1. 110509 Khaled M. Selim
In the Name of Allah,
the Most Beneficent, the Most Merciful.

2. Curriculum Vitae (C.V.)
Dr: Khaled Mohamed Selim Mohamed Abd Elrahman
Lecturer of Fish Diseases and Management
Faculty of Veterinary Medicine
Zagazig University, Egypt
Academic Qualification :
1- Bachelor of Veterinary Medical Sciences (B.V.Sc) May, 1998 from
Zagazig University, Grade Very good.
2- Master of Veterinary Medical Sciences (M.V.Sc), Fish diseases and
management since, July 27, 2002 from Zagazig University.
Title: Studies on Some factors affecting health and survival of Ornamental
fish.
3- Doctor philosophy of Science (Ph. D.), Reproductive biology of fish,
March 23, 2009 from Niigata University, Japan.
Title: Effects of temperature and methyl testosterone on sex reversal of fish.
4- Post-doctoral researcher for a year (2009 –2010), in Department of
Environmental Science, Fac. of Science, Niigata University, Japan.

3. Fish diseases

4. Parasitic Diseases
External or Internal or
Ectoparasitic Endoparasitic
Affect head, fins, skin, eye, opercula, internal organ- blood – swim
buccal cavity, the surface of nasal bladder and deeper layer of
epithelium or olfactory epithelium, muscles
crypts of the acoustolateralis system
or gills.

6. Metazoal Diseases
Lerneosis
Ergasilosis
Argulosis

7. Endoparasitic Metazoa
Digenetic trematode Cestode Nematode
Parasitic cataract Ligulosis Contracaecum
Yellow grub disease Diphylobothriasis Amplicaecum
Black spot disease Anasakiasis
Blood fluke Acanthocephala

8. 1-Monogenetic trematodes
• Diseases of bad water quality
• Affect external surface of fish
• Affect freshwater and marine water by
direct contact
• direct life cycle
• All are hermaphrodites
• the attachment occurs by haptor
( Opisthaptor- Prohaptor)
• They mainly fed on tissue debris and blood

12. Etiology and suscebitability
 Dactylogyrus spp (gill fluke) up to
2mm
 Gyrodactylus spp (Skin fluke) measure
up to 0.4mm
 Benedenia and Neobenedenia spp
mainly affect marine fish (oral and
cutaneous fluke) 5-12 mm
 Dermophthrius spp mainly affect shark

13. •The
identification of
monogenea
depends on
2. Haptor
structure

14. 2- Eye spots
or pigments
3- Body size

15. 4- Alimentary
tract structure
5- Reproductive
organ
[oviparous or
viviparous]
6- Site and
mode of
attachment

16. 7- Feeding behavior

17. very small
eye spots
8- Host specificity,
geographical distribution
and season Benedenia and Neobenedenia spp

19. Life cycle

20. Life cycle
 Dactylogyrus species at 24-28°C life cycle will
be around 11-13 days
 Mature eggs developed within 2-3 days
 Post-oncho-miracidium is sexually matured in
4-5 days.

21. Epizootiology
 Mechanical transmission by birds, reptile and
amphibians
 Nets and buckets are vehicle of transmission

22. Clinical signs
I. General signs
 Affected fish
appear lethargic
 abnormal
swimming
behaviors.
 Loss of reflexes
 Dark coloration
especially in heavy
infection
 Lower condition
factor in long
heavily infected fish

23. Abnormal swimming and movement

24.  Loss of appetite
 Remain at the
side or bottom
of the pond
 Restlessness
 Listlessness
 Emaciation
 Hyperirritability

25. II. General signs of body
surface affections
 Irritation of skin
 Swim against water
current
 Scratching body
against any hard
objects
 Copious quantities
of mucous
 Loss of scales

26. • Minute abrasions
or erosion
 Sometimes small
ulcer
 hyperemia at the
base of the fins
 Sometimes
secondary invaded
by bacteria or
fungi

27. III. General signs of gill
affections
 Aggregate on
water inlet
 Aggregate on
water surface
 Gasping of air
 Increase
opercula
movement

