FISH DISEASE
Kamonporn Tonguthai, Ph.D.
Lecture by Temdoung Somsiri, Ph.D., Somkiat Kanchanakarm, Ph.D.,
Titiporn Laoprasert, Jaree Polchana and Varinee Punyawachira
Inland Aquatic Animal Health Research Institute,
Inland Fisheries Research and Development Bureau,
Department of Fisheries, Thailand
Introduction
Fishes are subject to a wide spectrum of diseases. Scientific efforts have been
made to understand causes of disease in fishes and to attempt control. Disease of
fishes require a somewhat different approach to problem solving than diseases
involving terrestrial animals.
Fish are poikilothermic, and their internal biological systems are tremendously
altered by water temperature and other physiological factors of the enviroment, pH,
osmotic pressures, dissolved gases etc. These factors also determine if an etiological
agent can or will cause disease among fishes.
Fish disease diagnostician must have a broad knowledge not only know the
disease causing agents but also the aquatic environment in order to relate clinical
finding to disease entities.
The advent of more successful fish culture has enhanced the study of fish
health and disease problems.
Snieszko (1974) explained the relationships between host pathogen and
environment by 3 circles.
The disease state occurs through interaction of the host, pathogen and
environment.
Good management practice results in health fish and better growth. Adverse
environmental condition affect the disease susceptibility.
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Non infectious Disease
Fish is a poikilothermic animal. It is more sensitive to and dependent on it's
environment than the warm blooded terrestial animal.
This diseases occur due to adverse environment or water qualities changes. The
disease then sometimes calls “water quality disease”. The causes of non-infectious
diseases are:
1. Direct environmental effects
2. Nutritional effects
3. Dietary toxicity
1. Direct Environmental Effects
1.1 Temperature
This is probably the single most important factor in both pond and aquarium
situations. Fish has its own preferred range. Rapid changes within this range represent
stressful conditions.
In general terms, fish will tolerate a temperature drop better than a rise. Some
species are more susceptible to temperature stress than others and this is thought to be
due to a poorer ability to osmoregulate at the new temperature, Higher temperatures
cause an increased metabolic rate and hence an increased O2 demand necessitating
increased "irrigation" rates. The increased water flow past the gills causes an
increased water influx and thus possible compromise of the osmoregulatory
mechanisms.
Fish also appear much more susceptible to bacterial diseases in conditions of rising
water temperatures.
A sudden rise or fall in water temperature is a direct stress: survival rate and
the ability to combat disease are much lower outside the optimum temperature range
of the fish. High temperature causes respiratory distress, particularly if the respiratory
capabilities of the fish are already compromised by the presence of established gill
disease. This situation can lead to acute mortalities
1.2 Oxygen
Small fish have higher requirements than older larger ones. Fish will normally
demonstrate an 02 lack by gathering at inlets or by gasping at the surface. Gill
damage, or anaemia can be symptom of oxygen deficiency in water.
1.3 Supersaturation (gas bubble disease)
Water which is supersaturated with gas, either 02 or N2, may cause the
condition gas-bubble disease. Small bubbles forming in superficial blood vessels can
be seen, typically, on gills and fins and also behind the eye. The problem can be cured
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within the system by agitating, or just aerating. Those that recover will often be runts
or more susceptible to disease. Young fish are especially susceptible. A chronic form
of gas-bubble disease can occur due to low-level supersaturation, and may result in
cataracts, fin rot and gill disease.
1.4 Suspended solids
The presence of suspended solids in the water can cause irritation to the gill
epithelium and result in significant pathological changes and respiratory problems.
Overfeeding and high levels of fish faeces in the water will cause a general
deterioration in water quality and also contribute to the suspended solids.
1.5 Ammonia
Un-ionised ammonia (the toxic form) will primarily cause direct gill epithelial
damage with consequent hyperplasia and reduced ability to take up oxygen.
Depending on species, there may also be liver, kidney and brain damage with reduced
activity and growth. Low levels can produce chronic stress. The level will vary with
pH and temperature, being minimised by low values of both these parameters
1.6 Nitrites and nitrates
Nitrates are generally considered to be non-toxic to fish, but nitries are highly
toxic. If present at sufficient levels, nitrites can cause the production of
methaemoglobin with consequent hypoxia and cyanosis.
1.7 Carbon dioxide
Increasing levels of CO2 in the blood (or a decreasing pH) decreases the
affinity of hemoglobin for O2. Fish hemoglobin is very sensitive to CO2. Level of less
than 6 mg/l of free CO2 are usually recommended. High levels can interfere with
oxygen uptake and can also cause nephrocalcinosis, a condition where calcium
carbonate is deposited within the kidney tubules.
1.8 Chlorine
It is extremely toxic to fish, causing acute gill damage consisting of epithelial
hypertrophy and necrosis. Chronic exposure can result in epithelial hyperplasia with
consequent respiratory distress.
1.9 Toxic organic compounds
The number of organic compounds toxic to fish is huge and includes such
chemicals as PCBs, detergents and hydrocarbons. Usually problems are due to
accidental spillage or contamination of water supplies upstream. Clinical symptoms
and toxic effects will vary with the type of compound, but tend to include distress,
avoidance behavior, respiratory failure and death. Sub-lethal effects may occur such
as imbalance, blindness, anaemia, skin lesions, poor growth, tumors, etc.
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2. Nutritional Effects
There can be a wide variation in the quality of the diet received by farmed fish.
Factors include the poor availability of suitable constituents, poor formulation and
processing, lack of knowledge and understanding of dietary requirements, or
inappropriate storage. The formulation, quality and consistency of some fish diets are
probably much better than for species whose aquaculture is in the early stages of
development or in countries where appropriate constituents are not available.
However, problems can still occur with well established diets.
2.1 Starvation
Sign of starvation are easy to spot. Starvation may affect only a proportion of
fish in a group if there is a significant size disparity within the population. There is a
strong feeding hierarchy which becomes more emphasised as size differences
increase. The problem can be corrected by grading the fish into groups of similar size
and by attention to feeding technique, ensuring that all fish have access to the feed.
Singns of starvation will also be seen if there is a deficiency of certain essential
nutrients, e.g. an essential amino acid or vitamin. The nutritional value of the diet will
be limited by the level of the specific nutrient.
Deficiency of protein or essential amino acids will normally result in retarded
growth and symptoms similar to those seen in starvation.
A small number of pathologies have been linked with a specific amino acid
deficiency (e.g. cataract in methionine and/or tryptophan deficiency, and spinal
deformity also associated with tryptophan deficiency and possibly other amino acids
such as lysine).
Diets deficient in essential fatty acids can result in retarded growth, fatty livers
and fin erosion.
The most important pathology associated with lipids is that caused by an intake
of rancid (oxidised) fat. Lipid oxidation results in the production of compounds such
as peroxides and free radicals, which are toxic to the fish and also reduce the
nutritional value of other dietary constituents. The toxins cause liver and kidney
pathology and extreme anaemia. Symptoms associated with this 'liver lipoid disease'
include pallor of the gills, darkening of the skin, the presence of swollen, fatty, pale
liver and often ascites and popeye. Mortalities can be high in severe cases.
Experimentally induced mineral deficiencies have caused several pathological
conditions in a number of species. Cataracts in trout and carp, goitre in various
salmonids caused by iodine deficiency and irondeficient anaemias. Other mineral
deficiencies have been said to cause anorexia, poor growth and other relatively nonspecific symptoms.
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The problems associated with vitamin deficiencies.
Vitamin
Water-soluble
Ascorbic acid (vitamin C)
Thiamine (vitamin B1)
Riboflavin (vitamin B2)
Pantothenic acid
Pyridoxine
Vitamin B12
Folic acid
Fat-soluble
Vitamin A
Vitamin D
Vitamin E
Vitamin K
Symptoms of deficiency
'Brittle bones' and skeletal deformities
Poor wound healing
Poor growth and nervous symptoms
Cataract and corneal opacity
Pigmentation abnormalities
Poor growth
Fin erosion
'Clubbing' of gill filaments (nutritional gill disease
Nervous symptoms
Poor growth
Blood dyscrasias
Blood dyscrasias
Blindness
Pigmentation abnormalities
Few specific deficiency signs reported
Fatty liver
Muscular dystrophy
Steatitis
Haemorrhage
Infectious Disease
Disease causes by pathogenic organisms including: parasite, bacteria, viruses,
and fungi
Parasites
Terms commonly mention in Parasitology
Symbiosis is used to describe the cohabitation between two dissimilar
organisms, classified as mutualism, commensalism, parasitism or predation depending
on the advantage or disadvantage derived from the relationship.
