3'
uI I
ue
ue
e{3
lunI
pu
oql
sl u
qE
EJ?
.gIJ

0'9
-sd

46
6. Diagnosis: cysts can be seen with
naked eye on dissected gill arches
(Figure 42.1). Wirh 160 x magnification
it is possible to see the sporesinside the
cysts.
7.
Thansmission: with infested glass
eels, which often can be clinically apparently symptomless.When infested material entersthe facility - it must be considered infested as a whole. It seemsthat for
a clinical outbreak some specific and not
yet defined conditions must be fulfilled.
Thus, the degree of clinical manifestations vary completely according to the
type of recirculation system.
8. Prevention: suitable and effective
prophylactic control is not yet possible.
Inapparent latent infestations cannot yet
be identified. But anyway, parasite-free
restocking ee1material must be preferred.
9. What should I do? Fumagillin
mixed to eel feed 1 g / kg,2 - 3 7o of living weight / day,7 - 10 d is effective as
has been demonstratedby the Fish Health
Service of Lower Saxony. Damage to the
bio filter due to fumasillin was not
observed.

Recirculation system specific'ocommensalstt

These are a group of organisms which
can live in the system. If they develop
and multiply massively, they can also
occur in the fish tanks, where mainly
mites can colonise the fish. Mites are
small spider like animals, which are
known from warm-blooded animals
where they cause different forms of
mange.

mites
3.1. Causative
organism:
(Acara). The exact species is not yet
determined,but it is a aquaticform. It has
eight legs, is up to 0.5 mm in size and
motile. These mites can be observed on
fish between the secondary lamellae of
the gills (Figures 42.2).

3.4.9.What should I do? treatthe whole

system with trichlorfon. The water temperature during the day of treatment
should be below 20'C. Dosage: I g
trichlorfon in 2000 I of tank water. Two
repeattreatments.one week apart.
4.

3.2. Susceptible fish species: mainly in

eel systems. Also found on catfish
speciesand carp.
3.3. Reproduction: by eggs and by one
or more so called nymph stages (six
legs). The details of these life cycles are
not known yet.
3.4. Clinical signs: depending very
much on degree of invasion. Severenervous behaviour of eel. Rubbing of gill
operculaeuntil the opercular skin is damaged. Severegill swelling and an increasing production of mucus in the areas
where the mites are located. It is believed
that the mites feed upon gill secretion
products and epithelial cells. The eels
stop feeding. Mortalities are due to secondary infections. Comparableto mange
in warm-blooded animals and could be
termed fish mange.

Bacteriallnfections

Bacterial infections are frequent in recirculation systems. In 907a of such cases

the infections are by facultative fish
pathogenic pathogens and it is clear that
factors such as water quality and nutrition play an important role, leading to a
break down of the fish immune system
which then cannot withstand the massive
pressureof pathogensin the system. In a
later stageof this process internal organs
are infected which can lead to acute morrality.
Susceptible fish species : carp, eel, catfish and other fish kept in recirculation
systems.

Bacteria :
- motile Aeromonads, for example
Aeromonas hydrophila, Aeromonas
sobria and others (see section 16)
- Pseudomonads,fluorescing and non fluorescing
3.4.5. Mortality: dependingon degreeof
invasionand sizeof eel.Casesof massive - Cytophaga/F lexibact er sp.
invasions with severemortality rates are - Enterobacter (e.9. Edwardsiella tarda,
known.
seesection19)

Kee
orna
rece
in gi
for r
kept
The
colo
into
seve
taI I
shut
prod
bers
bree
cust
impr

SOml

3.4.6. Diagnosis: only microscopically,

scrape preparationsof the infected areas
(a high degree of mucus) on the gill at a
65 x magnification. The mite can be seen
immediately.
3.4.7.Introduction and transmission:
not known, probably normal occupantsof
recirculation system filters.
3.4.8Prevention: not known, the mites
come from the biological filter.

Therapy : after bacterial isolation and

antibiotic sensitivity tests, medicated
feed treatments can give good results.
The right antibiotic mixed in the feed will
not affect the nitrifying bacteria in the bio
filter.
On a long term basis resistance problems are to be expected in bacterial fish
pathogens in recirculation systems
because residual antibiotics can persist
for a long time in such systems.
Viral infections

',1ii.
r;.

Fig.42.1

sus
infe
in rr

-'i'i..zt.

.is

Because of the high water temperatures

in recirculation systems, viral infections
such as SVC for ca4) or eel are not to be
expected and have not been reported so
far. For catfish the situation differs, in fry
and fingerlings an Iridovirus has been
detectedwhich causeshigh motalities in
recirculation systems. The origin is
unknown and therapy as for all viruses is
not possible. It is not yet clear whether
Clarias (African catfish) speciesare also

ciali
mair
tom(
of tt
bek
conc
The
cial
troul
pricr
for a
Due
conc
to tt
have
ities
dise
fish
brea
rang
dire<
bloo
to de
than
Ther

47
susceptible to this virus. In general viral
infections do not play an important role
in recirculation systems.

Section43
Diseasesand
Problemswith Koi
Carp and other
Cold-Water
Ornamentals
Keeping koi carp and other cold-water
ornamentalshas become very popular in
recent years. These fish are mainly kept
in gardenponds. but for overwintering or
for sales purposes, these species can be
kept in aquaria or ponds as well.
The origin of koi carp is JaPan and
colourful breeding forms are imported
into Europe. In Israel, USA and Italy,
several koi carp and cold-water ornamental fish (for example, goldfish species,
shubunkin, etc) producersare now able to
produce good quality fish in large numbers as well. In northern Europe koi carp
breeding farms are rare and therefore the
customers here continue to depend on
imports. Because of the large demand,
some farms in norlhern Europe are specialising in trading in these fish. The
main periods for sale to private customers are spring and summer. Outside
of the main sales period, these fish may
be kept and fed up under rather intensive
conditions.
The ornamental fish trade has a commercial value higher than farmed rainbow
trout production and koi broodstock
prices of f5,000 or DM20,000 or more
for a single fish are no longer uncommon.
Due to intensive stocking and feeding
conditions in the salessites, and also due
to the fact many private owners do not
have enough knowledge of the complexities of keeping fish, management and
disease problems with these ornamental
fish are increasing. The majority of outbreaks of disease problems across the
range of cold-water ornamentals have a
direct link with the environment. Coldblooded animals are much more sensitive
to degenerativeenvironmental conditions
than are warm-blooded animals.
Therefore, it may be necessarynot only

to employ medication, but also to

improve the environmental and management conditions after diseaseoutbreaks.
Most of the problems first appear after
reduction of environment quality.
The most important environmental factors having adverseeffects on these fish
are:
. chemical water quality: for example
high amounts of ammonia in combination with high pH-values can lead
to toxicity; normal ranges are
describedin section42.
. physiological water quality: supersaturation of nitrogen, oxygen and carbon dioxide lead to chronic problems
or even to gas bubble disease(see
section7).
. biological watet qualitY:
high
water
in
the
waste
organic
of
amounts
reduceoxygensaturation.
. temperature: high water temperature
may reduce oxygen saturation; low
water temperaturedecreasemetabolic
activity.
. solarradiation: bright sun, particularly UV may causeskin Problems.
. adaptation to other environment systems: for example, different water
temperatures,different gas pressures,
etc.
. handling: grading, weighing, netting,
etc, can all lead to stress.
The following recommendations(mainly
for trade facilities) to prevent problems
due to environmental factors can be
expressedas follows:
. After receiving new fish: quarantine
and examination by a fish health service or veterinarian
. Reducing stocking density as far as
economically reasonable.
. Reducing feeding intensity as far as
economically reasonable.
. Water quality control in a recirculation system - employ a biological filter.
. Bacteria control by using UV or
ozonewatersterilisation.
. Proper aeration of water, prevent of
supersaturationwith nitrogen.
. Avoiding excessivehandlingas much
as possible: grading,weighing,etc.
. Minimum use of medications.
The most important diseasesobservedin
ornamentalfish are:
Viral diseasesin cold-water ornamentals:

Spring viraemia of carp (see section

11) - rarely obser.'red.
Carp pox.
No treatmentof viral diseasesis possible.
SVC may cause mortalitY; cary Pox can
have an adverse effect on the value of
broodstock. Optimising environmental
quality as well as the purchaseofdisease
free fish must be recommended.
Bacterial diseases in cold-water ornamentals:
.
.

Erythrodermatitis (see section 15).

Ulceration becauseof facultative bacteria. mainly Aeromonas(seesection
16) and PseudomonassP.
. Enterobacter,
example,
for
Edwardsiellosis(see section 19) in
intensive systems.
' Cytophaga andFlexibaclerinfections
on gills and fins (fin rot), as well as in
the intemal organs.
. Mycobacterial infections (fish tuberculosis).
Antibiotic treatment for most of these
bacterial diseasesis possible, after carrying out antibiotic sensitivity tests.
Treatment may be by feeding medicated
food, by immersion baths, bY local
antibiotic treatmentof ulcers or by injecting. Fish tuberculosis cannot be treated.
Slaughter of diseasedfish must be recommendedin most cases.
Fungal diseases in cold-water ornamentals:
Secondaryfungal infections are frequently observed in koi carp and other coldwater ornamentals. Treating the primary
cause and optimising environmental
quality may reduce the Problem.
Immersion bath treatments using malachite green or formalin may be used.
Parasitic infections in cold-water ornamentals:
The most important
infections are :

and frequent

Protozoa: Ichthyophthirlzs (see section

21), Trichodina (see section 29),
28)'
(see
section
Chilodonella
Glossatella(seesection30). Coslra(see
section 25) atd Cryptobia sP.
Trematoda: Dactylogyrus (see section
33), Gyrodactylus (see section 34).

48

Fig.43.1
Crustaceans: Argulus (see section 39),
Lernea (anchor worm) - a parasite frequently observed on cold-water o[ramentals (see Figure 43.1) - treatment
may be successful with the use of
trichlorfon.
Most of these parasitic infections can be
treated by immersion baths using various
medications. However, it is also very
important to improve environmental conditions in order to avoid further problems.

Section44
Disinfectionin
Aquaculture
Disinfection of:
1) eggs
2) equipment
3) ponds and basins
1.
Disinfection of Eggs
For egg disinfection in aquaculture
iodophores are preferred, such as
Buffodyne@ and Wescodyne@in Britain
and Actomar K30@Germany.
An iodophore contains iodine (the disinfecting agent) and surfactants which
ensure that the iodine reaches the surfaces to be disinfected. The iodophore
should be diluted in clean water as directed by the manufacturer. Remember that
the effective concentration of 100ppm
available iodine neededto disinfect eggs
does not mean that you should dilute the

iodophore at 1 in 10,000, but as recommended by the manufacturer.

Newly fertilised eggs may be disinfected
with iodophore solution, but such delicate green eggs must be protected by
diluting the iodophore in 0.9Vo saline
rather than plain water. This preventsthe
start of water hardening of the eggs - the
intake of water which occurs when
stripped dry fertilised eggs enter water
for the first time and which would also
pull the iodophore into the eggs and kill
them. Once eggshave eyed up the use of
saline is no longer necessary. Eggs
should be exposed to the iodophore for
ten minutes.
2.
Disinfection of Equipment (nets,
boots, etc.)
Equipment must be cleaned thoroughly
before attempting disinfection. Mud prevents the disinfectant from penetratingto
the surfaceto be disinfected.
2.1
Iodophores diluted to give 100
ppm available iodine are effective in disinfecting equipment, but iodophores are
relatively slow acting and rapidly inactivated by organic contaminants. They are
therefore expensive to use and are best
used on equipment which would be damaged by repeated use of cheaper more
aggressive disinfectants. If the brown
colouration of the diluted working
strengthiodophore begins to pale, replace
it with fresh solution, becauseit will be
loosing its disinfection effect.
May be used to spray onto vehicle undersides and tyres and is safer to cany in
vehicles than more aggressive disinfectants. Will corrode metal sprayerswhich
shouldbe rinsedout betweenuses.

