Khaledselimlefish diseases

Khaled M. Selim

110509

In the Name of Allah, the Most Beneficent, the Most Merciful.

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.

Fish diseases

Parasitic Diseases External or Ectoparasitic

Affect head, fins, skin, eye, opercula, buccal cavity, the surface of nasal epithelium or olfactory epithelium, crypts of the acoustolateralis system or gills.

Internal or Endoparasitic

internal organ- blood – swim bladder and deeper layer of muscles

Metazoal Diseases

Lerneosis Ergasilosis Argulosis

Endoparasitic Metazoa Digenetic trematode

Cestode

Nematode

Parasitic cataract

Ligulosis

Contracaecum

Yellow grub disease

Diphylobothriasis

Amplicaecum

Black spot disease

Anasakiasis

Blood fluke

Acanthocephala

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

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

•The identification of monogenea depends on 1. Haptor structure

2- Eye spots or pigments 3- Body size

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

7- Feeding behavior

very small eye spots

8- Host specificity, geographical distribution and season

Benedenia and Neobenedenia spp

Life cycle

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.

Epizootiology  Mechanical transmission by birds, reptile and

amphibians  Nets and buckets are vehicle of transmission

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

Abnormal swimming and movement

 Loss of appetite  Remain at the

side or bottom of the pond  Restlessness  Listlessness  Emaciation  Hyperirritability

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

• Minute abrasions

or erosion  Sometimes small ulcer  hyperemia at the base of the fins  Sometimes secondary invaded by bacteria or fungi

III. General signs of gill affections  Aggregate on

water inlet  Aggregate on water surface  Gasping of air  Increase opercula movement

 Vertical

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

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

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

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

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 1. Dipterex: prepare 50% solution in xylene and apply it to the pond at a dilution of 0.8ppm.

2. Potassium permanganate 20ppm with 4% Nacl 3. Methylene blue, Malachite green formalin, Ammonium hydroxide, masotene….etc 

Metazoal Diseases Ectoparasitic Metazoa Monogenetic trematode

Hirudinea or leech

Crustacean or Copepode Lerneosis Ergasilosis Argulosis









2- Hirudinea – leech – Annelid worm of fish, Parasites 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

 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 for cocoon deposition

Leave after the meal searching for shelter

Etiology / susceptibility  Class: Hirudinea

Phylum: Annelida Subphylum: Clitellata order: Rhynchobdellida Family: Piscicolidae (Cylendrical leech) – 4-8 cm 2) Family: Glossiphoniidae (flat leech)- 2-4 cm (Most important)

1)

 The

1.

2.

3.

4.

identification of leeches depends on Body shape Length of the body Pigmentation colour and pattern Numbers and arrangement of the eyes

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

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



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.

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

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

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 1. Dipterex: prepare 50% solution in xylene and apply it to the pond at a dilution of 0.8 ppm.

2. Masotene: 0.5-1 ppm in fish pond but harmful to zooplankton.

3. Neguvon 1ppm for 5 days is effective against adult leeches but not eggs 4. We can use OPC or chlorine * Marine water leeches have very little trials for treatment. 

Metazoal Diseases Ectoparasitic Metazoa Monogenetic trematode

Hirudinea or leech

Crustacean or Copepode Lerneosis Ergasilosis Argulosis

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.

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: 1. Lernea 2. Ergasilus.

3. Argulus 

General life cycles of Crustacean parasites Mature male or female Fertilized egg

Copepode stages

napuli

Meta napuli

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



Etiology and The are long slender copepod suscebitability

 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

Affect mainly freshwater fish • There was two common species which include 1. Lernea cyprinacea (host specific) affect carp fish and accidentally other fish species 2. Lernea elegans (non host specific) •

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

The cycle will not be completed at the following 1.Temperature lower than 15ยบC 2.Drying 3.Salinity of 1.8% 4.Lower pH 7

Epizootiology

 Contaminated water, infected

fish or carrier such as amphibians or birds.

1.

Clinical signs and pathology Lernea itself can be

seen by naked eye 2. They penetrate beneath scales and cause a lesion at the point of attachment (inflammationhemorrhagic and erythematic lesion)

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

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

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

4- Ergasilosis- gill rot  crustacean parasite affect gill of

fish.

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

• 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

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

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

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

Economic importance

 Highly significant epizootic of fish  Mechanical gill damage due to

hooks  Secondary fungal and rarely bacterial invasions  Decrease growth rate  High Mortalities

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

5- Argulosis- Fish liceBranchiurans 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

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 1. Two suction discs 2. Four pairs of thoracic legs 3. Two respiratory area 4. No egg sacs

pre-oral sting which injects digestive enzymes

Life cycle

7 molts to reach the adult

• 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.

Epizootiology 1. Argulus feed by first inserting a pre-oral sting which injects digestive enzymes (or toxin produced from poisoning gland) into the body.

2.This toxin lead to tissue lysis, lymphocytic degeneration and break down of the skin.