Mutualism is used to describe those close associations in which both animals
are benefited.
Commensalism is used to describe those close associations in which one
animal is benefited but the other is neither benefited nor harmed.
Parasitism is used to describe those close associations in which one animal
lives at the expenses of or harms the other. The organism is called parasite. Parasite
is an individual or species which nourishes itself at the expense of another species.
Which it affects adversely but does not immediately destroy.
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Host - Parasite Relationship to study this relationships requires knowledge not
only of the parasite but also of the host. Hosts are classified by the purpose served to
the parasite.
Definitive host known as the primary or final host in or on which the parasite
reaches adulthood.
Intermediate host is also called an alternate or secondary host to describe a
host in or on which the parasite passes a larval or nonsexual existence.
Transport host is a type of intermediate host in or on which the parasite exists
but no further development toward adulthood occurs.
Temporary host is a host in or on which the parasite lives briefly then leaves
to become free living.
Reservoir host serves as a source of parasites for other hosts by haboring the
parasite.
Life cycle is used to define the intricate association between the parasite and its
host. It is in actuality all stages of development in the life of the organsim.
A continuous life cycle is a life cycle in which the parasite remains in or on
the host from generation to generation. There is no need for the parasite to leave the
host. The parasite is designated as a continuous parasite.
If the parasite spends all its life on one host except for a brief time away from the host
as an egg or cyst, only to recombine with the host after the egg hatches or the cyst
returns to active life. It is called partial continuous parasite.
Parasitic Diseases
Introduction
A great number and diversity of animal species are capable of parasitising fish,
ranging from microscopic protozoans to grossly visible crustaceans and annelids.
In the wild, there is a large range of parasites but they are usually only present
in small numbers; they can be considered a normal finding and rarely cause disease
problems. There is a stable relationship between the parasite and the fish host in the
wild and regulating systems have evolved to ensure that parasitic burdens do not
increase to threaten the life of the host. It is only if these regulating systems become
disturbed, often by the action of man, that parasitic disease in the wild may be seen. It
must be borne in mind, however, that outbreaks of parasitism in the wild may go
unnoticed.
In cultured fish, there is a more limited range of parasites but they are often
present in much larger numbers than seen in the wild. There is always a risk of
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parasitic epizootics in farmed fish and this increases with the intensification of the
farm system. Many factors in fish culture will favour parasitic disease; an awareness
of these factors will allow remedial or preventive action to be attempted.
Factors favor parasitic diseases
(1) Stocking density is usually high in fish culture systems and the propinquity
of the host fish favours the transmission of parasites. This is particularly the case with
parasites having a direct life-cycle, such as the ectoparasitic protozoa, which always
have substantial reproductive capabilities to ensure that some offspring locate a
suitable host. Hosts are readily available in a farm environment and overwhelming
parasitic infestation can occur.
(2) Physical trauma Farmed fish are more prone to physical trauma due to
handling, grading, etc. These give an opportunity for parasites to colonise and feed on
damaged tissue.
(3) Pond water. Water in a fish farming facility is frequently sub-optimal in
quality and quantity. Low flow rates allow the accumulation of infective stages within
the system. High levels of ammonia irritate the gills and skin, causing an increase in
mucus production and an increase in surface bacteria and organic material producting
a very favourable environment in which protozoan parasites can flourish and cause
further damage to the surface of the fish. At the same time, high levels of nutrients
from waste feed and faeces will increase the local populations of bacteria and freeliving protozoa, again providing food for the parasites. In this situation many freeliving protozoa will use the fish as a convenient feeding platform and, while not
directly parasitic to the host, may cause problems due to the sheer numbers of
protozoa present. Some of the crustaceans and molluscs feeding on the waste organic
material may act as intermediate hosts to some of the parasites with indirect lifecycles. Increased nutrient levels in the water may also irritate the gills and skin of the
fish, again favouring parasitic invasion.
(4) Selective breeding Fish are often selectively bred for qualities other than
disease resistance and some strains may be particularly susceptible to disease.
(5) Exotic species the introduction of exotic species of fish may introduce new
parasites to existing (often highly susceptible) fish stocks. Any introduction of new
stock may precipitate disease in either the existing stock or the introduced stock.
(6) Predator. Fish stocks will attract predators (e.g. piscivorous birds) which
may act as intermediate hosts to some parasites.
(7) Environment. Environmental changes, such as a sudden rise in
temperature, may favour the parasite but stress the host. Outbreaks of parasitic disease
are common in overwintered fish whose disease resistance may be poor, making them
very susceptible to the increase in parasite numbers that occurs when water
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temperatures start to rise in spring. Any change in water quality may also stress the
host while favouring the parasite.
(8) Husbrandry System. The system of husbandry may be more likely to
expose fish to parasites. Earth pond systems favour the completion of the life-cycle of
some parasites, particularly the sporozoans, and also favour the presence of
intermediate hosts. Concrete systems reduce these risks but may cause more physical
damage. Cage systems expose the fish directly to the parasitic fauna of the wild fish
and allow the fish to feed easily on invertebrate intermediate hosts. The husbandry
system also dictates the ease with which treatment and control may be administered;
tank systems are more easy to treat than cages.
Animal parasitic. They appear in many forms protozoa and metazoa, large
and small with simple and complex life-cycle. All with tremendous reproductive
potential and an adaptation to the host(s) in or on which they live.
Animal Parasites
They appear in many forms, protozoa and metazoa, large and small with simple
and complex life-cuycle. AIT with fremendous reproductive potential and an
adaptation to the hoste in or on which they live.
Animal parasitic of fishes are including:
- Protozoa
- Platyhelminths of fish
- Acanthocephala
- Nematoda
- Hirudinea
- Crustacean
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Protozoa
CLASSIFICATION OF PROTOZOA PARASITES
Ectoparasites
Endoparasites
Protozoa
Protozoa
Flagellates:
Ichthyobodo
Flagellates:
Hexamita
Oodinium
Microsporidia: Pleistophora
Thelohania
Ciliates
Peritrichous (cilia
Coccidia:
Eimeria
Restricted to specific
Myxosporidia: Myxosoma
areas of the body
Myxobolus
Trichodinids)
Henneguya
Scyphidia
Thelohanella
Epistylis
Apiosoma
Holotrichous (cilia
Distributed
regularly
over the
body or
arranged in
rows)
Chilodonella
Ichthyophthirius
Flagellate Protozoa
The disease caused by flagellate ectoparasitic protozoa which important for
aquaculture are:
Ichtyobodiasis (Costiasis)
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Ichthyobodo sp.
General Characteristics
This disease causes by Ichtyobodo or Costia. It is the disease of freshwater and
marine fishes, more common in freshwater fishes.
There are two species Ichtyobodo necatrix and Ichtyobodo pyriformis which
are commonly found in SEA. Both are relatively small. Both species have one pair of
posteriorly directed axostyles and one pair of freely moving flagella. The axostyles are
short and tightly attached to the body. The free flagella are longer and are used for
propelling the organism and attaching to the host. The axostyles are used in feeding.
Both species have a small contractile vacuole and a rounded vesicular nucleus. The
body of both Ichtyobodo species is lentile or pyriform shaped in profile. The body is
concave on one side, thus forming a groove which leads anteriorly to a cytostome and
attachment of the flagells. Reproduction is primarily by longitudinal fission, though
sexual reproduction following conjugation may occur, Ichtyobodo species form
nonreproductive resistant cysts which are 7 to 10 micrometers in diameter.
Epizootiology:
Ichtyobodo species are obligate parasites. The trophozoite cannot survive long
away from its host. Ichtyobodo are transmitted from fish to fish through water.
Ordinarily the protozoan attaches to the skin or gills of its host by means of the
flagella. Some individuals may be swept away to become attached to new hosts.
Adverse conditons cause the trophozoites to encyst, sometimes on the fish and
sometimes free in the water. Cysts revert to trophozoites when conditions become
more favorable to the protozoa. Trophozoites derived from cysts must seek and find a
host within a short time or they will die. Thus there are two sources of trophozoites
for transmission to new hosts, those directly from host fishes and those derived from
cysts. Ichtyobodo are spread from one geographical area to another by transporting
infested fishes and water containing encysted Ichtyobodo.