2.2. Sodium hypochlorite. Normally

and most easily purchasedin the form of
dairy hypochlorite (it is extensively used
as a disinfectant in the dairy industry)
which is cheap,rapid in action and readily available. Dilute to give 100 ppm
available chlorine. Some dairy products
may have a coloured indicator in the
solution which will indicate loss of efficacy. Buy only sufficient for a few weeks
since hypochlorite is not suited to long
term storage. Use in baths and tanks for
disinfecting nets and boots, washing well
in clean water after disinfection.
To clean tanks and ponds hypochlorite
may be sprayed or brushed onto the surfaces to be disinfected. Does not contain
surfactantsto clean the surface being disinfected and therefore can be made more
effective by the addition of a suitable
detergent(e.g. Teepol L).
2.4. Sodium hydroxide (20g NaOH in
10 litres of water). Cheap and very effective, but is very corrosive and will damage skin, clothes and some metals. Take
great carein dissolving solid NaOH
2.4. 3-57o formaldehyde, is a cheap
and effective disinfectant, but very
aggressiveto some metals, clothing and
mucous membranes and should not be
used in closed spaces.It can be sprayed
onto concrete ponds adequately using
pressuresprayequipment.
Disinfection of Earth Ponds and
3.
Basins
3.1
Self disinfection by drying the
ponds completely. Disinfection results
naturally from the combination of drying
and the sun (UV) plus freezing in winter.
Unfortunately this method may not be
very effective in many cases because
complete drying can not always be guaranteed - the weather is very changeable
and not all agentsare eradicatedwith this
method.
3.2
Quick lime (CaO) is the most frequently used and cheapest disinfection
substancefor pond fish far:rning.It should
be used as far as possible in autumn to
allow enough time for building a productive pond top layer for new stock. For
routine disinfection 75glmz for sandy soil
and 400glmz for swampy soil is sufficient. The minimum amount for eradicating fish pathogenic organisms up to
a soil depth of 3cm is 1 kg/mz. To

achie
be er
surfa
Distr
froze
effec
wate
prev(
falls
appl)

co1T0

cloth

3.3.

40Vo
wher
crete
cloth
tles c

3.4
shou
The
relial
effec
uted
0.75
Calc
rema
of w
grea
ing.

3.s

tive ,
rarel
kg/n
quicl
not a

Note
myl

4.

The
disin
princ
wate
com(
emifl
be in
am a
ing r
avoi<
pass
teflor
radia
lamp
8700

-ce;ge.,(1eure.4xo
sr ouozo luerudrnbeeq1 -ursrp 'druu1qcee qlr.Adesn Jo sJnor{0018
q8rq eql etrdseq punore Jo oJII ecrlres u epnord sduruy
3uq1e1sur tsor
Jo
leqrur
'uoIl uels Uos peqcunel ,{llueceg 'uorterper
-oeJursrpSursnuordruocluetuleer euozo nn o1lueredsuerl sI qcrq,Lr.'Surdrd uogel
elenbepeur qlr.A Jelua eql e^pel lou
ur rue1s,(seql q8norql rele.& oql Surssed
seop elnporu e18urse Jo ssol eql os uuoJ fq luelxe eruos ol uoDelrruq sql prole
relnpou e ur peu8rsepfleunou sr 1ue1d sleporu re,^AeN 'dure1 eqt puno.re 3ur
uorlereue8 euozo 'prcu crlru Jo uorleru -ssedre1e,r,r
Jo ruru 9;o refel ruruurxruB
-JOJegl rlr llnseJ puu ,(cuercrgsQ
JQzruozo sr ereql leql reuueu e qcns ur pell]sul eq
eql ecnper ,tlteer8 IIL{\ rle lsrou se lsnur sdrueleqJ 'ruu VSZNtLl81Sur1ture
Iequossosr rre .,fuq 'tazruozoeq1q8norqt sdruel ,{rnc.reurernsse;d,l\ol ruoq seuroc
lJlorAsJllneq1 'suets,(sJeleA\
tr Surssedo1 .roud rre eql Surfrp se qcns uorlerpeJ
'sesod:nd reqlo roJ leeq sql Sursq4n .{q -BesJo qse4 Jeqlre ur elqrssod eldrcurrd
slueue;rnber ,(8reueeql ecnpeJueo slrun ur sr Jelu,4a
luengJe ro SururocurlceJursrp
o1 (An) uorlurpBJlelor^sJlln Jo esn erlJ
lsour 'Suqooc elenbepu eJnsue 01 uorl
-eIIDsur Suunp epuur eq lsntu uorsr,tord
'uorlceJursrpJelu.^A
'v
(an) uorlBrpBr lalol^Brllfl
Jo eeJSepqSrq B prre 'lueq sBlsol sr rezruozoeqt o1pelldde
Sur,terqceJo sueerulngre,tlode eJoJeJeql .(3reue eql lo ob06 q8noqtly 'peuuoJ
sr uorlreJurslp An fq pemollo; uorl
sr euozo pue IeAeI f3:eue lcerroc eql
-eaozo Jo uorluurquoc eqJ 'uoBceJursrp ol pelrcxo sr de8 eSreqcsrpoql q8noqt
ir(ur
rele,4aJo eerSep puorlrpp ue sepr.to,rd pedurnd .rre.ftp Jo 1(oU e ur ue3,(xo eq;
-ouoce osleJe sr 3u4ce;ursrplou :aloN
peqslqelse sr
osl? 1 eJurs uorlJnpelauozo Sur,terqcu 'secepnspyemdT uee,^Aleq
'.{uerureg ur pe,^d,oIIB
qcrq.Ll.ftrcu1ce1e
go eSreqcsrpe Jo lsrsuoc
lou
Jo sueeruluerue^uoc e sI An Jo esn eql
'wels.{s uonceJursrp(An) telortertln ue
1 nb
stozruozo IrJJeruruoJ'Iosse^ lseluoc sr o tu rl Joa p rro l q rJoasneql ' er - urpt
q8noJrpJele1(erp gu Surssed.{q ro 'epr pesopue ue urqlr.4aurels.,(sSurxrtu u puu roJ se Su4nqr4srp Jo poqtery 'zlul8>t
Jo
'pesn .(1e.rer
-xo.redueSorp.(q;o uonrppu eqt fq reqlre peleoJ.leq ol Jele,^A
oql olur euozo lcefur SZ'0-I'0 lB alnqlrlsl(
'ue3.{xo ol >Icqpocnpor eq ,(eru euozo ol lesnJJrpeuozo uB ss:rnbe;uorleuozo sr os 'ea.rsuedxesr lnq 'lulceJursrp elr]
's'
oqJ 'pe.{o1due oq ol e^eq ilr,4d,uorl ;o ssecord eq1 'sse13e.rqrg
ro 3n4n 3e -ceJJeue osl sr aurq Jo oplJolqJ
-epe;8epouozoJo eler eql 8ur1e:elecce;o 'JuEJSrser
auozo eq lsnru {Jo.la edrd eq1
'3uI
sueoru oruos 'e1rs-uouorleper8ep euozo 'uorlelrluel elenbepuglr.{\ ruoor eleredes
loJ er.urleJueprsalluelJrJJnsepr,ro;do1.ro e ur pJteJolsr lueudrnbeeuozolJe leql -qlolc elrlcelord 1ng Surree,t ewc luet?
'urruJ eql Jo tuee4s dn ecuelsrpelqereprs lueuodurr sr lI 'seruedurocpesqerceds qlr.4Aleer1 ;porred srql Surrnp rel.l.rJo
-uoJ le Jele/y\
oql lJsJursrp
o1elqrssodsr se;rnber lueurdrnbe sF11Jo uortelle]sur ,r\oglnoou 'slee^\ 9 ot dn Jo.los sutetuer
pue crxol ,(re.r. sr prureue,(3-runrclJ
ecueg pue snoreSuupfre.,l eq uuc euozo
tl sselufl 'euozo erll Jo uorlcnper ellzh
'surels.,(s
'ar,Ilp a^proJJa s,(up 7I - 8 'zu/34 9L'0
s JoJ selnurru 97 o1 dn e>lelu?c ssecord
elsB,4A
ur JellBrucr
-uu8-ro.rog
srql lnq '.(1urn1eu u,^aop s>leJq pu
luuprxo pye,Lrod u se ,{11uecer - S'0 oruFns puod lqou aql uo paln
elqelsunsr elnJolou ouozooqJ 'e.rtry8u eJour pue 'sree,( 97 punoJs ro; euenbu -qlrlslp sr pruruuu,t3-runrJluJ'tceJJe
eq tsnru uortuJluecuocIun eurJeu e3;u1ur puu Jele^\ Suqurrp 's1ood Sursryge; poo8 pue uortceJursrpelqerler
200'0
^\oleq
-prser eql qsr; 3uqpr1.ro Sursserlslue,terd Surururr,trsrog .{lnyssaccnspesn ueeq sprl eqt .{q pesl1?rneu ere slsoc ,req8rq eq1
'suorlceJur
ol JapJo ur te,Le,ro11 :e1e,LlSururocur uoIlceJuISIpJo Sueelu e se (gQ) euozo
snJr^Joesecur posneq plnor{s
ppueue.d3-urnlrluJ
lceJursrp o1 pesn eq osl uec euozo
NCeC)
V'E
'etnurtu.redse.r1r;
's
uollEuozo
000'gZ
'urFruroJ Jo serl
;o serlrcedec lueruleerl qlr^\ polletsur
'QfSH,D
puu 3urq1o1c
ueeq elq suiels.(selrlceJJeerurl luese,rd
srurl
rruec
-luenb
,(1dde
o1
s.role.rrdse.r
'(surseq elerc
eql lV 'luetuuoJrnue
srqt ur auozoSursn -4des cr8eq.uorueeqIeJrApue se,rodsooz e,Lrlcelord ree,tr ure8y
uerl^\ lunocce olur ue{l eq 01 e^uq ilr.44 oru3a1o.tdog'eeuec;eceleru u,mu,toJs -uoJ Jo sllezrr)elqrssodurrsr Sururrl e:eq.Lr
-old!(I'snr"nqtqdo[qtqrl'DllauapofqJ
pesn eq plnoqs (ep,(qepleruro1,ob1V
srrll eJoJeJeqlpuu prder eJorusr euozo Jo
''
- Eg eqt Io) (,bi apz(qappurrog
u,4.\op>leerq
eql 'rele.,1a
qse{ uI uuqt:eq8tq
'DurpoqruJ Surpnlcur'uorlurper AII
.{11e:eue8er senlel 11d e.reqzvrluetu
qlr.^apelloruoc .{lnysseccns ueeq eABr{
't1 .,(1dde
-uolnue JurJeu eql ul 'pueuep rruu8ro sueSoqledqslJJo sdnor8pre^es 'spqos
ol pesn eq tsnru 3urq1o1c
q8rq ro en1e,r11d qSlrl e e^eq tou seop pepuedsnsJo 'uoJrpe^lossp 'sprcucrlunr{ e,r.rlcelo.rd
goorfuelervrIInJ pue olrsoiloc
Jelel( eql Surprrr,ord'Ior1uoc IeJrA puu ;o ecueserdeql ur elrlceJJessel eJoJereql sr eurrl4cm| '(eruq lcrnb eqt 8ur.{1ddu
IerrelJsq roJ luercrJJnssr selnurru 9-z Jo pue Tnoloc pue erunlo^ rele,^Aeql ol pe reUE s>lee1vr
9-t) S'8 - 8 tnoqe 01 slleJ
gd rege .(1uo qsrg >Icolsed 'pe1ue.te.rd
oturllJeluoJe qtrn\elnuRuTeltrl
-llor sr urelsfs An Jo sseue^nceJJe
eqJ
1-8Lug-;
'palceJursrp
eq
01
Jele,^A
erun
eq lsruu Hd qBU e eleq IIrl( rlcll{^\ Jete,^a
Jo esop euozo ue'eldruexe ;og 'perrnbe,r
Jo
euozo Jo sesop ,4\ol eql ;o esneceq ,(1 -Io^ eql uo luepuedep eg m1vrslsoc uorl
ursJ ro relerrrSurleel Jo ,!\oulno 'lceJJe
-uruur'eprxorp euuolqc pue eluolqcod,(q -eilelsw 'eroJereql 's.laog rele.4d8ur.{rB,r uorlceJursrppelrjull e .,(po seq IIos uezo4
qlp,r edoc ol lrun rlnpolu e se peu8rsep puB ecr '1Y\ousuo orurl Jo uollnqulsl(l
'sruep pue sedols 1e3.ro;1.uoq 'ecBJJns
sr pue sged 8ur,r.otuou seq ruelsfs An V
rnoq red relervr puod lsroru eqt uo pelnqulslp .{1ue.l,eeq
Jo sertrl 6ggy ,(leleurxordde 3ur1ce; ptnoqsoull Jql IJoJJJtunurldo e,terqce
runrpos Surpnlcur 'uorlceJursrp Jo
poqteu loqlo qll, Ape;eduoc uaq,r 'role^\
eqt Jo .{11p1qrn1
eql Suue^\ol osl pu
rnopo Sura.orueJ'euelceq Surypl ur elrl