28.  Vertical
swimming
 Jump outside
water
 Die with open
mouth
 Infected gills
sometimes
appear pale or
be covered by
whitish patches

30. Economic importance
 Affect all types of fish
 Mechanical damage due to hooks
 Mechanical carrier for bacterial and viral agent
 Secondary bacterial or fungal invasions
 Eye affections lead to blindness
 Decrease growth rate
 Individual Mortalities
 Aggregation of ration may lead to high ammonia
level

31. Diagnosis
• History
• clinical sign and PM lesions
• Parasitic examination
• Molecular examination

32. A) Prevention
 Prophylactic measurements. predisposing cause source of infection
.Quarantine and restriction of movement of fish -1
. Good water quality -2
.Reduction of over crowding of fish -3
.Proper nutrition of fish -4
/ Periodical disinfection of ponds by 120 kg quick lime -5
.hectar
.Control of aquatic plants -6
.Control of organic matter -7
All utensils such as nets, buckets, aereators, must be -8
.disinfected
.Regular examination of fish for parasites -9

33. B) Treatment and control
 Prophylactic spray of chemical agents starting at
mid-April up to end of July as dipterex. Ammonia
can reduce infection so can be used in ammonia
tolerant fish as Japanese eel (40 ppm)
 Chemotherapy
3. Dipterex: prepare 50% solution in xylene and apply
it to the pond at a dilution of 0.8ppm.
4. Potassium permanganate 20ppm with 4% Nacl
5. Methylene blue, Malachite green formalin,
Ammonium hydroxide, masotene….etc

34. Metazoal Diseases
Ectoparasitic Metazoa
Monogenetic Hirudinea Crustacean
trematode or leech or Copepode
Lerneosis
Ergasilosis
Argulosis

35. 2- Hirudinea – leech – Annelid
 Parasites of fish,
worm
amphibians and aquatic
reptiles ( in both fresh and
marine water)
 blood suckling parasites
affect body surface, fins,
gill or mouth cavity.
 Carried to the farm
through contaminated
water
 Bisexual temporary
parasites

36.  Can be seen by naked
eye (2-4 cm) and swim
actively to reach the
prey
 Body formed from
several segments and
has 2 suckers( anterior
contains mouth and
posterior contains
suckers for attachment)
 They are temporary or
semi permanent
Leave after the meal
Leave for cocoon searching for shelter
deposition

37. Etiology / susceptibility
 Class: Hirudinea
Phylum: Annelida
Subphylum: Clitellata
order: Rhynchobdellida (Most important)
1) Family: Piscicolidae (Cylendrical leech) – 4-8 cm
2) Family: Glossiphoniidae (flat leech)- 2-4 cm

38.  The
identification of
leeches
depends on
2. Body shape
3. Length of the
body
4. Pigmentation
colour and
pattern
5. Numbers and
arrangement of
the eyes

39. 5- Crescent form pigments
on the body and caudal
suckers.
6- Arrangement of papillae
or tubercles.
It is better to examine the
leech in fresh and
relaxed state
• We can use alcohol or
menthols crystals for
short time in a Petri
dish before the change
of pigment colors

40. Life cycle
 Male put sperms through
spermatophore in female gonopore
 Mating occures on or off the host
fish
 Fertilized egg will be attached to
female body (within a special
socket) or deposited on aquatic
substrate (??) in the form of
cocoons(1-5).
 Off springs can survive for a week or
more before their first blood meal
 The period of nursing varies from 24
days – 4 months according to water
temperature
 After nursing leech need 3- 4 blood
meals to reach maturity

41. Clinical signs and
 Leech as it is can be seen
pathology
by naked eye
 Site of affection appears
well defined rounded and
sometimes oozed blood
 General sign of anemia
especially in young fish
( thin body, emaciation,
big head…)
 HB content drop from 50
to 20%
 RBCs count drop from 1.5
million to 300000/ml2.