3.They then suck out the liquidized body fluids with their proboscis-like mouth.

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

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

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.

Diagnosis

 History  Clinical sign  Parasitic identification  Histopathological section  Molecular studies

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.

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 20ยบC 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

Endoparasitic Metazoa Digenetic trematode

Cestode

Parasitic cataract

Ligulosis

Contracaecum

Yellow grub disease

Diphylobothriasis

Amplicaecum

Black spot disease white grub disease Metacercarial disease Blood fluke

Nematode

Anasakiasis Acanthocephala

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 1.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

2.Fish act as a final host: fish contain adult parasite and produce egg that leave fish to complete life cycle.

General life cycle of digenetic trematode

Die within hours

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

Epizootiology •The usual route of transmission from snail to

host fish is through water penetration of the cercria

and

active

• 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.

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)

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

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

B- yellow grub disease Clinostomum marginatum Etiology and Life cycle • Final host is aquatic birds • Site in the final 1. infected fish is eaten by a fish-eating bird 2. the fish passes down into the stomach of the bird 3.the cyst walls are digested by enzymes.

4.The freed grubs migrate up the esophagus to the trachea or the mouth cavity. Or drop with faeces 5.the grubs attach themselves and become sexually mature adults.

6.the bird thrusts its beak into the water to feed, eggs laid by the adults are released into the water.

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.

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

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

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

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.

Economic importance 1.

2.

3.

4.

5.

These parasites normally do not kill fish except in case of vital organ, but may reduce the growth rate if heavily infested.

The presence of digenetic trematodes often renders the fish undesirable by consumers.

It leads to sporadic mortalities Fish will be easily predated by enemy Proper cleaning and cooking will render the parasite harmless to man.

Diagnosis  History  Clinical sign  Parasitic identification

1.

identify the metacercaria

cyst can be released by enzymatic excystation using hatching solution or digestive solution 3. Complete the life cycle or developed in their natural host  Histopathological section  Molecular studies 2.

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.

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.

• 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.

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.

Clinical sign and pathology 1. Acute form occurs when heavy numbers of the

parasites present in brachial BVS (Occlusion, thrombosis, rupture and necrosis) leading to respiratory manifestation and massive mortalities.

2. subacute form occures when heavy numbers of the parasites present in kidney Bvs (Glomerular occlusion- chronic nephritis) leading to general symptoms of ascites 3. Chronic form occures when small numbers of the parasites scattered in the different body organs leading to emaciation and anemia.

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

Diagnosis     

History Clinical sign Parasitic identification Histopathological section Molecular studies

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

The following will help in the reduction of the occurrence.

1- Control of snails A- Mechanical control 1.aquatic vegetation act as a food and shade for snails so the reduction of aquatic vegetation will interrupt the life of snails.

2.The water inlet should have a small mesh size to avoid introduction of snails to the pond B- Biological control 1.Rearing of some snail eating fish such as snail carp 2.Rearing of some duck and geese that fed on snails 3.Some viruses and fungi that is fatal to snails and save to fish 4.Snails that fed on snails but not act as IH for fish pathogene C-Chemical control 1.Copper Sulfate used to control both snails and algae but should not harm fish 2.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

Monogenean infestations are more dangerous or digenean infestations 1. Have a direct life cycle.

2. Mode of attachment.

3. Rapid multiplication. 

Endoparasitic Metazoa Digenetic trematode

Cestode

Parasitic cataract

Ligulosis

Contracaecum

Yellow grub disease

Diphylobothriasis

Amplicaecum

Black spot disease white grub disease Metacercarial disease Blood fluke

Nematode

Anasakiasis Acanthocephala

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 1. vital organ ( Brain, heart ..)

2. Less vital ( body cavity, visceral organs and muscle) it will be dangerous in large numbers

Life cycle

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

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.

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 um)

(500

Second IH fish such as (pike, perch, salmon, trout and eel)

Hexacanth embryo

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.

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.

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

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

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

 If fish act as final host, use: 1. Di-N-butyl tin oxide 0.5- 0.6 %of diet for

3 days 2.Praziquantel bath 2 mg / liter for 1 - 3 hours or oral 50 mg / kg body weight / day  Summer drying season for copepode control

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

 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 1. Contracaecum 2. Amplicaecum 3. Anasakis

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

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

Clinical sign and PM lesions 1. encapsulated larval form of variable size in 2.

3.

4.

5.

tissues Round worms (red or white ) are found within the encapsulation and the lesions Free, non-encapsulated worms also occur in the abdominal and pericardial cavity and in sinus venosis (in case of heart worm disease) necrotic lesion in the dermis, the sub dermis and visceral organs deformed or atrophic gonads.

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

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.

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

 If third stage larvae consumed in row or

inadequately cooked fish, it will cause 1. serious gastrointestinal damage 2. acute pain 3. vomiting 4. Diarrhea and blood in stools 5. fever.

6. Larvae can penetrate the digestive tract and enter the body cavity.

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

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