o
ol
-I
-I
II
Jo
-c
0

P
u

sr
0l
-&
es
eq
'J

3
sl
OI

pu

3
p0
0q

p
dr
d

er
-I

q
0lq
0J

-s
up
-Jn

ellr
il0^
JO

3u
S{0

-IJ
eql
slc

ru
-lp
(,ft
po
Jo

fu

OV

Section45
Water Quality
Parameters
Limiting values for fish farming
The determination of water quality is best
done by experienced experts, because
there are complex interactions between
different componentsof the water.
In the following table guide values for
fish farming are presented for average
water quality giving values which are
generally acceptable.In specific casesit
is not impossible that fish damagemay
occur below theselimits.

Temperature:

carp: up to 28'C
trout: up to 20"C

Oxygen content:

carp: above 4 mg/l

trout: above 8 mg/l

Carbondioxide:

up to 25 mg/l
fry up to 10mg/l

pH:

above5.5. less than 8

A c i d B i ndi ngC apaci ty* * *

above1.5 vaVm3

Ammonia (NH3),forpH above8.5

up to 0.05 mg/l

Ammonium (NH+)''',for pH lessthan 8.5

up to 1.0 mg/l

Iron, total

up to 2.0 mg/l

Nitrite content*

up to 0.2 mg/l

Nitrate content*

up to 50 mg/l

Inorganic phosphate

0.6- 1.0mg/l

Chlorine (Cl2)

0.01- 0.03mg/l

HzS

up to I mg/l

Demand* (KMnOa)**
PotassiumPermanganate

up to 20 mg/l

ChemicalOxygen Demand* (COD)

up to 40 mg/l

Biological Oxygen Demand'''(BOD5)

up to 15 mg/l

Oxygen Demand (BOD2)

up to 6 mg/l

Cyanide

up to 0.1 mg/l

I
I

Tabk
Orga

The t
has ir
these
high
are h
salts
Dilut
with
Nerv
pirati
abno
are si

Note
whic
sis (h
orga
cle a
more
ples '
Infor
tion r
Merc
and l
main

IntensiveFish Culture:

COD maximum in outflow of raceway

up to 30 mg/l

(for 2 hours mix samplesand BOD5)

not more than 10 mg/l

COD maximum day limit of silo systems

up to 35 mg/l

(for 2 hours mix samplesand BOD5)

not more than 15 mg/l

if these values are increasing, this

points to an organic pollution of the water
(in case of high values mortality can
occur,especiallyfor pH above 8). Toxic
effects and limits may vary if other parametersare close to iimits.

'-"These substancesdon't causemortality, but have an undesirable influence on

the metabolism of the water svstem.

becauseof the low buffer capacity of the

water system. Take care with dosage of
therapeutants for immersion bath
treatment.

* * * T h e A ci d B i ndi ngC apaci tyi ncreases

xx*>r\z[us1
be less than 1.0 mg/l for
by a value I by liming with 280 kg of
quick limei10,000 cbm water, values salmonid fry.
below t have an indirect negativeefTect

It mr
used
defir
man:
agair
guidr
conti
mon
medi
ue tc
I na
pfov

eJB eJerp qcns su seurcrperu ,{reuuele,t

Jo esn eql uo suorlsulser 01 uonrppB uI
'puuq ul ere slutr I eseql
Surcro;ue pue Suuolruou JoJ slesodo,rd
pue tes ueoq seq (fU171) Ie^el enprser
ruruurxuru e sselun ng eql ur serceds
pooJul esnroJ posusJrleq,(eu ourJrpeur
,{reurrelerrou L66l;o Suruut8eqeqi {g
'rlslJ pooJ
rilr. A ueql pelcrJlseJ ssel lur{^\euos sr
[ISIJpooJ uou 'l?lueulelrro uo seurcrperu
.&uurrele,t Jo osn o1 preSer ur uorlenlrs

eqJ 'serJlunocuuedo;ng ..{uepeepur ro

6llur esnJoJelqulru^,(11e3e1
eq 1ou.{eru
sluJuleeJlpJpuounuoJo;eql 'seser,(ueur
uI 'leql sueelu srqJ 'eseesrpqcee roJ
lueuleeJl o^rlJeJJelsou oql eq ot peelSe
pueuluoceJ ol sI ue>lel
sr
'(1luerrnc luq,4A
ueeg ser{ tur{l qceo.rdde eqt eJoJeJeql
puu 3u4u,u Jo eurl eql le esuc eql lou
,(1e1rugep,tre,,lsr srql 'serJlunocJeqlo
fueru ro; ecrlpe olur elqelelsuer1eq ilI,\\
'lseel lB luJlxo uE 01 'qJtq,4puu ado.rng
Jo oloq,4aoql ssorcE ,(1ddu p,tr qcrqm

',{uerureg
uo^ uorDlnpord
'I4l/un}Iuerd
'8epen
914 '966I uoqrpepu7 '([ueqcsryess?.l.rgns
pun 1qcn7l ,,qsrd rete.^Aqserd
Jo uortcnpordpue 3urreeg,,rolrpg) 'gog uruetr^lreg? *
(s1run-flrprqrn;-uou1ce1) IIJI 0I :]norl

,t11p1qrn;

Irosec

y8urt0'0

(euqosu8'1or1ed)
eurzueg

y8ur0'I

I/8ru E'0

elozueqrolqcxeH

y8u o'I

slouer{d

v ? v L r-g

I '0

suorlepueruuoceJpue ecrlp epr,Lord

o1 elqrssoderuoceq1p.ur1r s.mef ,l.reJe uI
'oolo^op o] en
-urluoc uorun ueedorng eql ur seurcrperu
freurrelel uo sloJluoc Jo uorlesruou
-JqJo ssecordeql se e8ueqc snonulluoc
eql ur uellu^\ sl eptnS
Jo JturlEJo JIpprLu
s1{J 'uorlducserd .{reuuele,t e lsuru8e
peqddns uoqa pesn eq fluo feur fueru
lql pue sourcrperu.{reuuele,t uolllurJep
.(q ere eseesrplue.nerdro Ioruoc ol pesn
spcrueqc IIB luql poolsrspun oq lsnur 1I

JO

ql
Jo
eq

Sugrreg

qsl.{q seulrlpentr
iruulraleAJo esn
LVuoltres

t-

[unJIOIed

(HJH-^) euBPuI'I

y8u 08
y8u o't
(3urs-Oi- ruu I) l/8u Vl

,irlsrureqcrele,^aIlol uo Surpuedep
'y8ul 1'6
VSur 8 o1 dn uorle-re1o1

y8ur S0'0
IF.Jd

JCIC
slfueqdrg peleuuolqc.(1o4

1ury)ese8eueyq
(sy) cuesry
(IV) unrurunlv

(IN) IO{JIN

ySru g'g :d-rec

ySru 76'9 :1nor1

(rJ) euorqJ

y8urE0'0

ySur g'g :d;ec

lpru 1'6 :1nor1

(n3) reddo3

ItBu:Ay1:rele^\ preq
VBrut00'0 :rete,^A
Uos

(pJ) lunrlupBJ

vBlu l0'0 :uoneqncur33e

y8ru 1'g :drec
y8ru gg'g :1nor1

(qd peel

(8rus-6t = 3 I) I / ArJgg'6

(3g),{mc;ey1

're^rl prrB,(eupq ur perols ,{preru

or8 run[upBJpuE puel ts[q^\ le^rl pus
aJJSnuur solelnunJce,{1ureu,(,rnrre141
'sue8ro luereJJrpuI splelu .{.,reeq;o uorl
-nqlrslp eql Surpre8erslsrxe uorlerrlloJul
'3 gg1 ueqt sselSulq8re.trseld
-ruesroJ e,rrsuedxeool pue llncrJJrperoru
sr srsfpue enprsed'recsrl 3961 pue e1c
-smu 3gg1 sr (seprc4sedepr:olqcouuSro
- seprcrqJeq'seprcqsed's1e1eur
.(l,eeq)sts
-.,(1euu
enprserJoJue{et oq pFoqs qcqlrt
enssrt Jo lq8re,r runruluFu eqt :aloN
'suorJuloruqlr,t\uorleJrxolur
Jo su8tsere
qslJ Jo rnorlqeq Surururr,trspuuouqe
pue uorlJnpord sncnurpeseeJcul'uorlerrd
-sor rolsJ '(Suqseg) rnor^Bqeq sno,\reN
'Je1e,4Ae1S8,4A,{rlSnpUr
IcIIueqJ qlrA\
pelrcoss;epcrged ur ere leleru peln1q
'crxo1 flq8rq ol ,4aolruor; e8uer slps
Ftour elnlrp tnq qslJ 01 clxot ,(1p;eq eru
sluletu eJnd 'Sur8rurepeq uec slerrelqStq
'oJII roJ lueuodrul ,(:el ere spleru eseql
yo .{uuruqSnoqllv 'f,puece.rpeseeJculsq
sleleru Jo ecuecrgru8rspcr3olocrxol eq;
ur seprJusedpeleuuolqJ-Jruu3.r6
>FJJIeA\
pue sletontroluos roJ slFul'I I'9t oIqJ

seplrllsad
petBulrolqr-rIuBSro
puB sIBleHtraaBeH

gv uollres

52
existing and developing regulations for
the control of the dischargeof water from
farms containing such medicines. These
regulationstend to be set at national level
rather than Europe wide and the dischargespermitted are frequently local to
an areaor even to a specific farm, since
they form part of the control of the environmental impact of the aquacultural
unit. The effect of such controls will be
to fufiher limit the ability of farmer to use
the increasingly restricted range of therapeutic drugs which are currently available.
As an example - in Germany the whole
range of freely available simple chemicals like common salt, quick lime, calcium cyanide, calcium chloride, chloramine-T, malachite green,formaldehyde
(formalin) and potassium permanganate
was used for more than 100 years by fish
farmers. This use was not forbidden, but
also not explicitly allowed - because of
the fact that only at the moment when
these chemicals were applied to fish as
treatmentsfor the control of parasitesor
other pathogenic agents these chemicals
were literally promoted to medicines and
as such not licensed for fish. Of course
the pharmaceutical industry was not
interestedin applying for official licensing of e.g. common salt for use in fish.
The same applied to all the other chemicals becauseof the rather small and very
naffow national market because of the
very limited volume of fresh water fish
farming in Germany.
This situation is and was not unique to
Germany and applied to most other
Member States of the European
Community.