Ichthyobodo lives on the skin and gills of healthy fishes which are occupying a
favorable non-polluted environment; there they occur in an apparently commensalistic
state of symbiosis. The defenses of the host possibly keep the protozoan population
reduced to an acceptable level. A change in the health of the host or a change in the
environment to conditions usually associated with overcrowding in aquaria or fish
culture (low dissolved oxygen, high ammonia content or other skin or gill irritant, low
pH or other condition unsatisfactory to the host) allows survival of more of each
generation of Ichtyobodo. The defenses of the host are overwheimed and the protozoa
revert to a parasitic existence in which the host is harmed.
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Generation time of Ichtyobodo species is temperature dependent. Temperatures
between 10 and 25oC favor rapid reproduction, and generations are produced in a
matter of hours. Reduction of the temperature to below 8oC causes the organisms to
encyst. The organisms apparently cannot survive above 30oC. Tropical fish, therefore
has less problem.
This disease is commonly found in aquarium fish in early of the year when
temperature is low.
must find host within
short times within short
times
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Pathogenicity
Damage is due to the attachment by cytostome. In heavy infection, secondary
infection by bacteria may occur.
Clinical signs
In heavy infection, dull spots, white film occur due to thickening of mucous on
both gill and skin. Fish become lethargic and may refuse to eat.
Moribund fish rise to the surface become sluggish and die. Their sustenance is
derived from sloughed epithelial, cell and cellular debris from the host.
Prevention
As this parasite cannot survive without the host for more than 60 min.
Therefore, leave the pond or aquarium empty for a day or more.
Prevent wild fish or amphibian into pond because it was found in tadpole and
salamander. Raise water temperature about 1 or 2oC may kill the trophozoites.
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Oodiniasis
General characteristics
The disease is caused by Oodinium, which is a dinoflagellate parasite,
spherical and pyriform, about 100 u. Parasitic stage is called trophont. It has no
flagella. It life cycle comprises of three stages, the invasive stage, dinospore has 2
flagella and move freely in water and search for a fish host. Having attached itself to
the fish surface, it transforms into sac like-trophont which is equipped with an
elaborate attachment apparatus, which is a set of root-like cytoplasmic structures or
rhizoid. When the trophonts reach their final stage, detach themselves from the host
sink to the bottom assume a spherical shape and encysted. It starts a series of division
either within a common cystic envelop or the old envelop. The last division produces
the dinospore. Cytoplasm of Oodinium has a foamy appearance with numerous
granules. The species found in Thailand has yellowish pigment. Oodinium is found on
skin, gills. In severe infection the skin will have yellow or brown spot. These
appearance has given it several names velvet, rust, gold dust or white cloud.
Epizootiology :
This parasite is non-host specific. They have oftenly appeared among aquarium
fish. In many cases infection have killed fish in a few days or may be latent with no ill
effects over a long period of time. This parasite infects both marine and freshwater
fishes. Amyloodinium is in salt water.
Life cycle
When it has taken enough nutrient, it drops off, falling to the bottom, begins to
divide several times to obtain about 30-200 flagellates called
dinospores which can live free for only 24 hrs the most. They dies if they cannot find
the host. Once they do find a host they attach themselves to it and drop the flagella.
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Diagnosis
Disease cause by Oodinium is easily to observe by the coating ot the skin with
rusty colour.
Pathogenicity
Damage is due to the penetration of the rhizoids through the host epithelium.
Mechanical penetration may be aggravated by the lytic action of secretion. The skin
reacts by an inflammatory response and a proliferation of epithelial cells, focal
necrosis, hemorrhages and second infection by bacteria or fungi is occurred.
Prevention
Quarantine for 2 weeks
Treatment
Freshwater Oodinium
- NaCl 3-5% dip 1-2 min or 0.5% for 24 hrs
- Trypaflavin 10 ppm for 3-5 days
- 1 gm quinine (use quinine HC1 not sulfate) to 100 liters
of water as a continuous bath for 3 days.
- increasing water temperature slowly and not more then
1oC hourly, not quite recommended unless you have
good facilities
Saltwater Amyloodinium
- use freshwater (gradually change from saltwater to
freshwater.
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Hexamitiasis
Hexamita sp.
General Characteristics :
This disease is caused by Hexamita which is a common endoparasites in
alimentary tract . This protozoa is pyriform or oval in shape, tapering gradually
toward the posterior end. Rounded individuals are quite common. The organisms are
from 6 to 8 micrometers wide and 10 to 12 micrometers long. Hexamita species have
three pairs of anterior flagella which vary in length but are about one and one-half
times the length of the body. These flagella arise from the blepharoplast at the
anterior end of the axostyles. A fourth pair of flagella arise from the axostyles at the
extreme posterior end of the body. A pair of oval nuclei are present at the anterior end
of the body. There is a delicate membrane surrounding the nucleus.
Hexamita species reproduce by longitudinal binary fission. The organism
usually becomes round before dividing. Hexamita species may also reproduce by a
type of schizogony (asexual cycle) within the epithelial cells of the caeca or intestine.
Schizogony furnishes a rapid means of multiplication since the entire process takes
between 24 and 48 hours.
It is one of the most important disease in aquarium fish, particularly discus. In
discus fish, this parasites are found in pyrolic caeca and intestine.
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Epizootiology :
Transmission of Hexamita is probably by the oral route, although the anal route
has been mentioned in the case of free-swimming flagellated forms of the organisms.
Oral transmission may involve the encysted stage taken accidentally with food.
Life cycle
Clinical signs
Signs of hexamitiasis may be the signs of malnutrition, anemia, anoxia, gill
hyperplasia. Fish become dark coloration and listlessness, seek the sides or corners of
the tank. Refuse to take food, flashing, emaciated, extremely slender, abdomen
sunken, gill light in color, gut free of food, secrete white and slimy feces.
Treatment
At present time, methonidazone has been introduced to treat Hexamita in
discus fish at 10,000 ppm. 10-15 tablets/kg of fish (1 tablet has 250 mg
methonidazone). Feed the fish 3 times at 1 wk interval.
This treatment works very well in the early stage of the infection.
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Ciliate Protozoa
Several genera of sessile and motile ciliates have been involved in epizootics of
disease among fishes.
Due to the arrangement of cilia, there are 2 major groups of ciliated protozoa:
Peritrichous and Holotrichous.
Peritrichous
Peritrichous are ciliated protozoa with cilia restricted to specific areas of the
body. Among peritrichous, Trichodinids, Scyphidian, Epistylis and Apiosoma are
commonly found in cultured fishes.
Trichodinids
General characteristics
The major characteristic of the trichodinids are saucer shape, attachment organ
known as the adhesive or sucking disk arranged in the form of three concentric rings.
They can multiply well by simple binary fission. Trichodinid feed on bacteria.
Infected fish shows abnormal coloration, become sluggish, lost weight.
Infected clarias fry are seen to hang vertically at the surface and swirl, in frayed.
Pathogenicity
The harmful effects of Trichodina are aggravated by their mobility so that each
individual extends its influence even a large area. Skin become irritated. Degenerated
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and necrosis of the epithelial cells occur accompanied by proliferation of mucus.
Secondary bacterial infection are facilitated. The disruption of the respiratory process
is the most serious effect of infection and is often causes lethal to fry.
Prophylaxis
Trichodina are capable of living on frog, tadpoles and panktonic crustanceans.
Therefore it is necessary to get rid of these animals.
Dry pond completely for 3-4 days before restocking.
Treatment
- Formalin 25-50 ppm is recommended for prolong treatment
- NaCl 3% dip for 5-10 min.
Epistylis
It is a peritrichia sessilina, cup shape. The cells themselves are capable of
contractile and withdrawal of the peristome into the cell, attach to the host by a
slender cylindrical stalk called scopula, stalk non contractile. Macronuclei are
relatively shorter and sausage-shaped. Stalk compresses the epithelial cells causing
deformation and resulting in functional disorder of epithelial cells. Heavy infection
stimulate mucus production, skin becomes hyperaemia. Macronuclei are relatively
shorter and sausage-shaped.