47. Economic importance
 Affect all types of fish
 Young fishes are more seriously affected especially that live in
the bottom….lead to reduction in vitality and death ( so it will
lead to great damage to hatcheries).
 Mechanical damage to skin and scale pockets (sever epidermal
erosions) due to suckers followed by Secondary bacterial or
fungal invasions
 Vector transmitter for haemoprotozoa
 Mechanical transmission of viral and bacterial diseases
 Leech can suckle about 150 ml of blood within 2 days leading
to marked anemia
 Produce Hirudin enzyme that acts as anticoagulant leading to
oozing of blood from fish after leech leaving host
 A predisposing cause for opportunistic pathogen
 Decrease growth rate
 Individual Mortalities

48. Diagnosis
• History
• clinical sign and pathology
• Parasitic examination
• Molecular examination

49. Treatment and control
 Prophylactic: remove aquatic vegetations, apply net with
small mesh size to prevent leech or gravels and stone
entrance with water, summer drying season (chlorinated
lime is able to destroy both live leech and cocoons),
 Chemotherapy
3. Dipterex: prepare 50% solution in xylene and apply it to the
pond at a dilution of 0.8 ppm.
4. Masotene: 0.5-1 ppm in fish pond but harmful to
zooplankton.
5. Neguvon 1ppm for 5 days is effective against adult leeches
but not eggs
6. We can use OPC or chlorine
* Marine water leeches have very little trials for treatment.

50. Metazoal Diseases
Ectoparasitic Metazoa
Monogenetic Hirudinea Crustacean
trematode or leech or Copepode
Lerneosis
Ergasilosis
Argulosis

51. III- Copepodes – Parasitic
crustacea
 Many of crustacean parasite are lethal under
certain circumstances, other depilating and other of
major importance to fish culture and the fishing
industry
 It showed exoskeleton with jointed appendages and
segmented body.
 Affect mainly external surface of body.
 Many of parasitic copepods burrow into the flesh
and cannot be dislodged by chemical treatment
 Treatment is directed toward killing larval forms.

52.  Oviparous parasites with separate sex
 They have a complex life cycle which involves
mating of the parasites and attachment of the
female to the fish with subsequent production
of eggs which pass through several distinct
larval stages.
 The most important organisms are:
4. Lernea
5. Ergasilus.
6. Argulus

53. General life cycles of
Crustacean parasites
Mature male
or female
Fertilized egg
Copepode stages
napuli
Meta napuli

54. 3- Lerneosis - Anchor worm
 Are the most harmful parasite of cultured
fresh water fishes
 They most commonly found in warm water
fish
 The destructive activity of lernea is due to its
relatively large size and its mode of
attachment and feeding

55. Etiology and
 suscebitability
The are long slender copepod
 give the appearance of soft strikes with two eggs
sacs attached at the end of the body
 the head is buried in the flesh by large horn-like
appendages ]anchors} that help in identification of
the parasite

56. • Affect mainly freshwater fish
• There was two common species which include
• Lernea cyprinacea (host specific) affect carp fish
and accidentally other fish species
• Lernea elegans (non host specific)

57. Life cycle
• infective stage id 3rd copepode stage
• Mature stage is 5th
• mating occures on 6th copepode stage
• male will die after mating while female will die after
production of 3 pairs of egg sacs or 20 days

58. The cycle will not be completed at
the following
2.Temperature lower than 15ºC
3.Drying
4.Salinity of 1.8%
5.Lower pH 7

63. Epizootiology
 Contaminated water, infected
fish or carrier such as
amphibians or birds.

64. Clinical signs and
pathology be
Lernea itself can
seen by naked eye
e They penetrate
beneath scales and
cause a lesion at the
point of attachment
(inflammation-
hemorrhagic and
erythematic
lesion)

65. 3- Irritation- fish rub itsbody against hard
objects- excessive mucous secretion
4- General sign of fish diseases
5. When affect gills lead to respiratory
manifestation
6. When affect eye lead to blindness
7. When affect fins lead to difficult
movement
8. When large number of infestation
occures within the same fish lead to
emaciation and thinning

73. Economic importance
 Affect all types of freshwater fish
 Mechanical damage due to Anckors
 Secondary bacterial or fungal
invasions
 Eye affections lead to blindness
 Decrease growth rate
 Individual Mortalities

74. Diagnosis
 History
 Clinical sign
 Parasitic identification
 Wet mount of skin or gills showing
developing stages
 Molecular studies

75. 4- Ergasilosis- gill rot
 crustacean parasite affect gill of
fish.