Section 48
Glossarv of Terms
and their Meaning
for Fish Farming
Practice
U

Acid Binding Capacity-Value: showing

the hardnessof water (Lime content).It is
important to know this value becausethe
dosageof chemicalsto the water depends
strongly on this value. For example copper sulphateis applied 20 g/10m: for an
ABC-value of 6.6-13. For values below

hyde, but concentrations are normally

expressed as Vo formalin not Vo
formaldehyde. Because of its irritative
effect on mucous membranes is should
not be usedin enclosedareasunlessgood
air exchange can be set up. Formalin is
very effective for treating against
ectoparasites(flagellates). For control of
Costia,concentrationsof 1:4000- 1:7000
(1 ml fresh formalin in 4 - 1 I water) are
used. The formalin should not contain
any white sediment - this is sedimented
paraformaldehydewhich is highly toxic.
Furthermore formaldehyde may also be
used for disinfection of equipment (3 47o). Formalin should be stored tightly
closed, cool and dark.
Incubation time: The time between
infection and outbreak of disease.
can be used against
Trichlorfon
Dactylogyrus, Gyrodactylus, Ergasilus,
Argulus andPiscicola:
Trichlorfon is an organophosphateinsecticide and is known in some markets as
Masoten@. It is very toxic and its use is
closely controlled everywhere. The related, more toxic product dichlorvos
(Neguvon@, Aquaguard@) is used in
mariculture to control sea lice.
Medicated feed treatment: fish feed to
which has been added a veterinary medicine so that the fish absorb the drug
through the gut. Specific rules apply to
the supply or manufacture of medicated
feeds,in most countries they may only be
usedundera veterinaryprescription.
Masking: through indiscriminate use of
drugs the signs and whole picture of a
diseasecan be heavily falsified - masked
- so that proper diagnosis becomes difficult or even impossible. In caseof bacterial infections a medicated feed treatment
prior to bacteriological examination and
20'c.
Drug resistance: Some bacteria are less antibiotic sensitivity testing can make it
sensitive to particular antibiotics than are impossible to isolate and identify the
others. Continued use of a single antibi- pathogenicbacteria responsible for about
otic. panicularly if the concentrations 30 days and therefore an urgently needed
employed are lower than they should be, antibiotic sensitivity test - to select the
will select those resistant cells. Some correct therapy - is impossible unless a
types of resistance may be transferred small stock of untreated fish have been
retained separately.
betweendi fferentbacteria.
Facultative Fish Pathogens: Organisms Notifiable Diseases: These are diseases
which can grow and survive in the aquat- whose presence must be notified to
national diseasecontrol authorities
ic environment but which are capable of
- Viral Haemorrhagic SePticaemia
infecting fish and causing diseasedependent on certain conditions (decreasing ffHS) of salmonids
- Infectious Haematopoietic Necrosis
health conditions from poor water quality or high stocking densities, over feed- (IHN)
ing at lo.w water temperaturesetc. (See There are variations between European
Union Member States, e.g. SPring
Section16).
Formalin: formalin is 3l7o formalde- Viraemia of Carp (SVC) is notifiable in

0.8 copper sulphate should not be used

because even small amounts may be
toxic.
Antibiotic sensitivity tests (also known
as an antibiogramme) : to establishthe
suitability of a therapeutic agent in an
outbreak of bacterial disease. The
pathogen, after isolation and culture, is
grown in the presence of candidate
antibiotics. After a suitable incubation
period the effect of the presenceof the
in terms of a reducantibioticis assessed
tion of growth of the pathogen to determine if the pathogen is sensitive to that
compound. The most effective drug
found in the sensitivity test should be
selectedfor therapy.
Carrier: Animals which, although showing no clinical signs of infection, continue to be infected and therefore continue
to carry the pathogen and continue to be
a source of infection to other susceptible
fish. If for example trout fry survive an
IPN outbreak, they may be expected to
releasethe IPN virus for the rest of their
life.
Disinfection Barrier: To decreasethe
risk of disease introduction or of its
spreadat least, boots and equipment disinfection should be carried out before
entering the farm or between the different
areasof a farm (e.g. hatchery,fingerling
accommodation, grow on accommodation).
Disinfection: to make free of pathogens
by physical (heat, etc.) and / or chemical
(for example formaldehyde) treatment.
Dosage: lgl3mz water for cyprrnids, or
Igl6mz water to allow survival of food
where fish are dependanton natural food,
lg 4mz water for salmonids.It should not
be used at water temperatures above

the UX
Membe
Aquacu
SVC,
Gyroda
plague)
untary c
Obligat
or pathc
natural
Exampl
da, ci
Aphano
plague.
Suppor
reatmer
by cont
tions m
fish pat
allow pr
not dire
pathoge
Withdn
period v
pletion
wit h a'
may be
tion. Tl
able dn
meat.
now ma
Sensitiv
such ret
ing pro6

E
I

lon

The infr
ation ir
publica
A.
(Januar
health r
on the t

produc
Europe
46/18)
June l
Europe
r75/37

gI pu?zI selcluv 01perreJer

eururerSord
oql ur porJrcads
eq o;

(rcotso saa[taouoqdy) an3o1dqs$ot3

suoaJDtsruJ

sltvlDs sn1&copo.t{g
(I ftM eseesrpqlnouper 3uelua
(optcruow1os souou.to,r
ay) srsolncurund

.\LEI9LI
-I -VEISLI1 'o51'serlrunururo3 ueedorng
a q r Jo l e u rn o f l B l rIJJO) t 66l aunI
lo Jgg/rg/6 tuaupuauv str pue (UtgV
j -I/9n T 'oN 'seltlunuruoJ ueedorng
eqt Jo Ieurnof 1elclJJO) slcnpord
pue slrurueernllncenbe Jo le>Ireru eql uo
Surceld eqt SuruJa^o8suoqrpuoc qlpeq
Ieurrrru eql Sururecuoc (166I ,{renuel)
e^rlserrc IrcunoJ Jg7/19/16 - 'Y
:oJesJuoruncoplueleleJ eql 'uorlucqqnd
eroJeq ,{lelerpeuru 966I IIJdv ur uoqe
-ruls eql 01seluler.4aoleq
uorlsrrrroJuleql

rn"op;:$i"",ruor

alnllnJBnb
sosBasrp
oql Jo slBlluessfl

UI
o
U

3l
ol
s
u

ln
0ql
11

p
lua
-el
-IJ
pel
vl l
Jo

(56n) srsorceucrteodoleureqsnorlceJul

(Sfn) erureecrldescr8eqrroureeqprrn

(vsD ruleuuuuolul?s snorlceJul

ueSoqled/ eseosrq

suBaJElsnJJpuB sJsnllotr{'rlslJ
Jo V xouuv ruo{ lcerlxg I 6t olqsJ

0q

'ecueqdruocoJnsueol seururerSord8ur
-Jolruou ur pe.{oldrue eJe senprseJqcns
lcolop ol senbruqcellecrfpue eAIlISueS
's.(ep eerSep ur pesserdxe ,(lureur .trou
er qsrJ ro; spoued IB^\BJprlUly\ 'teeru
eql q lueserd eJe senprseJ Snrp elqu
-ldeccuunou leql eJnsueol sr srql 'uoll
-drunsuocuurunqro; pe:elq8nels eq fuur
,(eq e.ro;eqJurJrpau ,(reuuate,rB qllr\
qslJ Jo luerulee4 Jo esJnoc e ;o uotleld
-ruoc eql;egu esdelelsnu qcrq.ldpoued
er11:porrad (3qp1oqq1p,r) parurpql;11
(sn-n,te '3'e) ueSoqled
qsrg ,fteurud eql spr/!\ol pelcerrp lou
'uorlrpuocqsrg;o Suuerrocerlerged .ato1p
o1 se 'srusrue8ro-orcrurcrueSoqled qsrg
e^uBllnJuJqlr^\ pelerJosse,(1uteusuotl
-ceJurleuelceq frepuoces 3uq1o.4uocfq
seDrleuouI Je,rol 01 pepuolu lueruleJl
peeJpepJrperu B :luorulueJl Sulgoddng
'enBeld
qsrgfurc Jo esnuc 'lJDlsD sac,(tuouoqdy
puB srsolnJunJnJ Jo esnBJ 'Dp
-rJluowIDSsDuoxuoravepnlcur seldruexg
'lSOq eql eprslno lueruuoJl{ue IeJnleu
oql ur eArAJnslouuuc qcq,l ueSoqpd.ro
elrse;ude ,(pcutg : suaSoqled a1u3;1qg
'(IoJluoc Arelun
1o,r.) elqugoder ,(po ,tpreur eru (en8eld
sn1{lcopot{g
'JAS
'c)s

'(EilgLr-r-tztgLr qsrg^{er3 pue suolos

-I 'oN 'serlrumuruo3 ueedorng eql
Jo Ieurnof IeITIJJO)seseesrpqsrJ ureuec
Jo sernsueru Io4uoc Sururecuoc (9661
eunl) e.r,qcerrq[cunoJ Jg;1]Eglt6 -'1.4

0
p

(AXg) eseeslq,,(eup1y
Ieuolceg
(CzfS) dreC Jo Brrueerr1SuFdg
(g4f srsorceucrleercuedsnonceJul
TISTf,

TII JSI-I

6t uollres

(sntcnl rosg) frg e>114

sercedspruorules
l(sntutwul snu.qoqlqdocg)toqrnl
l(sntcn1xosg) e414
'.('dds snuoSato3) qsge1q11
| (sn7pu{qt snpout(q1) 3u1.{erg

'sercedspruorules

qsI.{
II JSI'I

VDIDSorar)sJuolulessnuupv

qstd
I JSI-]
sercedselq4decsng

;o sue8oqle;.,tsosBaslqJo sfslA Jgg/lgll;

'vztLtt
-I -gI / LEt T'oN'serlrunuruoJ ueedo.rng
eql Jo leuln of l eIJ UJ O) seseos rp
qsrJureuec Jo uorlerun]uoc pue uollcolop
roJ spoqteu c4souSerp pue suuld 3ur1d
-ruBSeql u,trop 3ur,(u1(7661 reque.to1q)
uorsrcec uorssruuroJ JawzE9l7,6 -'J

'hlug

'srsolncunrng

'NdI) JA1I 19il6 e^\calq ernlpcunby

Jo seseesrp-ilI lsrT selBls JeqIuoII
eql
reqlo q '(,{emrop ut pue) )n

P
oll

3r
-Ip
olt

ul l
so
-wl
SI
S3 S

-c
,S
lsu
U00

,{
-L)
0q(

'c
Pel
ulsl
em
00
JOI
JSU

qul
po
pp
sAr
ob
.,(1

LY

E/

A.
91167 EEC Council Directive concerning the animal health conditions
governing the placing on the market of
aquacultureanimals and products.
The general principles of this basic
Directive can be summarisedas follows:
- To contribute to the completion of the
intemal market, avoiding the spread of
contagious diseases.
- Taking into account that the animal
health situation for aquaculture animals
is not the samethroughout the territory of
the Community, to introduce the concept
of approved zones which are free for one
or more diseases.
- To define the concept of approvedfarms
situatedoutside free zonesand enjoying a
special animal health status.
- To define the trade patterns between
approved zones, approved farms and non
approved zones.

from approved zones or farms "down" to

the whole non approved area.