Apiosoma
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When fully relaxed have the shape of a funnel, when contracted, lose their
pendunclate appearance. The distal end forms the peristomal disc. The scopula or the
attachment organelle at the oboral end with macro and micro nucleus. Macronucleus
has compact and oviform or subconical.
Scyphidia
No clear distinction from Apiosoma, only it has less pronounced peduncle.
Macronucleus is band-shaped and run through a large part of cell.
These three genera are very common in Clarias batrachus and C.
macrocephalus.
Pathogenicity
Heavy infection by these three genera provokes a copious exudate of mucus.
Skin covered by a pale blue coating and whitish mucus appears on the gill. The skin
becomes hyperaemia and the scales might bristle.
These three genera found mostly in the aquatic habitat which are rich of
organic matter. Feed on microorganisms and small protozoa. When associated with
the damage area of the integument may benefit from feeding on the aggregations of
microorganism associate with superficial lesion.
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They are common on juvenile fish, favour soft skin, devoid large scale. They
are found on skin fins, gills buccal cavity and nose.
Dense colonization of these protozoa results in skin irritation. The stalk
compress the epithelial cells causing deformation and resulting in functional disorders
of the epithelium. Heavy infection on the gill can disturb opercular movement and
affecting respiration. Generally cause growth retardation and weight loses, mortality
may occur.
Prophylaxis
- reduce organic matter in the pond by changing water then treat the water
with 25-50 ppm. formalin
- NaCl 0.5% in pond
- NaCl 3% dip for 5-10 min.
To treat with formalin, it is necessary to observe the level of phytoplankton in
pond. Formalin may kill phytoplankton and cause O2 drop which may kill the fish.
Holotrichous
Holotrichous are ciliate protozoa with cilia distributed regularly over the body
the body or arranged in rows. There are found on the skin, fin and gills of fishes.
These organisms are usually commensals but dermal and branchial pathology. Several
of them have been involved in epizootics and disease among fishes.
Normally these ciliates cause no harmful effects to the host unless present in
large numbers. But there are a few which cause severe skin or gill damage even when
present in small numbers.
These ciliates have the most complex body organization of the protozoa. All
possess cilia, cirri or tentacles for locomotion or for use in feeding. Reproduction
mostly by binary fission
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Chilodonella
General characteristics
It is a motile ciliate heart shaped with the posterior end broader and slightly
notched. The ventral side is flat with parallel ciliary rows. The oral opening is on the
ventral side near the anterior end. There is a large oval macronucleus in the posterior
part of the body. Reproduce by binary fission
Disease sings
Chilodonella are very small cannot be seen with naked eye. They cause
excessive mucus secretion. The result may be the appearance of white or grey-white
or pinkish slime patch on the dermal surface or gill. These patches may be localized or
extensive over much of the body.
Diagnosis
Scrape the skin or gill arches of the affecting live fish; quick place on slide
with drop of water and observed under microscope.
Therapy and Control
- Formalin 25-50 ppm in pond 3 times on alternate days, 200 ppm for
flushing
- Formalin + Malachite green : 25+0.1 ppm., prolong for aquarium
- NaCl 3% for 5-10 min
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Ichthyophthiriasis
The disease causes by Ichthyophthirius (Ich) commonly called white spot
disease. The name derived from numerous white swellings covering all external
surface of infected fish. This disease is relatively non-host specific. It is one of the
most prevalent disease of fish. It has been recorded among cultural, aquarium and
wide ranging fishes especially among warm water fishes. I. multifilliis is a very
common species found in freshwater cultured fish.
General characteristics
"Ich" the largest protozoans 0.5-1.5 mm, has body subspherical to ovoid with 2
nuclei, crescent shaped macronucleus and micronucleus which is not visible unless
stain. Body covered with many rows of cilia arranged longitudinally, the cytostome is
anterior, the buccal apparatus is relatively simple with no accessory oral membrane. It
consists of a single ring of approximately 65-75 cirri-like structure surrounding the
mouth opening. Each cirri-like structure is composed of a row of three cilia fused at
the tip to form a pointed spike. The cirri-like structures are relatively stiff and
arranged in a ring formation a circular row like collar. The oral cirri-like structure is
believed to be used for burrowing and rasping. Such actions could account for the
extreme irritation, hemorrhage and excess mucus production.
White spot disease in marine fish causes by Cryptocaryon irritans.
Life cycle
"Ich" spent sometimes under the skin and gill of host where repeat binary
fission to many trophozoites (tomonts). They encyst between epidermis and dermis
layers of the host and feed on host cells. When these mature breakout of the skin get
into water or attach to the aquatic plants, form gelatinous cyst, begins to devide to
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daughter cells, tomites, to about 100-2000. Cyst ruptures and releases tomites free
swimming and search for host. They will die within 3-4 days if cannot find host.
These tomites equipped with perforatonium, an organelle enabling it to penetrate the
skin of the fish. Tomite must find host within 48 hrs. When tomite becomes lodged in
the skin the life cycle is completed. There was a report that muliplication complete
within 10-20 hrs at 24-26oC. The life cycle is completed in about 4 days.
Disease signs
White spot is seen with naked eyes. Fish with light infection, shows signs of
irritation and tend to move toward the pond surface. Heavy infection fish rub and
scrape against the side, cease to feed, become discoloured, lethagic. Increase in
infection is fatal especially in young fish.
Diagnosis
Removing one or more of the white spots mounting on slide with few drops of
water and a cover glass and observing under the microscope. Crescent shape
macronucleus will be seen. Tomite may be observed.
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Prognosis
Mobidity level of Ich infection usually reach 100% especially in aquarium.
Generally, fish with small scales are more susceptable to infection than those with
large scales. Infection of Ich are sometime seasonal and infection levels may increase
during winter.
Pathogenicity
Penetration of "Ich" results in extensive changes in the surrounding integument
tissues. As the parasite grows, the epithelium is pushed outwards, spongy layer
collapses forming a depression under the parasite. Where parasite break out the skin,
the epithelium is completely distroyed and the dermis exposed. Heavily infection to
gill cause respiratory surfaces become non-functional.
This disease occurs in wild population. Fish with low degree of susceptibility
can become carrier. Therefore fish must be quarantined until it certain that there are
free of the parasite.
Prophylaxis
- quarantine more than one week
- prevent wild fish to get into the pond.
- left pond empty for more than 4 days.
Treatment
It is not possible to elimate this parasite when they are under the epithelial layer
of fish. Therefore treatment must be aimed to eliminate the unprotected free
swimming stages. There was an experiment to immunize fish with antigen prepared
from the cilia of Tetrahymena pyriformis which is close relative to Ich result in high
degree of immunity.
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Therapeutic procedures for control of ichthyophthiriasis
Compound
Formalin
Dosage and Time
1:5,000
Method of Use
1 hour bath
Remarks
Destroys tomites; other life
stages may be affected;
intradermal stages not
affected
Destroys tomites as they are
released, but will not after
intradermal life stages
25 – 50 ppm
Continuous for 5 days
(Prolong)
Malachite green
plus formalin
0.1 + 25 ppm
3 to 5 hour bath on Destroys tomites as they
alternate days
emerge; will not control other
external or intradermal life
stages
(recommend for aquarium)
*Potassium perma
nganate
4 – 5 ppm
30 minutes to
bath
*Sodium chloride
3%
1 hour bath daily for
7 consecutive days
Temperature
Raising to 30 - 31oC
5 days in aquaria
(close observation)
1 hour Destroys tomites; no effect on
other external or intradermal
life stages
Destroys tomites as they
emerge, will not control other
external or intradermal
life stages
Destroys tomites as they
emerge; probably weakens or
kills other external or
intradermal life stages
* Accepted by the U.S. Food and Drug Administration (FDA) for use with food-fish
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Agmasoma
It is a microsporidian reported in Penaeus monodon. This microsporidian is formerly
called Thelohania.
This disease can aftect a wide range of shrimp species including P. merguiensis and
Acetes spp. It has associated with significant losses in P. monodon.
Diseae sign
It infects the muscle of the abdomen causing it to turn opaque and white. The
appearance of the muscle has led to the condition being called “cotton shrimp or milky
shrimp.
Epizooliology
At present the mode of transmission has not been confirmed but is thought to be
through an intermediate host. P. mondon an thought to be susceptible only in the early stages
of growth. There is also evidence that levels of infection are incresing in wild stock.