76. Etiology and susceptibility
 Ergasilus spp
 most commonly found in warm water fish
 Affect freshwater and sometimes brackish water
fish
 Carp fish less affected and increase in fish which
live at the bottom
 Severity increase in high water temperature and
lower salinity.
 Cyclopoid in shape
 Female only is parasitic

77. • Cant be easily
seen by naked eye.
2mm
• The antennae will
be transformed into
hooks leading to
damage of gill
tissue……………..fed
on blood and tissue

81. Life cycle
• infective stage is 4th copepode stage
• Mature stage is 5th
• mating occures on 6th copepode stage
• male will die after mating while female will die
after production of 3 pairs of egg sacs or 20
days

82. Epizootiology
Hooks penetrate gill tissue leads to hyperplasia
Interfere in blood supply of the squamous
epithelium and respiration in fish
Different area of necrosis giving marbling
appearance
Ended by sloughing of gill filaments

83. Clinical signs and
pathology
1.General sign of fish diseases
2.Respiratory signs
3.Marbling appearance of gill
4.Parasite can be seen by wet
mount preparation

89. Economic importance
 Highly significant epizootic of fish
 Mechanical gill damage due to
hooks
 Secondary fungal and rarely
bacterial invasions
 Decrease growth rate
 High Mortalities

90. Diagnosis
 History
 Clinical sign
 Parasitic identification under the
microscope
 Molecular studies

91. 5- Argulosis- Fish lice-
Branchiurans of fish
 Non specific Temporary parasites of
skin, fins, gills or opercula mucosa
 It called fish lice due to it ability to creep
about over the surface of fish
 Flattened against the side of the body
 Can be seen by naked eye
 Heavy infestation may lead to death
even of large fish

92. Etiology and susceptibility
 Argulus spp affect both
fresh and marine water
fish
 Dorsal surface have a
rigid or semi-rigid chitin
exoskeleton
 Ventral surface has
4. Two suction discs
5. Four pairs of thoracic
legs
6. Two respiratory area
7. No egg sacs

95. pre-oral sting which injects digestive
enzymes

97. Life cycle
7 molts to reach
the adult

98. • After mating female leave host
and swim to aquatic plants or hard
objects to put egg with sticky
mucous material “sometimes
mating occurs in water”.
• life cycle take about 30-100 days
according to water temperature.
• water temperature must be
above 16ºC for completion of life
cycle.

99. Epizootiology
• Argulus feed by first inserting a pre-oral
sting which injects digestive enzymes (or
toxin produced from poisoning gland) into
the body.
• This toxin lead to tissue lysis, lymphocytic
degeneration and break down of the skin.
• They then suck out the liquidized body
fluids with their proboscis-like mouth.

100. 4. This feeding activity causes
intense irritation and localized
inflammation
5. Transmitted via water
supply, mechanically by birds
and amphibians

101. Clinical signs and pathology
1.Fish lice are one of the biggest parasites
(5-10 mm) and visible with the naked
eye.
2. The site of bite appears as red circular
depression with raised margin ( Button
like lesion)
3. skin Hemorrhage and ulcer
4. irritation and jump outside of water to
get rid of parasite
5. general sign of fish disease

108. Economic importance
•They can cause significant morbidity and
mortality
• direct tissue damage
• opportunistic bacteria such as Aeromonas or
Pseudomonas sometimes infect these damaged
areas leading to skin ulcers and gill disease.
• It is also believed that the stylus may
occasionally ‘inject’ viruses and bacteria into the
fish.
• all these lead to severe stress, which often
leads to secondary parasite infestations such as
white-spot and Costia.