The
ket I

1.
mals
ease

2.
Special conditions List II diseases
- principle - from high health status to
low health status(Figure 49.1).

For movements of approved farms (in

non-approved zones) to an approved
zone special safeguard measures can be
establishedfrom the side ofthe approved
zorrc (Art. 14 9I/67/EEC) - if serious
hazardsto animals or humans inside the
Community or in third countries arise.

Figure 49.1 Principles of movementsin

relation to disease status under
Aquaculture Directive 9l/61|EEC.
Horizontal" trade: approved zones or
farms - trade is only possible between
facilities of same status "Verlical" trade:

3.
Special conditions list III diseases
to be defined case by case
National control progralnmes at Member
State level can be supplied to the EEC
Commission. If approved, additional
guaranteesmay be permitted.

The
was
app
non
Ann
the r
tain

eggs and gametesare defined.

1.
General conditions
- no clinical signs of disease
- not fall under schemeof eradication
- not from farm subject to prohibitions

Ann

z0ne
approved

aquaculture animals
- fish
- crustaceans
- molluscs

farm
approved

-.H

farm
approved

List II diseases
2.
- seriouseconomicimpact
- presentin the Community
- approved(free) zonesand farms (in non
approvedzones) can be identified

2.G
- fou
- tw(

3.M
- fis
zon
- twl

pr0gramme
Tone
llarm

-.H

prOgramme
zonellarm

The Directive gives a definition of diseasesand groups them into three lists:
1.
List I diseases
- exotic to the Community
- seriouseconomicimpact
- eradication measures(Directive
93/53IEEC)

A.C

1.D
-wa

The scope of the Aquaculture Directive

9I/61|EEC is to define the animal health
conditions for placing on the market of:

aquaculture products
- for reproduction: eggs, gametes
- for human consumption

z.
- ev
appr

zoneI larm
unapproved

zoneI Iarm
unapproved

farm
suspect
/ contagious

.<+

farm
suspect
/ contagious

- re

4.S
drav
- ab
eda
-im
- res
- res
- res
four
-Cc

B.C

List III diseases

3.
- diseasesfrom which Member Statesare
lree or havea control prograrnmein force

2.G
pen

Anr
ther
tain
app

Table 49.1 summarises Annex A of

91| 6'7IEEC indicating disease/pathogen
and susceptiblespecies"
Within this framework - movement patterns for live fish, molluscs, crustaceans, Fig.49.l

1.D
- es

(after: T. STRUBELT)

(0) 6t+ 'teJ

69822/IZV9q,
watr{JrL\vLLLj
z9'JISJJ0(I

(goottpdv t ro Jwvzug6
uorsrce(
uorssrururoJ)
:peer8e
ereurr(seuozpe,torddu uou ur) sure;
pelordde 3ur.tro11o;eqt S66I qcrulN uI

ssnu'ruBd
Jeuqcr
(seerelueruqclucJelu,,ta
peurJeporrrl
t
Joquellerod
;o uorldecxe eql qlr.^dtuegpg :go ged)
vsz}slgLE9E(0) 6t+ 'IoJ eruerd 'uEI tr Jo eIsI '(l ged) ryuuueq
>Icruqlepur)gg966 'pueleq 'pwlerl urequoN '(eq8tC Jo elsl
tqcnzqcsrd eq1;o uoqdecxe eql qlrm) urelrrg luerg
Hqurc >Icruqlopury
LgttlrE9(o) oruel

'(euoz pe,r.ordde
uou e ur) uue; pe,to-rddeJo snlels eql ure]
-UBIUpuu qceeJol se suorlrpuocumlu eql
sesuBrurunsJTE/L9/I6 eql Jo J xauuY
seuozIelueunuoc ol Jelrrursuorsued
-sns pue ecuuuelur{u'pedde Jo lueJg 'Z
urels,,{sfrenlse uolllurJecl'I
qslJ JoJ seuoz IulseoJ 'g

:sHA rod

uzles-uesneqproN
porrrjoJureq lsruu uorssrurruoJ ?9166
soseosrp pue lsl-I
ee"rg
ree,{.rno;
7 Se.Lrepeg
lI
I
Jo
pue uorlucrpure:1e.r.ordde
Hqtuc ezles]qcnzqcsrd
Jo uoqt?JolseJ'pueleq 'pueloq urequoN 'urelug leerc
u,^aJprprl\
lulordde :e.LrlrsodllnseJ peJolseJplordde :e,rrle8eullnseJ vLzztvL}gt (0)
6?+'Ior
epleJeure-I
:NHI roC
qsrJ>lcrsJo uorlsurruBxeelBrpeurur LZELT
slqro a lqcnzqcsrg
pepuedsnsp^,lordde- perJrlou puu pe
eploJoure'I
:uorufl ueedorng eql ur lsrxe seuoz -1e8qse,rureq lsnru fllpuour
truulsroCreSurrnq;
1euuouq
pe,\ordde 3urno11o; eqt S66I IIrdV uI
I.&Jp
-q l r.,!\' l u e ru q sq q e l se-eJ ' uor suedsng' 7
twzt,69E (0) 6t+ 'ter
ue8urureyq
g xeuuv ur paqrJcsep
11996
do11e11
erurrg sB JBI(urs lE,4^erpqlr/$
'erueuelure;41^
uorlerlsr8er JBe^/Suorlururexe
luode
IO4UOCOAUulruJ Jo euoz
IZE|ILSqE(0) 6t+ 'teJ II pue I lsrl Jo uorlJrulsep eql s^\oIIB
qcq,r urels.(s e fq perlddns eq lsruu pe,r.ordderuo4 eq lsnru pecnpo.r1ulqslJ lpelsoJJ
9t986
utpquelneJerurrg
plorddu Jo ecuuuelurcI I '
qslJ roJ suuBJ
'fl
lulsuoS
(ue8uu11ql)u;8ugnq; Jo etetslurepeC
.ree,(7 suoqcedsurq11eeqorg pelruoJureq lsruu uorssrurruoJsesuesrp pu lsITJo eer; sree.{rno; 11
I
saseesrp
:leeddeJo luerg 'Z
11pue I lsr'] Jo ear3.rea,(;no.;
88t/9E9S(0) 6t+ 'teJ pue uorlecrpere: pa.orddeJo uorlsJolseJue8ugory99119
u,^a?rpqlr,4a
p.Lordde :elrlrsod llnser tl Jo ued ro BeJsluerurlclec rele.l\ rell!!trtrurupnDpw e>lrrln
poJolseJplordde :e.Lrle8eu]Inser :uoDrurJecl'I
qolslepercJoquellerod
qsrJ>Icrs uorleuruexe el8rpelulur Jo
pepuedsnsle,rordde- perJrloupuu pe
- rlslJ roJ euoz leluourluoJ 'Y
(0) 6t+ 'IoJ -le8nse,lur eq lsntu ,$11egourIeurrouqe LV9S/10V9
eilnquerrerus
3rceg y716p
sauoz pa,r,ordde'g xeuuy
IeA\eJp
91 ue11en|ueqors - glr1('l ueruqsrl qel se-er' uorsu e d sn g ' g
uege8uesoA'g:q
:snlels e qcns urel
ue11en|ueqerslqcnzuelleroC
uorle.rlsr8e.r
-urBrupu qcseJ01s suorJrpuocure{u oql
ree.(7 uorleurursxelo.Duoceuo sesrrsrurunsJsglL9lI6 eql Jo g xeuuv
'(euoz pe.,lo.rddeuou
u ur) urre; pa,rordde puu ouoz pa,rordde
;o sldecuoc orll Jo uoqcnpolur eql se^\
uor1e1sr3e1
slql Jo lcedsu ,treu urcru erlJ

.>rleruuec
.rr^ jf:1Ti"-i,"#3
ecu'Ic

(0) 6t+ 'ter

IruBJ JO OUOZ
LIZT,/V995
Iessec98918 pe.r,ordderuo4 eq tsnru pecnpoJlurqsrJ (sesofundcrJrtuercs
- freqcleq)sneqqcsld
p.norddeJo ecuuueturutrl 'Z
ueBupteC
'lull

rep uesner{erlle5ln8sqcns,ren
ree,{7 suoqcedsurqlpeq ozrrlseseesrp
rnol ll pue I tsl-1Jo ae.gs.lue,(
ruBe4su,^(\'op
qsrJsnolu
0lnztljlg (0) 6t+ 'IeJ
>lcelque>IreH-ue8ururueg996g g
-orperrEroJ relueq Iulcupr ro Iernleu eloqeJoqJo lle,,la,(q perlddnsrol1d8Z >lurrqurels
relleow 'l INZd:
p.,to.rddeJo luerg 'I
{celque>lJHlqcnzqcsrc
qslJ roJ srrrreJIetueunuoJ 'Y
(uesqcusreperN)
e}els IerepeC

,{uoxug

Ja^ro.I

euoz perrordde
uou ruoq 3u4uur8uo Jr rISrJpoleJocsrlo 'Z
:euoz pe.a,ordde
olur uorlcnpo4ul
esee
-slp Jo u8rs pcrurlc ou .roqs qcrq.ry\sleru
'I
-rue tuo4 eleurSuo lsruu slcnpord

I8
Jlli
r0
s0
'i

eql
sno
p0
eqr
p0

u1

Jo

z(uuurrag

sauoz pa,l,ordde
uou ul sruJBJ polorddu '3 xauuv

:are uogldrunsuoJ uurunq JoJ la{

-JBru oql uo 3u1ce1dJoJ suoglpuoJ aql

ol ,,

q9

Additionally some special problems

are covered by 9ll6TlEECz

health situation in the Community

through the following generalmeasures:

Non susceptible farmed species (Afiicle

14) introduction into approved zones or
farms
- from another approved zone
- from approved farm in a non approved
zore
- from any farm in a non approved zone
if such farm does not contain susceptible
speciesand is not connectedwith watercourse or coastaVestuarialwater

1) all farms must:

- be officially registered
- keep record of livestock movements
and mortalities

Derogation is possible where practical

experienceand/or scientific evidencehas
shown that there is no passive transmission of disease.
Principles apply also to ornamental
speciesexcept to ornamentaltropical fish
kept permanentlyin aquaria.
Wild species:
- introduction into approved zone only
from another approved zone.
- introduction into approved farrn situated in a non approved zone only from
approved zone.
- when fished in deep sea and introduced
into approved zones or approved farms
for breeding purposes, quarantine is
required.