Pathogenicityc
The systs are formulate between the muscle cells.
Treatment
No suilable treatment
Control involves removing the affected individual which will often swim on the
surface of the pond at night.
Microsporidiosis
It is a disease causes by sporozoan parasite, microsporans, which are
endoparasites. When this parasite get into the fish, they are either coelozoic or
histozoic. This parasite has a tremendous reproductive capacity, therefore, they form
tumor like called xenomas. Spore itself is about 7.5 x 3.5 u. Each spore has a single
polar filament coiled within the cytoplasm. This filament is used to anchor to the host.
Spore transmitted into new hosts increase in number by binary fission or schizogony
at first. Enormous number of spores are produced, causing hyperthrophy of the cells
in which they occur, resulting in the formation of cysts oval or elongate. Common
Microsporidian found in fish and shellfish are Pleistophora, Thelohania.
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This disease is as a chronic condition normally gives little effect on the host
unless it occurs in vital organs. Fish with advanced stage of this disease may become
lethargic and emaciated. Development of microsporidian parasites within the host
depends on many factors which determine the outcome of the infection. Among
environmental factors, ambient temperature is positively known to influence the
development. Temperature below 15oC was found to retard the infection. Spores
retain their viability in water at 4oC for at least on year. They are transmitted directly
perorally. Young fish can be infected very early in life. As is evident from
spontaneous infections, some species have a broad host rang. Some microsporidia are
known from one host only.
Life cycle
It is monoxenous (requiring but one host) Spore are present in hypertrophic
cells of the host until death of the fish. Spore release. Ingestion or infected fishes by
other fishes also releases spores from the infected.
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General life cycled of a microsporan
1. Spores taken into the new host orally of reinfection in the same host.
2. Sporoplasms enter the host cell and are called tropozoites at this stage.
3. The tropozoite reproduces by schizogony to an octonucleate schizont.
4. Nuclei divide again.
5. A sixteen-nucleate pansporoplasm forms. Each of the sixteen spores are released to complete
the cycle.
Clinical signs
Disease is characterized by massive invasion of host tissue. The tissues are
hypertrophied and altered so that they become opaque with accumulation of spores.
Destruction of muscle leads to abnormal swimming behavior, Tumors of individual
cysts or groups may be so extensive as to cause occlusion of the affected organs.
Mortality may be very high due to destruction of the respiratory epithelium.
Pathogenicity
The growth and proliferation of the microsporidian within the host cell always
results in the complete destruction of the latter. In developmental stages, mature
spores, gradually replace the cell contents until the host cell (or syncytium in muscle
fibres) becomes a mere envelop containing the parasite. In some species,
developmental stages are separated from the intact sarcofibrils only by an amorphous
layer about 0.2-0.6 m thick, with an external layer of small vesicles. In other genera,
the microsporidian stimulates the infected cell to an enormous hypertrophy. Such
hypertrophic cells can reach dimensions up to 14 mm.
This disease gives little effect on the host unless they occur in vital organs.
However there was a report of almost a complete loss of 170,000 rainbow trout
fingerling occurred in California from Thelohania californica.
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Treatment
No treatment. Infected fish must be removed to prevent spreading after the fish
died.
Microsporidiasis in shrimp
Agmasoma
It is a microsporidian reported in Penaeus monodon. This microsporidian is
formerly called Thelohania.
This disease can affect a wide range of shrimp species including P.
merguiensis and Acetes spp. It has associated with significant losses in P. monodon.
Disease sign
It infects the muscle of the abdomen causing it to turn opaque and white. The
appearance of the muscle has led to the condition being called “cotton shrimp or
milky shrimp.
Epizooliology
At present the mode of transmission has not been confirmed but is thought to
be through an intermediate host. P. monodon an thought to be susceptible only in the
early stages of growth. There is also evidence that levels of infection are increasing in
wild stock.
Pathogenicityc
The systs are formulate between the muscle cells.
Treatment
No suitable treatment.
Control involves removing the affected individual which will often
swim on the surface of the pond at night.
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Coccidiosis
This disease causes by parasite in coccidia group. Eimeria is one of the
etiological agent to cause coccidiosis of fish. Over 40 species of Eimeria have been
reported from fishes.
General characteristics
It lives in air bladder, liver and blood. The infective entity of coccidiosis is the
sporozoite in the oocyst. Mature oocysts usually with four sporocysts each with 2
sporozoites. Sporozoites transforms into a schizont multifission into large number of
daughter cells.
The oocysts are extremely capable of withstanding the rigors of external
existence and remain viable for long periods of time probably a year or more or until
swallowed by a new host.
Disease signs
Signs of coccidiosis include emaciation, lethargy and general poor health.
Internal signs of coccidiosis include white blisters on the intestinal wall, the intestine
swollen with fluid and the feces light in color and made up of many oocysts.
Diagnosis
Oocysts may be observed in intestinal scrapings or focal smears viewed at
magnification of 200 to 400 x
Prevention
- Quarantine and restriction of movement will reduce the possibility of
spreading the pathogen.
- Removal of infected fishes.
- Test and slaughter
Treatment
No chemotherapeutic agents known to control this disease.
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Myxosporidiosis
The disease is caused by myxozoa parasites. They are exclusively
endoparasitics. The key feature is the spore. The spore usually consists of two valves.
Within the cavity enclosed by the valves there are one or two polar capsules
containing spirally coiles. The remainder of the spore cavity is occupied by
sporoplasm. Myxosporeans are either coelozoic or histozoic.
The genera commonly recorded in the fish are:
- Myxobolus
- Henneguya
- Thelohanella
Key to myxosporean genera
1.
2.
3.
4.
Spore compact, without outgrowths or processes .......................................…........... 2
Spore with pair of long processes at the pold opposite to polar capsule .....................4
Only one polar capsule present ............................................................. Thelohanellus
Two polar capsules present ........................................................................................ 3
Sporoplasm with iodinophilous vacuole ............................................……..... Myxobo
Two polar capsules present ....................................................................... Henneguya
Four polar capsules present ........................................................................... Agarella
The taxonomic of the vacuole is currently under debate. It is not a permanent
structure and may be present or absent in the same species depend on the age, maturity
of the spore.
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Whirling diseases, is a salmonid disease which causes by Myxosoma
cerebralis. It is a highly infectious disease. Many reports in drastic lost by this disease
in Europe and America.
Life cycle
Spore with broadly posterior and sharply tapering anterior. Moderately well
developed suture ridge valve smooth polar capsules, pyriform, long, slender,
occupying between 2/3 and 3/4 of the spore with iodinophilus vacuole.
In Indonesia Myxobolus koi was recorded to form spherical cysts in connective
tissue of the gill and subcutaneous, of cyprinid. In Thailand there were recorded on
Clarias batrachus, C. macrocephalus, Ophicephalus striatus, Trichogaster
trichopterus, Helostoma temmincki. In Philippines in C. batrachus.
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Henneguya
They are among the most cosmopolitan myxozoan of freshwater fishes in the
world. There were recorded to be found in freshwater fishes such as Oxyeleotris
marmoratus, C. batrachus, Osphronemus sp., Puntius porctozysm, Trichogaster
trichopterus, Anabus testudineus.
Henneguya spore fusiform slender with greatest width at level of posterior end
of polar capsules, anterior end bluntly round valves smooth, posterior processes of
valves partly fused long and slender with iodinophilous vacuole. It has two long whiplike caudal processes about 8-24 u in length.
Cyst were found inside and between respiratory fold. Vigorous response of the
host tissue resulted in hyperplasia. A severe infection is capable if causing heavy
mortality.
Disease
signs
This parasite causes opaque masses in various tissue, form cyst in gill, skin or
some internal organs.
Pathogenicity
Infected site was infiltrated with blood cells and the branchial arteries were
conjested, vigorious response of the host tissues resulted in hyperplasia.
A severe infection can cause heavy mortality to fish especially small fish.
Treatment
When the cyst is formed, no chemotherapeutic treatment.
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Platyhelminthes
Platyhelminthes is called flatworms. Most of them tend to be flat, although
many of them are fusiform or even filiform. They may be segmented (some Cestoda)
or unsegmented, and all are equipped with characteristic attachment organs, designed
to maintain hold of the host under specific conditions of their host-parasite
relationships.