109. Diagnosis
 History
 Clinical sign
 Parasitic identification
 Histopathological section
 Molecular studies

110. A) Prevention of crustacean
parasites
1. Summer drying season
The parasites will die if dehydrated. If a pond or tank is
infected therefore, complete draining and leaving dry will kill off
any parasites
2. copper sulphate as prphylactive treatment
3. Quarantine and restriction of movement of fish.
4. Good water quality .
5. Reduction of over crowding of fish.
6. Proper nutrition of fish.
7. Periodical disinfection of ponds by 120 kg quick lime / hectar.
8. Control of aquatic plants.
9. Control of organic matter.
10. All utensils such as nets, buckets, aereators, must be
disinfected.

111. Treatment and control
1. Chemicals interrupt life cycle
a chitin inhibitor drugs such as Dimilin will stop the
juveniles developing as they moult their exoskeleton, most
of the results have shown these compounds such as
Lufenuron and Diflubenzuron to be entirely nontoxic to
fish or other animals.
2. The most common treatments are organophosphates,
Masoten and Malathion. Using three treatments over the
estimated life cycle of the parasite. At typical summer pond
temperatures of 20ºC or higher, treatments at 10-day
intervals will kill existing adults and juveniles as well as
emerging juveniles.
3. In small number reared fish mechanical removal of the
parasites and dip in disinfectant (Potassium permanganate)
and antibacterial drugs
4. Potassium permanganate is useful in Ergasilus

112. Endoparasitic Metazoa
Digenetic trematode Cestode Nematode
Parasitic cataract Ligulosis Contracaecum
Yellow grub disease Diphylobothriasis Amplicaecum
Black spot disease Anasakiasis
white grub disease
Metacercarial disease Acanthocephala
Blood fluke

113. 1- Digenetic trematod
• Trematodes that have a complex life cycle need one or more
host
• Most digenetic trematodes are not a serious threat to fish
health; however, their presence often renders the fish
undesirable by consumers.
• There are 2 main groups
•Fish act as intermediate host: fish contain metacercaria or
encysted metacercaria until will be eaten by final host such as:
a- Diplostomum spathaceum, parasitic cataract, eye fluke
b- Clinostomum species, yellow grub disease
c- Apophilus donicus, black spot disease
•Fish act as a final host: fish contain adult parasite and
produce egg that leave fish to complete life cycle.

114. General life cycle of digenetic trematode
Die within
hours

115. a- parasitic cataract - eye fluke
Etiology and Life cycle
Diplostomum spathaceum
Final host is aquatic birds
Site in the final host intestine
First IH is snail as Limnia snails
Second IH is Fish
Site in fish eye tissue

116. Epizootiology
•The usual route of transmission from snail to
host fish is through water and active
penetration of the cercria
• Very rare the transmission is possible by fish
feeding on snails containing cercariae.
• This parasite lodges itself in the eye of a fish
and induces cataract formation (from it's
metabolic waste) this in turn increases
predation on intermediate fish, because the
fish is less able to get away from predator due
to its new vision handicap.

117. Clinical signs and pathology
• The fluke occurs
in the lens and fluid
portion of the fish’s
eye.
• A popeyed effect
is sometimes
created from
accumulation of
fluids in the
eyeball.
(Exophthalmia)

118. • In advanced
cases, the eye
becomes opaque
white and the
fish becomes
partially or totally
blind.

121. This is a photo of a fish eye encysted with Diplostomum Spathaceum

123. B- yellow grub disease
Clinostomum marginatum
Etiology and Life cycle
• Final host is aquatic birds
• Site in the final
3. infected fish is eaten by a fish-eating bird
4. the fish passes down into the stomach of the bird
5.the cyst walls are digested by enzymes.
6.The freed grubs migrate up the esophagus to the
trachea or the mouth cavity. Or drop with faeces
7.the grubs attach themselves and become sexually
mature adults.
8.the bird thrusts its beak into the water to feed, eggs
laid by the adults are released into the water.