Greece:
Centre of Athens Veterinary Institutions
2) compulsory notification of suspected Fish Diseases
25 Neapolios
presence.
15310Athens
The control measuresfor List I diseases
Spain:
are:
Laboratorio de Sanidad y Producci6n
* classicalmeasuresin caseof suspicion: Animal,
Cta. Madrid-Algete, km5400,
- official diagnosis
- restrictions on suspectedneighbouring 28110 Madrid
farms
France:
x measuresin caseof confirmation:
CNEVA Laboratoire Central de
RecherchesV6t6rinaires
- stamping out
22, rue de Pierre Curie
- disinfection
BP 61
- epizootic investigation
94703 Maisons-Alfort Cedex
- inspection of neighbouring farms, etc.
The control measuresfor List II diseases
atei
* in approved zones and farms:
- stamping out
- 4 year testing programme
x in non approvedfarms in non approved
ZONES:

Importsfrom third countries:

1. Third county must appear on list (not
yet published) - criteria:
- state ofhealth livestock
- organisation of control services
- information on infectious and contagious diseases
- control measures

- official diagnosis
- infected farms must be listed
- official supervision of infected farms
- fish/eggs/gametesmay leave infected
farms only to other infected farms or for
slaughter

2. Third counf,J must respect special

health conditions.

Further imporlant aspectcovered are the

establishmentof national referencelaboratories and of a Community laboratory
as listed below.

3. Consignments must be accompanied

by health certificate.

National Reference Laboratories for

Fish Diseases:

Directive 9I/61IEE;C was followed by a

more detailed follow-throush Directive:
B.

Council Directive 93l53lEEC

This Directive applies to fish diseasesof

List I (ISA) and of List II (IHN and VHS)
as well as to take quick action in case of
outbreak of such diseaseand to preserve
and, where possible, to improve the

Germany:
Bundesforschungsanstaltfiir
Viruskrankheiten der Tiere
Anstaltsteil Insel Riems
17498InselRiems

Belgium:
Institut National de Recherches
V6t6rinaires
Groeselenberg,99
1180Bruxelles
Denmark:
StatensVeterinere Serumlaboratorium
Landbrugsministeriet
Hatg4vej 2
8200 Arhus N.

CNEVA Brest
BPTO
29280 Plouzand
Ireland:
FisheriesResearchCentre
Abbotstown
Castleknock
Dublin 15

Un
MI
Th

we

Do

SO
PO
Vic
Ab

Co
Fis

Sta
Lar
Har
82C

Thr
Cor
sun

1)t
Cor
the
dise

2) l
out
Me
isol
act(

3) tr

Italy:
Instituto Zo opr ofilattico delle Venezie
SezioneDiagnosticadi Basaldelladi
Campoformido
Laboratorio di Ittiopatologia
Via della Roggia 92
33030 Basaldella di Campoformido
(Udine)
Luxembourg:
Institut National de Recherches
V6t6rinaires
Groeselenberg,99
1180Bruxelles
Netherlands:
ID.DLO
Postbus65
8200 AB Lelystad
Portugal:
Laborat6rio Nacional de InvestigayS5
Veterin6ria,
Estradade Benfica,701
1500Lisboa

exp
vier
tecl

4) l
dial
pet(
whr

Vac
app
non

Alsr
plar

1)r

cen
mea
cen

2) a
cofi
co-(
at a

JoJ spoqletu crtsouSerppue sueld Suqd

-tues oql u,^AopSurfel (7661 requre,tog)
'E
uosrcoc uorssnuruoJ JEglzESlz6

'81/9V-r

go godurr eql roJ sp;en8e;eseql sE IIea

se )n .eqt ul (CztS) d;el Jo enueurr1
Surrdg go Iorluoc eql roJ eurruer8
-ord eq1 u,trop ,{e1 suorsrceC eseqJ

oN sertrunuruoJ
ueedorng
IlgV
T
Jgg/s98/t6 puB
.c
eqt Jo Ieurnof IelclJJO) 'slcnpord JggJvnltt
suorslra0 llrunoS
pu? spturue ernllncenbe
orp
uo
le{Jeru
Jo
Surculd eqt Surure^o8 suo4rpuoc qtpeq
'selets requetr l
Ierurue eqt Surureruoc (166I ,{-renuel) -uorull uuedorng ,(q AAl Ieuorleu
.Z otur pourqsueeqr^eq plnoqs
e^rlcorrc
IrcunoJ
J!lE/
LglI6
Jg3/sl86
pue JgalLgl[6 se^rlcerrc eql lsel le
'62/LVE-I - LZlLV.-I oN serlrunruuoJ
eurluuotuaql ur teql pelcedxaeq ot sl ll
u eedo.r ng eql
J
o
l
eulnoI
l
el
r$J
O)
soseesrppruru urcuecJo Suuolruou pue
',$runuruo3 eq1
uorlecrpeJeer{l JoJ auolrJc flrumuuro3
srerureJ
pelserolur
o11r,(1ddns
lnoq8norql
u,r\op 8urfu1 (OOOt requre,tog)
ueJ
serJoleJoqs-IecueJeJeJ
IeuortsN lnq .I
uosrcec uorssruruoJ JEil/g'g/06
JroqprlreleprrqunJ eq louueJsrql eceds
Jo {cl Jo esnceg 'slueure;rnbe; 3ur
-rolruoru NHI pue sHA eql slrElopqcrq^\
S66I IIrdV Jo sB uolun
ueadorng aql u1 e.rnlpcunbe .ro1ea,r
.J
qsa{ ol luBAaIaJ suorsrJa(vsaallJeJl(
JgElzgglz6 uolslroo lrrunoJ
.g
IrrunoJ
ns/Jf,fl
Jo lslf
ur ue,tr8 ere sue8oqled
(smcn1rosg') e>pd 11 lslT Jo uortucrJrlueprry 3ur1se1frol
(sruo13sntn1tg)qsrJler ( uuedo"rng) -uroqel pue Suqdures'srsou8erp- ,{11eurg
(smsso"ucc
smssDJDJ)druc uurcruc
'sue1d
(snpt sncsnnaT) ecep
,(cue8urluoc
eql
uorlulueru
Jo
(ocut1ncurl) qcual -eydrureql JoJ,fuesseceusre,Lrod
1u3e1eqt
(snw1oqrydotqitta snrurprDe5)ppm
ernsue o1 peldopu eq il?qs suorsr.r,ord(6
(snp1n.tsn14ny) qceot
(sn7otnosmssoto3) qsrgploS
i(se1d
lxL"tLllou,t -tues Jo uorlegodsuerl prder -rog eperu
s[qrq crupqtqdo d[g) d;ec (re,rps) eq
sluerueSue.ue
'.pue sqt o1) srs
lsnru
(o11aptuooZur"rcqdoual druc (sse;8) -ou8erpprder
rog
sIIDIS
eql urelurcrulsnu
3)
(otd.tncsnut"td,(3)drr-c pue '4'ote',{3o1o1srq
',(3o1oresro; ,Qrceduc
: (JAg
,{;esseceu eql 'uorluunuxe rueuoru
598/V6)
pelretepe,rcsercedselqrldecsns
eql -1sod rog serlrlrceJ e^uq lsnru serJol
JAS
pue (Jag
-eroqel crlsouSurp'elerrdordde ereq,lrl(g
WltO pepu.o.rdsr uortecrJrileclercedse 'ssore ee4
ruo4
lsernpecordelrlurlsrurupu pus plorJ
JAS
qsrJ qlr^\ ,{po pellured Suolcotse-r ur sllDISdolelep pue urlureru ol peqs{
'pelceJursrp -qelse oq
ileqs seruue.rSordSurururl (1
pue pe4drue ueeq eABq
eore er{l ro lsnru
'pe,ro.rdueeqe^Bqtsntu
:uorl
JAS Jo eruesqe ue serceds elqrldecsns -eultusluoJ Jo uorlceJurJo uorleurrrJuoc
pue uorcrdsns uo uo>luleq ol uorlce uo
;o suorlelndodur osle 'euop ueeq eleq
lsnur Surlsel 1ecr3o1orr,tsreef ee.rql yo peprlo;d eq ileqs suoncnlsur pepelep (9
runlurullu e suoJspalcoJul r(1snot,,rerd
ur 'lno peluec s1se1
yecrSoloJrlpuu >leorqlno
iflredo;d
sernseeru
JAS ue rege srue,( o1(1Jo runrurullu e
3ql lno ,(.r-rec
ol olqpltp^p
loJluoJesosrp
roJ pelsel ueeq e^eq lsruu seerepelceJureq IIEqs sluueteur pue luerudrnbe (g
's eerepal ceds ns ;o
polceJur-J^S ruory eq tou lsnu
oql
:>lEeJqlno
uB ur pe^Io^ur
)n
ol lrodurr roJ peurtsepqsIJ urSo"roeq1.{llcerrpur ro f11ce:rp ere r{crq,ry\suorlesr
Jo
'serpelcoJur.{lqrssod
-ueSroTsuosred
,(lprdur l3eluoJ ol elqp oq
1o"r1
lsnru er1uecIo4uoc eseesrppcol r{J?o(t

-uoc
01e^us
serlrroqt.:"#:fjffiffl;

e oq tsnru
'u@po go ,{glunoc eqt q lserlrlrqrsuodseJ
rrerp pue sllDISrroql
3ng
-: snqJ ')n eql o1 seleure8 'sernsEeulIoJluoc ur pe^Io^ur JJels eql
serceds elq4decsns-3ng uo ue,tr8 eq IIEr{suortsuuoJurpelplep (g

Jleqt puu

:Ie^oI IEcol e te
seJnsBoru
IoJluoc osBesrpeql eleurpJo-oc
ol sonrlrcq elenbepeglr^\ serluec Iortuoc
es?osrpIucolJo pepr.,lordeq IIBqs lsII u (Z
lpeu-rec
-uoc selels regruetrAleql q sernseoru
IorluoJ II? elsurpJo-ocilqs rl3rrl,r eJ]uec
srsuJ Iuuorluue Jo lueuqsrlqelse eqt (I
:sA\olloJ
sEpeutllnoere sueld
,{cue8urluocJoJ erJolrJcuruururur oslv
'uepplqJoJsr (seuoz pe,rordde uou
ur) surE pe,to;ddepuu seuoz pe,l.ordde
ut sospostp
II tsl-t ]sure8euouEurJJeA

'1ue1u.terd
ew seseosrpesoql eJoq./y\
sorrlunoc pJlql q serrolEJoqIluelod
-uoc eql qlr.,tl'seseesrpI lsll Sursou8ery
Jo spoqteu spre8ersB olsroqelloc ot (?
i,{1rumuuo3oril lnoqSnorgl senbruqcel
crlsou8urpJo uorlesruouJeq eql ol A\erA
p
qlr.r\
srsou8zrp
,iro1e;oqe1ur sgedxe
go Surure.rler
ro 3ururcr1eql elulrlceJ ol (g
:selp$s crloozrdepu uonesrrolce
-reqc 'srsouSerpdroleurrr;uoc JoJ selelosr
ueSoqled Surlrecer ,(q se1e1gJeqruotrI
ur osBesrplu?^eleJ eql Jo s>leJqlno
go srsou8erpoqt ur flelnce lsrsse o1 (7
:peuJecuocoseesrp
oql SursouS?rproJ sele1s requory eql
ur pe,{oldure.spoqleu eql '4uorssrunuoJ
eql qll{\ uorlullnsuocur 'eleurpro-oc o1 (1
:sA\oIIoJsB pesueuruns
ere f.roleroqel ecuereJer .{lrunurruo3
oql Jo serlnp puB suorlsunJ eqJ
'N
snqrv
0028
z letd,?ueH
leuelsrurursSruqpw.I
runuolsJoqslr.uruos
eJauuele^ suelels
:sasBasroqsld
ro; froluroqu'I eJueJoJaU.dlrunuuro3

sc8 6sv ueepreqv

peod euolcr^
I0I xog od
fuo1e:oqe1
eurretrl CICVOS
sn8 tIC lesrocl
qlnoru.{e11
eqloN eqJ
,(ro1aoqe1 seseesrqqsIC CdVIAtr
:urop8u1y pellufl