Three classes of platyhelminthes infect fish cultured in South-East Asia. They
can be distinguished with the aid of the key below.
Key to the classes of Platyhelminthes
1.
2.
Ectoparasites one posterior attachment organ, with one or more pairs of median
hooks and varying numbers of marginal hooks and/or clamps
..............................................................................................……....... MONOGENEA
Endoparasites, attachment organs not as above ................….......................................2
One attachment organ, armed with hooks and/or suckers (some without attachment
organ). Gut absent, body ribbon-like, segmented or unsegmented
.................................................................................................……............ CESTODA
Two sucker-like attachment organs, one anterior, terminal or subterminal, other
ventral (either sometimes absent). Gut present, usually bifurcated. Body unsegmented, flat to fusiform ........................................…........................... TREMATODA
Monogenea
Monogenea are largely ectoparasitic, but not among those species infecting
South-Asian cultured fish. All monogeneans of South-Asian fish are either small (less
than 1 mm) or medium-sized (1-5 mm). Their importance is much greater than their
size.
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A typical monogenean has a bilaterally symmetrical, dorsoventrally flattened
body. The most characteristic structure is the opisthaptor a shallowly concave
attachment organ situated at the body’s posterior extremity. It is armed with chitinoid
structures important for attachment called hook or anchor and, because of their
morphological diversity, equally important for identification. The anterior end of the
body often carries a much smaller and less well developed sucker-like structure,
associated with the mouth opening or independent of it. It serves to fasten the anterior
end of the body to the host surface during feeding, as well as to provide an additional
grip on the substrate during locomotion. The anterior end can be rounded or
subdivided into two or more lobes. The cuticle covering the body is also pierced by
the genital orifices and the openings of the excretory ducts.
All monogeneans reported from South-East Asian fish have relatively simple
opisthaptors, subcircular and armed with one or more of three prehensile structures.
The anchors fix the parasite to the substrate. Acting together as a unit, their
synchronization is assured by the presence of a connecting bar or bars of various
shapes with hooks are arranging along the rim of the opisthaptor called marginal
hooks.
Life cycle
They are hemaphroditic having both male and female reproductive organs.
Most monogenea have direct life cycles. They use only one host. Most are oviparous.
Only a minority, the gyrodactylids are viviparous and will be considered in more
detail later.
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Small numbers are little damage to their hosts. Large numbers cause trauma to
skin and gills. Therefore, the diagnotician has to determine why the large population
has developed.
Usually the primary cause is poor water quality, malnutrition or some other
physiological alteration of the fish which gives the parasite an advantage in
reproduction and survive.
Two common occuring families are
Dactylogiridae
Gyrodactylidae
Dactylogyridae
The family Dactylogyridae contains at least seven genera and over 150
recognized species on freshwater and marine fishes of the world. These organisms are
never more than 2 mm in length and most often between 0.2 and 0.5 mm. They all
have seven pairs of marginal hooks and usually one pair of median hooks on the
opisthaptor;
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The dactylogyrids have two to four pigment (eye) spots located in the anterior
part of the body. The ovary is round to oval in shape and the testes are unpaired. All
dactylogyrids are oviparous with no uterus, only an ootype structure containing one
egg at a time. The genus most commonly found on fishes is Dactylogyrus, its species
sometimes known as gill flukes because most are located on the gills of their host.
There are at least 100 identified species of Dactylogyrus.
Gyrodactylidae
Gyrodactylids are found on many of the lower vertebrates (fishes, amphibians
and reptiles) and also on in invertebrates. At least 85 species have been identified on
fishes. Gyrodactylids have eight pairs of marginal hooks on the opishaptor, with one
or more pairs of median hooks and often two six sucking valves. Those with sucking
valves are oviparous, those without are viviparous. The gyrodactylids have a
copulatory organ on the ventral midsection of the body which is a corona of chitinized
hooks. Gyrodactylus species are small flukes rarely over 0.4 mm in lenght. All species
of the genus are viviparous, with one to three daughter generations in the V-shaped
uterus lying behind unpaired round testes. Dactylogyrus is bigger than Gyrodactylus.
Epizootiology
By direct contact. Depletion of disolved O2 low enough to affect or suffocate
fishes does not affect the flukes. They even increase oviposition.
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Disease signs
Signs of excessive parasitism with flukes depend on the species involved,
location on the host, environmental, temperature.
Pathogenicity
Gill flukes cause loss of gill function and behavioral characteristics. Fish
become lethargic, swim near surface, seek the side of the pond and refuse food.
Suffocation is generally occurred.
Fish with skin flukes may rub against bottom or sides of the holding facilities.
They may race through the water as if attempting to remove the irritant. Some may
develop gray white areas of thickening mucus on the skin.
Diagnosis
Some monogenean flukes are relatively large and can be seen without
magnification. Recommend to see while fish in water. Most are small need to scrape
and look under microscope. Monogenea found in grouper are small and mostly under
the scales. Scaping may not possible. The monogenea will drop from fish, if fish is
put in freshwater.
Treatment
Formalin
25-30 ppm. in pond, prolong
Dipterex
.25 ppm. in pond
Close observation while treated fish especially in pond with high
phytoplankton.
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Digentic Trematode
Digenean are predominately endoparasites. They possess dosoventrally
flattened unsegmented bodies usually oval or lanceolate, long than wide, but
sometimes transversely oval, wider than long.
They are equipped with two attachment organs, the oral sucker at or near the
body's outerior and the ventral sucker or acetabulum, the positon of which varies
from near-anterior to near posterior with all position in between.
Adult trematode may be found in the intestine, gall bladder, urinary bladder.
Nearly all digenean of fishes are hemaphroditic having both male and female genital
system. Most of them are host-specific. Many of freshwater and marine forms exist.
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The life cycles of Trematoda involve more than one (often three) hosts and include
several morphologically and biologically dissimilar stages. The most elaborate type of cycle
includes eggs, miracidia, sporocysts, cercariae, metacercariae, as well as the adult. Most
cycles, however, leave out one or more of these stages.
Cultured South-East Asian fish serve either as second intermediate or as
definitive hosts of trematodes. In the former case they harbour the metacercarial stage,
quiescent, encysted in various tissues and organs. Only if the fish are eaten by the
definitive host can the cycle be completed and a new generation of adults produced.
The usual way for the fish to acquire metacercariae is through being attacked by
cercariae that penetrate the skin and move to their target sites. When fish act as
definitive hosts, they harbour adult worms ingested with the second intermediate host,
an invertebrate or a small fish. Adult trematodes often inhabit the lumen of the
alimentary canal but can be found in other internal spaces. They are attached by their
acetabula, but are often quite mobile and in post-mortem examinations are commonly
found detached.
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Diagnosis
Metacercariae are sometimes large enough to be seen with the naked eye or
with no more magnification than the hand lens. Cysts are disected and the
metacercariae released.
Identification of the metacercariae to species is usually quite difficult and
transmission experiments may be necessary to obtain adults.
Pathogenicity
Adult trematodes are considered either harmless or nearly harmless. Fish that
serve as intermediate hosts certainly suffer tissue damage. The process of invasion has
two phases.
During the first phase the new metacercariae actively migrate to their target
sites leaving behind a trail of tissue destruction. Their pathogenicity depends an their
numbers and on the paths they must travel before encysting. During the second phase,
the metacercariae are encysted and quiescent. Their effect depends an their numbers
and on the location and size of the cysts.
Necrotic tissue changes around cysts have been observed. In vital organ, the
presence of cysts can cause function disruption and mobidity. Severe gill damage may
be caused by the presence of trematode cysts. Effect can be grave when fry or
fingerling are infected.
Prevention and control
Prophylactic measure is likely to be the best method.
Treated pond when no fish with lime 10 kg/rai, Sodium pentachorphenate (a
wood preservative) at 2-3 kg/rai. In China, used tea cake 20 kg/rai soak for 24 hrs.
Eliminate of a link in the transmission cycle may be possible in small bodies of
water. Large bodies usually impossible.
Immunization had been tried and seem to be possible but need more
confirmation. But it is not recommended in the case of our fishes because infection in
general are low and cause little damage to fish unless for those with human as a
definitive host.
There are no specific therapeutic measures effective against endoparasites.