124. First IH is snail as Helisoma
Second IH is Fish (Cercaria burrow through
the skin and encyst forming encysted
•
metacercaria). Metacercaria released from
their cysts are large and yellow in color ,
reaching up to 5-6 mm in length and 2 mm in
width
Site in fish under the skin, gills and
muscles sometimes in body cavity and
internal organ
The grubs can live for four years in
individual fish.

128. If the cyst is broken open, a yellowish or whitish parasite will be found

130. Clinical signs and pathology
1- Yellowish vesicle can be seen in
skin, muscles, gills and sometimes
in internal organs
2- when affect gills show respiratory
manifestation
3- general sign of fish sickness
4- in human Inadequate cooking
lead to haulzun disease

131. c- black spot disease- Apophilus donicus
Etiology and Life cycle
Final host is aquatic birds
Site in the final intestine
First IH is snail as Planorbella
Second IH is Fish
Site in fish skin, tail base, fins,
and musculature

135. Clinical signs and pathology
1. Variable sized black spots (1 to 3 mm) in the skin, tail
base, fins, and musculature.
• The metacercariae of the black grub become
encapsulated by host tissue
• melanophores surround the outer layers
• the dark color of the embedded grub causes affected
fish to have a “peppered” appearance
2- Until the black grubs become encapsulated in the host,
the host loses lipids (fats) and their oxygen requirements
increase.
• Heavily infected cold water fish often enter the winter
months in lipid depleted (low fat) state; consequently,
these fish have few energy reserves to last over winter
and that would affect their ability to survive.

136. Economic importance
1. These parasites normally do not kill fish
except in case of vital organ, but may
reduce the growth rate if heavily infested.
2. The presence of digenetic trematodes
often renders the fish undesirable by
consumers.
3. It leads to sporadic mortalities
4. Fish will be easily predated by enemy
5. Proper cleaning and cooking will render
the parasite harmless to man.

137. Diagnosis
 History
 Clinical sign
 Parasitic identification
• identify the metacercaria
• cyst can be released by enzymatic excystation
using hatching solution or digestive solution
• Complete the life cycle or developed in their
natural host
 Histopathological section
 Molecular studies

138. D- Blood fluke
Sanguinicoloiasis
Etiology and Life cycle
Final host is fish
Site in the final flukes of the vascular
system of freshwater and marine fish.
First IH is snail as Limnia
found in cyprinid and salmonid fish in
which it is a serious pathogen,
especially in cultured carp.

139. Etiology and life cycle
Blood flukes
(Sanguinicola) live
as adults (in
groups /solitary)
in the arterioles of
the blood
vessels of the
mesenteries,
hepatopancreas,
pericardium,
eye, gill, and
caudal kidney of
salmonoides and
other fish species.

140. • These tiny worms lay eggs that
become trapped in the capillary
beds of the gills and other organs
where they developed into
meracidia
• The ciliate miracidia burst from
the gill to be eaten by the
operculated snail, the only
intermediat host.
• Cercaria emerge from the snail
and penetrate fish to complete the
life cycle.

141. After Cercaria penetrate the skin pass to
blood and then to internal organs cause
inflammation and decrease the
physiological and mechanical efficiency of
these organs. In some cases, they kill the
host.

143. Clinical sign and pathology
Acute form occurs when heavy numbers of the
1.
parasites present in brachial BVS (Occlusion,
thrombosis, rupture and necrosis) leading to
respiratory manifestation and massive mortalities.
subacute form occures when heavy numbers of
2.
the parasites present in kidney Bvs (Glomerular
occlusion- chronic nephritis) leading to general
symptoms of ascites
Chronic form occures when small numbers of the
3.
parasites scattered in the different body organs
leading to emaciation and anemia.