L9

58
the detection and confirmation of certain
fish diseases (Official Journal of the
European Communities No L 337118L331l2l
4.
93l22lEEC Commission Decison
(November 1993) laying down the model
of the movement documents referred to
in Article 14 of Council Directive
9I/67|EEC (Official Journal of the
European Communities No L16l8 -

Lr6/12)
5.
93/14|EEC Commission Decison
(December 1992) conceming the status
of Denmark with regard to infectious
hematopoietic necrosis and vital haemorrhagic septicaemia (Official Journal of
the European Communities No L 27135L27/36.
6.
93l44lEEC Commission Decison
(January 1993) approving the prograrnmes concerning spring viraemia of
carp submitted by the United Kingdom,
and defining the additional guaranteesfor
certain fish species for consignment to
Great Britain, Northem Ireland, the Isle
of Man and Guernsey(Official Journal of
the European Communities No L 16/53 Lt6t54.

defining the additional guaranteesof certain fish speciesfor consignmentto Great

Britain, Northern Ireland, the Isle of Man
and Guernsey (Official Journal of the
European Communities No L 352175

Section 50
Fish Health
Laboratoriesand
Advisor-vServicesin
the EuropeanUnion
AUSTRIA
VeterinzirMedizinische Universitiit
Institut fiir Fischkunde
ll
Linke Bahngasse
A-1030 Wien
Tel. +43 (O)222 I'71155-0

94l450lEEC Commission Decison

9.
(June 1994) amending Decision
93/'741EECconcerning the status of
Denmark with regard to infectious
haematopoieticnecrosis and viral haemonhagic septicaemia(Official Journal of
the European Communities \lo L 341121
-L347t29
10. 94l865lEEC Commission Decison
(December 1994) amending Decision
93l44lEEC approving the programmes
concerning spring viraemia of carp submitted by the United Kingdom, and

National Veterinary and Food Research

Institute
Oulu Regional Laboratory
PO Box 517
SK-90101Oulu
Tel. +358 (0) 81 5541666
FRANCE
CNEVA Alfort
Laboratoire Central de Recherches
V6t6rinaires, 22 rue Pierre Curie,
94703 Maisons-Alfort C6dex,
Tel. +33-l 49 7l 13 50
CNEVA Brest,
Laboratoire de pathologie des animaux
aquatiques,B.P. 70,
29280 Plonzanl,
Tel. +33-98 22 44 62

t
I

1
j
I

Bundesamt fiir Wasserwirtschaft

Institutftir Cewrisserokologie.
Fischereiwirtschaft und Seenkunde
Schar{ling l8
A-5310 Mondsee
Tel. +43 (0) 6232 I 3847 or 3848
BELGIUM
CER/Pisciculture
Centre bconomie Rurale
1, Rue du Carmel
8-8900 Marloie
Te(. +32-84-220244

7.
93l53lEEC Commission Decison
(Ju n e | 993) int r od u c i n g mi n i mu m
Community measuresfor the control of
certain fish diseases(Official Journal of
the EuropeanCommunitiesNoL 115123
K. U. Leuven
- Ll15/33
8.
93/54|EEC Commission Decison
(June 1993) amending Directive
9l/61|F,F;C concerning the animal health
conditions governing the placing on the
market of aquaculture animals and products (Official Journal of the European
CommunitiesNo L 175134- LI15l31)

National Veterinary and Food Research

Institute
Kuopio RegionalLaboratory
PO Box 92
SK-70701Kuopio
Tel. +358 (O) | 201469

Zoologisch Instituut
Namensestraat59
8-3000 Leuven
Tel. +32-16-283966
DENMARK
Danish Trout Culture ResearchStation
Br@nsMollevej 7,Br@ns
DK-6780 Skaerbak
Tel. +45-'74753234
Ministry of Agriculture
Danish Veterinary Service
Section for Aquaculture
Skomagewej 38
DK-7100 Vejle
Tel. +45-75857820
FINLAND
National Veterinary and Food Research
Institute
PO Box 368
Fin-00101Helsinki
Tel. +358 (0) 3931880

Laboratoire V6t6rinaire D6partemental du

Finistdre
7, rue Turgot,
29107 Quimper
Tel. +33-9882 88 88
Laboratoire V6t6rinaire D6parlemental de
1'H6rau1t
306, rue Croix Las Cazes,
34000 Montpellier
Tel. +33-67 10 11 17
Laboratoire V6t6rinake D6partemental du
Jura,
B oulevard Th6odore Vernier,
B.P.316,
39016 Lons-Le-SaulnierC6dex
Tel. +33-84 24 37 34
Laboratoire Y ltdinaire D6partemental des
Landes
1, rue Marcel David,
4004 Mont-de-Marsan
Tel. +33-5806 08 08
Laboratoire V6t6rinaire D6partemental du
Pas-de-Calais
Rue du 19 Mars 1962,
Dainville, 62022 Anas
Tel. +33 21 51 46 54
Laboratoire V6t6rinaire D6pa.rtementaldu
Haut-Rhin,
21, rue dAgen,
68020 Colmar C6dex
Tel. +33-89 73 37 5'7

\F

\rTL
D
T

F
L

D
T(

Fi
Ti
C
D
T(

B:
Fi
Ti
Se
D.
Te

Fi
Z't
Ba
DTe

Br
Fis

Ve
Lel
Sc
D-(
Tel

900t086t (0) 6+ IoJ

e^oped6zIgt
'z 'sruo 'c l?r^
'erzeue^ellepsleluerupeds
ocrlellrJoJdooz
olnlDsI
'ErSolorr^rp ouolroge.I
96t199ZEV\0 6+IoJ
(qn) opruroyodruu3gpellepusleg0g0e
'76 'e63og ellepErA
'arzeue1e11ep
eptueuruedg
ocrlep;ordooTo1n1qs1
'e6o1o1edor11y
ep olueurrgedrq
A'IVII
'teJ
69S99-I6-t9+
,(u,tr1eg'Cln'e4uel c4sou8erq
FuoqeN
puBJerI
gJJeeserorg
dno.rgfueuuele1rrlenby
99tZ/ILVZ|6LrZ:$e ' I L89LZ-r.,-E;E+'rer
,rrro6
'
lcedsor4
ryoJ
cqenby
]run secr^Jes

Ejrgtz/ rt6| (0 6v+'rel

Iepuels91968-A
9EI -Ztl 3e16relrerqte;ug
lruesAunqcnsretunlenrursueqe-I
pun -J?uuele^
uaqcr11ee]S
rue tsuerpstreqpunse8qcsrg
:1pquy-duoxes / tprluy-uosqres

vzjgztI IvE\0 6v+'IFr

8reqee14ryuyq
gIWy-Cl
lIg eu?JlseqcsEurog
- ?rzdrc1
]suerpslreqpunse8qcsrg
elsuerpslreqpunseS:erg
esse{ueqcnesJerJeqJsrsqJes

zvzg/ t6898(0)6t+'teJ
"qer) 90620-q

3 rlsreprea,lsre,{o11
eqrsr{ FreJou

f{serN
rues8unqcnsreruffi[Tt
LE90V0V
I r9Z \U 6V+'Ipr
zualqox gtogg-c
t eg"4sreqcnlg
lrues8unqcnsrelurueuuelelsapu?-I
ru? tsuerpslreqpunse8qcsrg
:alBuqelud-puelouFlu
/ zlJd-puBlulorJu

'lpr
vv909v8-I-E9t+
ullqn('oJ
epqel?IN ',(pesury
llun qllEeH qsrd
eJlueJ
qrr?esed
seueqsrd
euuul
luerulredeq
I
Jo
ONV'IflUI

z96LL to 06LL I EZLZ(O)0t+ 'ter

uneqlv ' uepunqqcrr) 66ELs-{
l&dN reregrsrd 4rJ
llulsuusepue.IJep u lsuepqreqpunse8qcsrg
:u1pqd1sa76-auFlg qiloN
/ ualBJlsa \-uloqrproN

060I09-I-0+ 'teJ
SUEqIVOI9I
sollodseN gz
seseesrQ
qsrd
suoqqrlsul freuuelen
sueqtv
Jo e4ueJ
flJfltrUC

0E8rL6/ IW \06V+'IFL
3mquep19IZI7Z_CI
I e$eJ]s-rnoJ-el-sr?I
surg-Jesed\lrueslreqpunseSrerl
ure lsuorpslreqpunseFqcsrg

6VrLr8/ 09(0)6V+]pr
ezpsue8uel
pe11
LV666-C
6 egeJlsrelpelsuueJ
ezpsueSrrE.Ipeg
uopuEts lnlDsul IellFUSueqe-Ipun -reuuele
O I I I I ? I I V qE\ U 6T + ' I EI
E ue Iw L L j -q
q96 egerlsre8rnqurneN
8u3I
uopu?]s lnlrlsul IeurursueqeTpun -Jeuuelo^
:erFul.rnq; / uo8ulrnqJ

6,n069r
/ tw 6) 6r+]pr
IerJIgrrvz-a
17- gTage4s?requotnD
'lsuerpslreqpunsaBqcsrd
Sunpelqe;elun
'ute1s1o11-3r,,r,rselcS
rerrue{sU?qcsUr,r\spu?-I
rep'IJI / tpllpnbleprursuoqe-I
pun lrepunqse8rerJJnJ .]sul

(elqrssod
{colc eql punore se8esseur- eurqseru
Sune.r,rsue
osp) ZIIISZ / IIS (0) 6V+ .pI
re^ouueH ELIW_A
1y 8e,r1qce4urg
(err^res qtl?eH qsrd pue ,(uoxeg
Ia,t\oT Jo aJIAUAS -IOUJNOJ JIWgCIIdg
pun
HSIC AJVJS)'tsuerpslraqpunse8qcsrg
uesqcesroperNJSNaICISDNOgdWVXSS
NAHJNIISHJSIS dAH JI-IJVVJS
:,{uoxeg Ja.troA / uosqrusJaporN

0Ez8L
tsgt (0)6v+'IpL
snquoJvro'o-q
8I egB4sJowqcIqcs
lu?s8unqcnsJelunlenlusueqe-I
pun -JBuLreleA
ueqrrneelsrrle lsuerpslreqpunse8qcsrg
:SJnquepuBJg
LVL\8E (0) 6'+'rel
uepredt Lt9z6-a
zlelduueuneg
rlreqserulv e[elsBrel(Z
ue,(eg lsuerpslreqpunse8qcsrg

z9z1606to
t9zt606
/ 68(0)6v+'ter
qrug-3uro4
9gg9g-A
gze8pls-rensrec
roleues
A'e rue{Bg lrueslraqpunse8rera
u?
lsuerpslreqpunseBqcsrg
ura,{efl / elreaBg