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Cestode
Cestode is an internal parasite and called tapeworm. Adult stage of cestodes
usually live in the intestinal tract of vertebrate. Intermediate stages lie in a wide
variety of body locations in both vertebrate and invertebrate hosts.
The bodies are ribbon-shapes and divided into short segments called
proglottids. A hold fast organ at the anterior end is called the scolex followed by
neck and the remainder is the strobila. The strobilae of most cestodes are segmented
consisting of many compartments the proglottids.
Each proglottid is a complete reproductive unit having both a male and a
female repreductive organs.
Fish can be either intermediate or definitive hosts for cestodes. All records
from freshwater fish in SEA are of adult cestodes. Their life cycles involve either one
or two intermediate host, mainly various invertebrates but sometimes small
vertebrates also.
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Life cycle
This parasite has two stages in fish
1. as intermediate host, larval stage is histozoic, therefore migrate through and
encyst and cause inflammatory response, cell proliferation but the extent of injury
depend on the injured size.
2. Adult stage cause little tissue damage especially at the point when scolex
equipped, interfere with absorptive process of intestine and may reduce the food in
take.
Disease signs
Adult (normally in intestine) or plerocercoids may cause reduced growth,
emaciation, anemia, dark color erratic swimming ability and suceptible to secondary
infections.
Location of plerocercoids in vital organs (for example brain) may be
significant to survival. If in gonads, may become atrophied and non productive from
only a few plerocercoids.
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Prognosis
Unthriftness, susceptibility to other disease, evidence of malnutrition and other
indication of poor health with heavy burdens of cestodes.
Best example of transport this worm to new geographical area when carp was
moved from Asia to Europe and North America. They carried cestode
Bothriocephalus acheiloghathi. This tapeworm then occured in golden shiners and
fathead minnows.
Pathogenicity
As they are not cause massive mortality, no attention have been given to them.
Therapy and Control
The best control is good pond management. Draining and allowing ponds to
dry completely will remove infected intermediate hosts and cestode eggs.
If cannot dry, treat pond with chlorine or lime.
Di-n-butyl tin oxide 0.5 to 0.6 % of the diet fed for 3 days.
Mebendazole has been used experimentally to remove larval from the intestine.
Using an oral dose of 100 mg/kg of fish for 14 consecutive days
* There is no therapy for removal of plerocercoids from fish
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Acanthocephalans
They are wide distributed. All are endoparasites in the digestive tract of
vertebrates. Worms with anterior proboscis covered with many hooks, called thornyheaded worms. The body of acanthocephalans is made up of three regions proboscis,
the neck and the trunk. The trunk is more or less cylindrical in shape. The proboscis
is a hollow, subglobular or cylindrical structure always armed with a set of posteriorly
pointed hooks use to a extent for taxonomic classification. This organ is one of the
most outstanding features of the worm, especially on first observation of the
organism.
The proboscis functions to anchor the worm in place more or less permanently,
by penetrating the host's intestinal wall. The neck, a short section of the body directly
behind the proboscis, is also retractable. The trunk is a sac-like structure
subcylindrical or bilaterally flattened.
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Life cycle
The life cycle of acanthocephalans involves crustaceans or occasionally
mollusks and insects as the intermediate host, each acanthocephalan being somewhat
host-specific in relation to their intermediate host. Eggs released from the female are
swallowed by the intermediate host and fully formed larva or acanthor released. The
acanthor uses its hooks to bore through the intestinal wall and into the hemocoel. It
develops into an acanthella and becomes surrounded by a connective tissue capsule
formed by the host. The acanthella then becomes a young thorny-headed worm or
cystacanth inside its capsule. Sexual maturity of the worm is reached when the
cystacanth is ingested by the primary host.
Pathogenicity
Pathogrnic effect of acanthocephalan are due to its attachment
Inflammation may occur at the attachment area. The number of worms persent
is important in determining the severely of damage.
It has been suggested that some acanthocephalans produce toxins,
secreted into the host tissues through pores present in the proboscis hooks.
Occlusion of the gut lumen can occur, especially when the fish is small
and the intensity of infection heavy.
Prevention and Control
Prophylactic procedures are considered sufficient to prevent serious
infections. Quicklime provides a good disinfectant.
Bithionol at 20,000 ppm as food additive, a single application.
di-n-butyl-oxostannate 3.25 b mg/kg of fish, 3 applications on each of
three successive days.
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Nematoda
Nematode is called roundworm, they are widely distributed in both fresh and
saltwater. A fish with hundred of nematodes can live relatively mormal life. It widely
distribute in both fresh and saltwater but it was given very little attention as it does not
give severe effect to fish.
Nematodes mostly are cylindrical, filiform and covered with a strong
protecting cuticle that is flexible but does not stretch. The cuticle usually has fine
transverse striations, occasionally is it armed with spines or annular bands carrying
spines on their free margins.
The most important taxonomic feature is the head. At its simplest, the mouth is
an unarmed opening, it may be surrounded by two, three, four or six lips the highest
number being the primitive form.
The posterior end of the body carries on its ventral and ventrolateral walls
preanal and postanal papillae, often quite prominent and club-shaped. Their number
and arrangement provide an important taxonomic clue. The posterior extremity,
particularly that of the male, is often flexed ventrally or coiled in a tight spiral.
The structure of
A. Adult female; B.
nematodes
Adult male
Species commonly found in culture fish in SEA are Camallanus anabantis
occurs in the intestine of Clarias batrachus and Anabas testudineus.
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Life cycle
The nematode life cycle typically comprises four larval stages, followed by the
adult. The fourth larva is infective to the definitive host but earlier stages may require
an intermediate host or hosts, and sometimes a carrier host, to develop to the next
stage. The life cycle of nematodes parasitizing South-East Asian cultured fish involve
more than one host.
Disease signs
Anemia or emaciation, unthriftiness when nematodes are too numerous in
alimentary tract.
You may see lot of larval forms in mesentary or muscle.
Diagnosis
Must cut the fish open and look in intestinal tract. Those in mesentary mostly
immature forms.
Pathogenicity
Nematodes that use fish as intermediate hosts much more injurious than adults,
mainly because they infect the tissues. During migration to their target site they cause
damage; the seriousness of which depends on the extent of migration and on the
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importance of the affected tissue to the host’s vital processes. The host’s defensive
response results in deposition of a fibrous capsule around the encysted larva.
Extensive degenerative changes and necrosis may occur around the cyst.
Because they are coelozoic, adult nematodes rarely cause serious injury. At
most they cause local lesions of no great significance to the host’s general health.
Heavy nematode infections, especially in small and young fish, may be more serious.
Nematodes usually do not constitute a serious treat to successful aquaculture.
However, because some nematodes can infect man, they may pose a danger to public
health Gnathostoma spinigerum, for example, produces painful swellings in humans.
Therapy
- Phenothiazone 0.1% of food for 3 days may remove the worms.
- Tranisol 0.1% for seven days.
- no treatment for larval form
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Crustacean Parasites
Crustaceans posses an exoskeleton with jointed appendages and a segmented
body. The digestive tract is completed and the circular system consists of a hemoceal.
Respiratory is by tracheae, gill a through body surface. The sex are separated. All are
oviparous.
Crustacean which have become fish parasite no longer resemble free living
crustaceans. Bodies have been modified tremendously. Each modification serving a
vital purpose for completion of the life cycle and survival of the crustacean.
The common fish parasitic crustacean fall in to these orders:Copepoda
Branchiura
Isopoda
Key to parasitic crustaceans
1.
Entire dorsal surface of body divided into many narrow segments, tagmata poorly
developed; parasite immovably attached to external surface, buccal or branchial
cavity of fish .................................................................................….......... ISOPODA
Dorsal surface of body with reduced segmentation and well developed tagmata, or
unsegmented ..............................................................................……………….......... 2
2.
Pair of compond eyes; body covered anteriorly with dorsal shield; main attachment
organs suckers of modified first maxillae; parasite capable of movement over host
surface ........................................................................................BRANCHIURA Compound
eyes absent; double median eye present or absent; shape of body varied;
parasites anchored and sessile, attached more or less firmly to surface of fish, or able
to move over its surface ..................................................................... COPEPODA
Copepoda
Copepod parasites on fish has about 1,600-1,800 species only 5% are found on
freshwater fishes. Only 4 genera are found on cultured fish in SEA.