145. Economic importance
1- Massive mortalities when
affect fish in acute form
2- loss of fish flesh
3- anemia and fish become
predisposed for opportunistic
pathogens
3- Damaged kidney and
spleen

146. Diagnosis
 History
 Clinical sign
 Parasitic identification
 Histopathological section
 Molecular studies

147. Prevention and control
 All control measurements to
metacercaria are difficult because of
the complexity of the life cycle,
shortage of blood supply and disease
condition.
 There is no known control of
digenetic trematodes in ponds,
other than the possible control of
the snails and the birds

148. The following will help in the reduction of the occurrence.
1- Control of snails
A- Mechanical control
4.aquatic vegetation act as a food and shade for snails so the reduction of
aquatic vegetation will interrupt the life of snails.
5.The water inlet should have a small mesh size to avoid introduction of
snails to the pond
B- Biological control
7.Rearing of some snail eating fish such as snail carp
8.Rearing of some duck and geese that fed on snails
9.Some viruses and fungi that is fatal to snails and save to fish
10.Snails that fed on snails but not act as IH for fish pathogene
C-Chemical control
•Copper Sulfate used to control both snails and algae but should not harm fish
•OPC and CHC
2- Aquatic bird control
• control the disease in the surrounding birds
• Deep water at the pond edge discourages birds that feed in shallow water
3- Summer drying season

149.  Monogenean infestations are more
dangerous or digenean infestations
2. Have a direct life cycle.
3. Mode of attachment.
4. Rapid multiplication.

150. Endoparasitic Metazoa
Digenetic trematode Cestode Nematode
Parasitic cataract Ligulosis Contracaecum
Yellow grub disease Diphylobothriasis Amplicaecum
Black spot disease Anasakiasis
white grub disease
Metacercarial disease Acanthocephala
Blood fluke

151. Cestodes of fish
 Ribbon like parasite, divided into scolex, neck
and stroblia
 Fish may be act as final host: present in the
intestine and pyloric caeci of fish as sexually
mature worm eg Proteocephalus
 Fish may be act as IH: larval form
(plerocercoid ) present outside intestine
4. vital organ ( Brain, heart ..)
5. Less vital ( body cavity, visceral organs and
muscle) it will be dangerous in large numbers

152. Life cycle

153. 1- Ligulosis
 Ligula intestinalis larva
Final host is aquatic birds
Site in the final intestine
First IH is copepodes as cyclop
Second IH fish body cavity (length
20-40 cm, width 0.5-1 cm and
express 10% of body weight).
Perch, pike perch, numerous cyprinids
and trout are susceptible

160. Clinical sign and PM
lesions
1. Reduced growth and emaciation
2. Anemia and dark coloration
3. Enlargement of the abdomen in post
cephalic region
4. Peritonitis and atrophy of internal organ
5. internal organs showed hemorrhage,
necrotic white areas and ascites.

161. 2- Diphylobothriasis
 Diphylobothrium latum
 affect fresh water and marine water fish
This is the longest tapeworm found in man, ranging
from 3-10 meters with more than 3000 proglottids.
Final host are man sometimes fish eating
mammals such as dog and cat
Site in the final intestine (3-10 m)
First IH is copepodes as cyclop and diatoms (500
um)
Second IH fish such as (pike, perch, salmon,
trout and eel)

164. Hexacanth
embryo

165. Etiology and Life cycle
 Eggs discharged from gravid proglottids in the small
intestine of final host are passed in the feces.
 The egg hatches in fresh water to produce a ciliated
coracidium which needs to be ingested by a water flea
(Cyclops) where it develops into a procercoid larva.
 When infected Cyclops are ingested by the freshwater
fish, the procercoid larva penetrates the intestinal
wall and develops into a plerocercoid larva
 Man and other animals are infected by eating
uncooked fish, mature into adult worms in 3 to 5
weeks.

169. Clinical signs
1. Plerocercoids are found encysted or lying in
the viscera and musculature of marine and
fresh water fishes.
2. migrating larvae can cause much damage
with adhesions, sterility and even mortality
3. The presence of this cestode affect the
market value of fish.