0Er90s
/ tzzg(0 6r+ 'reJ
Sreqyeprell
9I169-A
qryzzSuu^urezJ
Sreqyepreglurus8unqcnsrelull ueqcrllzrgrelJ
ueqclltu?lstue tsuerpslreqpunse8qcsrg

z;zz\il | t9L(o)6v+''eL
Ernqre.rg
80I6t-C
z rqle1Ksool
trIuY
tsrnqrerdlrullsul
ueqcsruer8fqrerlrue lsuerpslreqpunse8qcsrC
EEZZV6
/ 9791\0 6V+ 'Ipr
JJopueFV 92988-c
0z eus4selrerque,{\o'I
Jropuelnv lu?sSunqcnsrelun ueqrrllzrgrerJ
uil{JrlluulSIu? lsuelpslleqpunseSqrsr{

sw-6v8tI rtL (0 6?+'r{

I rrE8ilrusvLIoL_a
9l auellsSrequezv
uz8pnl5 lruus8unqcnsrelun ueqcrllzJgJerJ
ueqJrIselSuE lsuems]leqpunseAqJsrJ
3raque1gLr6-uopsg
'ses?esrpqslJ JoJ
serlqrqrsuodser
qlri\{ uorlqqsul,{reupelen
e 1e,fio1e.roqelB Jo eJr^res qllseH qsrd
e seq (e1e15prepeg) plreT rlc?e ,(uuuuag u1

s0IL I I9E8t (0)-6t+ 'Ier

surerllIesul86vLI-a
sIeIuruv
srur^ JoJe4uec qcJeesel{
Joseseesrcl
preped/ ererJrep uelrerppurtlsnrr^

9L'89 '0n-9008I rV9 6) 6V+'Ier

uegerc g6tg-(
tg eueI]sreSrnqrery
uesseqlegrtr
l lues8unqcnsrelun-1-.T-'W

lllJ ll?lsuEsBunqJSJoJsepun
B

ueqcrll?elS
ruelsuerpslreqpunse8qcsrg
: sr ErodeJ eseesJpeIqU
-Ilou JoJ,{role.roqq eJuaJoJeJIsuopsu aql

:uossoH

6069sI IZW \0 6V+'IpL

retsunurneNLtgvz, _ a
'9 egers $fg xeli
toqel seqcsrSoloJrAqcsrd
'urelsloH
-8r,rse1qc5sepu?-Jsop lues8unqcnsrelufl
ryuljele^ pun IenrursueqeT
:ure1qo11-Spuselqcg

ANVWUSC

vgzTrt/ Itt \0 6V+'IFI

upslod69vnl-q
67 eelpledde4
luresFunqcnsrelunleilrrusueqe-I
pun -Jeuusle^
ueqcqleels ru? lsuerpslreqpunse8qcsrg

z0 z0 EL9t-+ 'IeJ
xep93ueno'u9LI9l
'smoJ pusJc np enue^v
'eluDlrtrAtr
eures
?l opplueureuedgqerruuugl91erroteroqeT

69

60
Istituto Zooprofillatico Sperimentaledel
Piemonte, Liguria e Valle DAosta,
Via Bologna, 148,
10154Torino
Tel +39 (0) 11 26861

SPAIN
Ministerio de Agricultura PescaY
Alimentaci6n, Central de Algete, 28110
Algete, Spain.
Tel +34 1 629 03 00

Departamentode Biologia Celular

Facultad de Biologia
Universidad de Le6n
Campus de Vegazana
24071 Le6n

Istituto Zooprofillatico Sperimentaledell

Abruzzo e del Molise,
Via r. Paolucci,
65100 Pescara
Tel +39 (0) 85 4310337

Centre Nacional d'Aquicultura

Carr. de San Carlos a Poblenou del Delta
43540 Sant Carles de la Rdpita (Taragona)

SWEDEN
Fiskhiilsen FH AB,
81071Alvkaileby
Tel +46 (0) 26 726 30

Istituto di Malattie Infettive, Profilassi e

Polizia Veterinaria.
Via Tolara di Sopra, 50,
40064 Ozzano Emilia (BO)
Tel +39 (O) 51 792002
NETHERLANDS
ID-DLO
PO Box 65
8200 AB Lelystad
Tel. +31-3200-383'/3
RIVO-DLO
PO Box 68
1970 AB Ijmuiden
Tel. +31-2550-64646
Wageningen Agricultural University
Dept. of Fish Culture and Fisheries
Laboratory of Fish Diseases
PO Box 338. 6700 AH Wageningen
Tel: +31 317 483307)
PORTUGAL
Institudo Portugu6s de Investigaydo
Maritima,
Departamento de Aquacoltora - Lab. de
Sanidade,
Avenida de Brasilia,
1400 Lisboa,
Tel. +351 13016361
Faculdade de Medicina Veterin6ria,
Rua Gomes Freire,
1199Lisboa
Tel. +351 1 3522595
Instituto de Zoologia Dr Augusto Nobre,
Faculdade de Sci6nciasdo Porto,
4000 Porto,
Tel. +351 2310290
Laborat6rio Nacional de Investigaydo
Veterin6ria,
Laborat6rio de Patologia,
Estradade Benfica, 701,
1500 Lisboa
Tel. +351-1-7165139
Instituto de Cidncias Biomedicas Abel
Salazar
Laborat6rio de Sanidade
Largo Prof. Abel Salazar,2
4100 Porto
Tel. +351-2-310290

Tel. +34-73-74542'7
Depafiamento de Biologia Animal, Vegetal y
Ecologia
Facultad de Veterinaria
Universidad Aut6noma de Barcelona
Campus de Bellatera
08 193 Bellaterra (Barcelona)
Tel. +34-3-5811746
Departamentode Microbiologia Y
Parasitologia sanitarias
Facultad de Farmacia
Universidad de Barcelona
Av. Diagonal
08028 Barcelona
Tel. +34-3-3309061

SVA,
Fiskenheten,
Box7073,
750 07 Uppsala
Tel +46 (0) 18 674000
UNITED KINGDOM
In the United Kingdom there are three
govemment laboratories with responsibilities
for the statutory control of notifiable fish
diseases. Any suspicion of outbreaks of
notifiable diseaseshould reported to the
responsiblelaboratory either directly or by
the farms veterinary practitioner who should
be consulted in regard to non notifiable
mortalities.

Departamentode Microbiologf a
Facultad de Biologfa
Universidad de Valencia
Burjassot
46100 Valencia
Tel. +34-6-3864300

England and Wales

MAFF Fish DiseasesLaboratorY,
The Nothe Weymouth,
Dorset, DT4 9UB
Ter+44 (0) 1305 206600

Instituto InvestigacionesMarinas
CSIC
EduardoCabello 6
36208 Vigo
Tel. +34-86-231930

Scotland
SOAFD Marine LaboratorY,
Victoria Road, Aberdeen,
AB9 8DB
Tel +44 (0) 1224 876544

Centro de InvestigacionesBiol6gicas
CSIC
cl Yel6zqrez,144
28006 Madrid
Tel. +34-1-5611800

Northern Ireland
DANI, Veterinary SciencesDivision,
Stoney Road,
Stormont,
Belfast,BT4 3SD
Tel +44 (0) 1232 520011

Instituto de Acuicultura Torre de la Sal

CSIC
Ribera de Cabanes
12595Castellon
Tel. +34-64-310325
Departamentode Microbiologia
Facultad de Biologia
Universidad de Santiago
15706 Santiago de Compostela
Tel. +34-81-596904
Area de Microbiologia
Facultad de Ciencias
Universidad de M6laga
Campus de Teatinos
29071MLlaga
Tel. +34-52-131899
Priniedby WarwickPress
Estate,
CambridgeRoad,GranbyIndustrial
Weymouth,Dorset,U.K.DT4gTJ
Tel:(01305)779494 Faxi (01305)776266

EOZZ-90086
Vt(\'en elleg''g'N onue^vwjEI'\zLI 'qcsng'u'rc o/c''JNI ollruolg
VCIUf UUVJO SfIVIS OSIINN
.VdI
.pul
,gI
9dSslueH.e8puq8uprog..lsg Weqelpues llun.p1ThII{VHdIUJAA
'pu?llocs'IaEIHd'I+Ied'leeJlsnoss 'NoIJVIJossv sugt(\odc Noht'IVS HSIIIOJS
gC9 61y\J'erlqseqJ'qrlq^\roN'Iuerlcul!\'EUnI'InJVnoVA,nOUJ
'fAI 0ISJ xessg'ueptet11
uo.gJes
''tS ptog qZ-VZ'(ILy) ''pl] S1INIJJVAiIUnJ.InJVn}V

tNoocN|)o3JNn
'8reqz1ng'ZZ67-HJ
re,r.lg'DV NNV1ICCOH'n'H
''rlseutsnpul
'.retlnJuelleroC-dn3
ONV-IU3ZII/\AS
'efleuepe5
xofl 'gV flUnJTOJVn}V SOA\A
'819
LZ
t;I
S
N303l S
'olso
'deC
trrtuoJ'te1roJe4ueJIeuoDN)
ZE00-N
OOtgxog Od '(qc.ruesea
OSSA
re8uu.tul5I00t-N'619 xog Od'S/V C51111AU)S
'oISOI gtg-N'7'uere,tsuSosIUVN1UAJAA JCO)DIJNI.I1V1Ir1
'gZ6g-N'ue83erq'Z1lLxo1;Od 'Z oqeleluog'S/VUION
'ue3;eg'900E-N'SS
r8uelouuoqJ''S'V
OISIION
JAAUAJNI
'rerg>ls
xog.
ueddogqnl
'7
'lZV
'S/V
Iftl-N
94
Vn}V
SO./y\A
're8uezlelg
xo1.;
r{croso;
'ZES
'e4ueJ
ernlyncenby
'NOIIIXJ1N dg
I00t-N
Od
'eil,qs
xog
'g8tI-N'tII
od's/v
acuoN
uit vg
'0ISO'9t20-N'
uoeile4rqreH'wlndoJ\auosv.I

silNui[xaHJodv
AVA UON
'uuore1'eueluudpnrp olurn| VE1LE'DIBIeueluedlen
IA ''V'd'SVNOUAAISANOUAA
'eulpn'olueureqSel
otl1'S
gtggg'L
osr^e{
el1
''V'd'S
le
MIICNVI{
TVSUAAIN1
'eulpn'olorileg
rp
otue1g
'Ze^qdul1
''V'd'S
OditUJS
V.IOJIUCV,
VJEIJOS
'uuore1'
euecezzol4l
ouez
rrES
euorzrd''V'dS
LE'
090
XIUCNAH
'Buore1
orolsT
elel1'erluecrr8y
o/c
''TVII
SEILE'9
Iep
HOJ.IOJISId1INOIZ\.IJOSSV
'u^oped
'elozzerroJ
BIA''J'N's HSaJV1}JV
'eurssulg
0209t'I
AlVII
'(nSBIIV)
ueldurey
'S61ggdVhl'IV
L*Lg
C 'I egrsJouqeqrso
ANVINHSO
'sur^re^
sel
eurctuod
op luod el 'gf,Nvud ,tnodJ sllnoodd
'euerd
0vIZ0
'orunoqrTI09Et'9zI d8 'erQrlselleg
uI ep 'I'z 'iIlvwINV NOIJIUJ0N gJNVS IdoNVS

pln

uo,qr006ererurec
jf''uilT[;91;iy#":J::1"&T""r"H';i'_.'xnsrdqhtr-nNeHd
fCNVUI

seII

.OISIUd
.SSAJ/JWHAJ
OOZIZ-dS
NOISIW
'DIrnJ'I
g90Z-dS'
xogod IO VnoV SO./y\iINNId
619
ONV'INIJ
'epuergggry'

gg'fe,r.suesq8pA'tft{'(S/V
USCOSCI1ptrSO
)NVC) SAr'rehtrotg
)|HVl/UN:IO

'OSI
.{qu.{o6lse 11,(J;IHI-IV11HV1DV
AI
J
Igd'uaolellolreqJ'ryed
Ierrtsnpq
VOVNVC
'3ure.reg
ZUV - g 'uee1tS srog np eru 'y1 'e8nogesuoJel ep eqcreqcegep cred''JgIOIg AC ANNAAdOU1AiIJiilJOS

runtclfs

suf g1^r31/u
cNrNtvrsns
dJVS