170. Economic importance of
cestodes
Migratory larval stages leads to peritoneal
adhesions or damaged viscera because of
pressure necrosis, other species may affect eye
leading to blindness
 Poor growth and chronic mortalities
 Sterility and stop spawning
 Miserable appearance of fish affect marketing
 (Diphyllobothrium latum) can have hypochromic
anaemia because it takes up vitamin B12, which
is necessary for red blood cells to mature

171. Diagnosis
 History
 Sign
 PM lesions
 Parasitic identification
 Molecular study

172. Prevention and control
 Prevent human being from infection
by Freezing for 24 hours, thorough
cooking or pickling of fish kills the
larvae.
 Fish reservoirs should be kept free of
raw sewage
 Treatment of adult worms in final
host using suitable anthelmentic
drugs

173.  If fish act as final host, use:
• Di-N-butyl tin oxide 0.5- 0.6 %of diet for
3 days
• Praziquantel bath 2 mg / liter for 1 - 3
hours
or oral 50 mg / kg body weight / day
 Summer drying season for copepode
control

174. Nematodes of fish
 It is cylendrical parasites with separate sex
 Either oviparous or viviparous
 Fish may be act as a final host or intermediate
host or both at the same time
 The larval form in fish either uncapsulated or
capsulated by host CT
 When fish act as final host the mature parasite
will be found in the intestine
 When fish act as IH the parasite will be found
in the abdominal cavity or musculature

175.  When fish act as IH it will be more dangerous than
FH where it will usually affect a vital organ not
intestine as well they infect the tissue and cause
tissue damage during its migration
 Nematodes are more noticeable than other
endoparasites due to their cuticle are more
resistant to the post mortem autolytic enzyme
in the dead fish and remain alive.
 The most common nematodes are
4. Contracaecum
5. Amplicaecum
6. Anasakis

177. A- Contracaecum
Mesentry worm disease
• affect mainly freshwater fish, sometimes
brackish
• Final host fish-eating birds, marine mammals
and sometimes carnivorous fish.
• Site in the final intestine
• First IH is copepodes as cyclop
• Second IH fish
• Site in fish in the body cavity and mesenteries
• human act as a reservoir host if ate uncooked
infected fish

178. B- Amplicaecum
Heart worm disease
• affect mainly freshwater fish
•Site in fish in the body cavity and mesenteries
mainly in the pericardium and heart

179. Clinical sign and PM
lesions
1. encapsulated larval form of variable size in
tissues
2. Round worms (red or white ) are found
within the encapsulation and the lesions
3. Free, non-encapsulated worms also occur in
the abdominal and pericardial cavity and in
sinus venosis (in case of heart worm disease)
4. necrotic lesion in the dermis, the sub dermis
and visceral organs
5. deformed or atrophic gonads.

194. C- Anasakiasis
Herring worm disease
• occur worldwide and all species of
fish are susceptible.
• common in marine mammals
especially Herring fish.

196. The infected crustacean is subsequently
eaten by a fish or squid, and the nematode
burrows into the wall of the gut and encysts
in a protective coat, usually on the outside of
the visceral organs, but occasionally in the
muscle or beneath the skin.

197. Clinical signs and PM
lesions
1. In the live fish larvae may be free or coiled in
capsule of host connective tissue
2. Distension of abdomen will be observed OR
sometimes affected fish show no external
signs
3. They can be found on or in the viscera, body
cavity, skeletal muscles and mesenteries

198.  If third stage larvae consumed in row or
inadequately cooked fish, it will cause
2. serious gastrointestinal damage
3. acute pain
4. vomiting
5. Diarrhea and blood in stools
6. fever.
7. Larvae can penetrate the digestive tract and
enter the body cavity.

202. Economic importance
1. decrease the commercial value of
affected fish
2. Cause many diseases in fish and man
3. Larval migrations lead to dangerous
effect on vital organ
4. Poor growth and chronic mortalities
5. Sterility and stop spawning

203. Prevention and control of
Nematode
1. Anisakiasis can be avoided by rapid evisceration
and preparation fillets, deep freezing to -30 and
sufficient marination or thorough cooking
2. Regular examination of fish for parasites.
3. Mature parasite use:
• Fenbendazole orally 25 mg / kg body weight / day
for 3 days or prolonged immersion 2 mg / liter
• Levamisole HCL orally 2.5 – 10 mg (8mg) / kg
body weight / day for 7 days or prolonged
immersion 10 mg / liter