- Lernaea
- Lamproglena
- Ergasilus
- Caligus in marine fish species
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Lernaea sp.
Lernaea spp. are among the most harmful parasites of cultured freshwater fish.
The destructive activity of Lernaea is due to is relatively large size and its mode of
attachment and feeding. These copepods undergo a profound metamorphosis that
results in their assumption of a vermiform shape with an anterior holdfast organ,
buried in the host tissues. The body shape and attachment organ have earned for
Lernaea its vernacular English name ‘the anchor worm’.
The structure of their appendages is remarkably uniform and cannot be used
for specific diagnosis. The definitive shape of any individual holdfast is largely
determined by the consistency of the fish tissue within which it grew and developed.
Five species of Lernaea have been recorded from South-East Asia. The
greatest economic harm has been caused by L. cyprinacea and all control measures
developed against Lernaea have been directed primarily against it.
The key below provides a rough guide to the identification of adult females.
1.
2.
3.
4.
Holdfast with definitely dorsal and ventral pairs of branches..................................... 2
Holdfast with two pairs of braches arranged in anteroposterior plane; anterior pair curved,
longer than posterior; latter more or less straight................…...... L. arcuata
Both pairs of branches well developed ............................................................ 3 Ventral pair
of branches small, almost papilliform, dorsal branches usually (though not always) with
one or two secondary times.................................….... L. polymorpha
Dorsal pair of branches usually longer than ventral .................….............................. 4
Ventral pair of branches usually longer than dorsal, both pairs usually (though nor
always) bifid .......................................................……………….............. L. oryzophila
Dorsal pair of holdfast branches divided some distance from base, often T-shaped;
ventral pair usually simple ........................................….............. L. cyprinacea
Both pairs of branches simple, sometimes club-shaped or nearly papilliform
.............................................................................................…..................... L. lophiara
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Lernaea are found in eyes, gills, opercular, fins, skin, lips and other body
surface. It is not host specific and it is not selective in the site of penetration of the
host.
Life cycle
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The female become adult on a fish host. Metamophosis, body form change to a
bizare creature. The head region is thrust through the skin or gill epithelium of the
host and continue to develop. This structure is called cephalic process could develop
to anchor to hold the organism in place during the remainder of life. This female have
two pair of eggs sacs.
Disease signs
Small number of this parasite may cause behavioral or clinical changes in the
host. For example, a single L. cyprinacea was reported on the head region, cephalic
process of the parasite penetrates the brain cause lethal. Slight infestation, cause fish
to rub against the side or bottom of the pond or tank in an attempt to dislodge the
irritating copepodid or adult. Heavy infestation cause fish to become lethargic, seek
the side of the pond and have difficulty in maintaining equilibrium. Fish may dart
about as if attemping to dislodge the parasite, leaving them completely exhausted and
swim upside down. Skin, fins and gill secrete excess mucus from irritation.
Hemorrhage on infected areas appear.
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Pathogenicity
It injures its host as the result of attachment producing disruption of the host's
tissues. It feeds on tissue debris and erythrocytes and cause fish to secrete excess
mucus, skin hemorrhagic. May cause secondary infection by bacteria. Young fish in
particular are in danger of death.
The first tissues to be damaged are the skin and muscle which in the
attachment area become hyperaemic and swollen. Ulcers with swollen margins
appear, scales are damaged or lost and necrosis sets in. Secondary infections,
particularly fungal, are not uncommon. The host’s connective tissue reacts to the
parasite, forming a thick fibrotic capsule around its embedded end. Fins may be
damaged or even completely destroyed. Wounds caused by the parasite’s implantation
occasionally develop into fistulae, penetrating the visceral cavity and sometimes
resulting in peritonitis and death. On the other hand, early parasite removal from the
cavity of implantation is often followed by rapid and complete recovery of the skin,
particularly when it has not been penetrated through its entire thickness.
Attachment to the head or mouth, particularly in yound fish, may cause
twisting and deformation of both jaws. Small fish are in danger of deeper penetration
and internal injury.
The general effects of Lernaea infection are often marked by serious weight
loss. The blood picture is affected due to a significant increase in monocytes and
polymorphonuclear agranulocytes. Gonadal development may be retarded. Infected
fish often experience repiratory difficulties in oxygen-poor water and may display
sluggishness, a typical sign of debility. Mass die-offs are not unusual.
Therapy and control
It is very difficult to get rid of adult stage. Earlier life stages are usually more
susceptible to chemical therapy.
It is recommended to use dipterex 0.25 ppm for big fish, can increase to 0.5
ppm about 3 times consecutive at 3 days interval.
Adult cannot be removed, if you try to pull the Lernaea from fish, anchor will
remain under the skin may cause bacterial infection.
Fish recovering from infestation are thought to be somewhat immune to a
secondary infestation by the same parasitic species.
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Selected procedures used for control of crustacean parasites on fishes
Commpound
Dose Level
Time & Method
Remarks
Ammonium
Chloride
1,000 mg/L
4 hour bath
Useful for adults and
early life stages;
will not affect eggs.
*Benzene
Hexachloride
(lindane)
1:8,000,000
0.1 – 0.5 ppm
Indefinite
Add to the water and
allow to dissipate; use
one treatment only;
removes all life stages.
**Diptery
(Masoten)
(Neguvon)
1:4,000,000
0.25 – 0.5 ppm
Indefinite
Add to water and allow
to dissipate; use two
Applicationas at weekly
intervals; removes all
life stages.
3 to 5%
30-second to
one-minute dip
Removes all life stages
of Lernaea
1%
3 days
Removes all life stages
of Lernaea
Sodium
chloride
* Has not received clearance for use with any fish species.
** Has been cleared for use with bait minnows and aquarium fishes; not for food fishes
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Ergasilus
It is a gill parasites capable of colonizing the skin and fins but typical habitat
is the gills. They are difference in shape. Males are not parasitic.
Cephalothorax of E. thailandensis is about twice as long as wide,
dorsoventrally flattened, anterior margin forming short, central, truncated protrusion;
lateral margin with identations sligntly posterior to midlength eyes clearly visible near
anterior end; four free thoracic segments deminishing in size in posterior direction.
First antenna indistinctly six-segmental bearing short setae. Second antenna well
developed with very strong hooked claw of sutchela.
Pathogenicity
Damage due to attachment by the extremely well adapted second antenna and
by its feeding activities causing gill surface erosion. In severe infections a significant
proportion of the respiratory area may become non functional. Mobility is also added
to the damage each individual being capable of occupying several attachment sites in
the course of its life.
Treatment
Dipterex 0.25 – 0.5 ppm in pond prolong treatment
Dipterex = Dylox = chlorphos, = Foschlor = Neguvon, = Masoten
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Caligus
Caligus is one of the most successful genera of parasitic copepods of fish. As
might be expected in a very large genus, its species are diverse in host ranges, habitat
and distribution. Caligus is almost exclusively marine. Some Caligus species
parasitize fish in brackish inshore waters, though this must be considered atypical for
the genus and is, at least, rate.
Not less than 12 species of Caligus occur in South-East Asia, but only C.
patulus is of interest to fish culturists of the region. Others occur only on wild
populations of sea fish.
Caligus patulus infests the skin and fins of Chanos chanos, in brackish-water
ponds in the Philippines and in Indonesia.
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Life cycle
Caligus patulus hatches from the egg as a free-swimming nauplius and passes
through a second nauplius stage before moulting into the infective lava, the
copepodid. Before reaching maturity, it moults several times, passing through four
chalimus stages and two preadult stages.
Treatment
The copepod can be eliminated by Dipterex, applied to closed water system
tanks at 0.25 ppm for 1 day. Aeration of the tanks during treatment was essential.
Lamproglena
All parasitic of freshwater on freshwater fish. The primitive nature of this
genus if evident in the absence of extensive metamorphosis during post larval
development.
It is a gill parasite, body consists of 3 distinct parts. cephalothorax, trunk and
abdomen, having uniseriate egg sacs with relatively few eggs.
The body of the adult-female consists of three distinct parts: cophalothorax,
trunk and abdomen.
The maxillipeds are strong and prehensile, ending usually in three claw-like
spines. In most species there are four pairs of biramous swimming legs, the fifth leg
being vestigial and uniramous. Lamproglena differs from other lernaeid genera in
having uniseriate egg sacs with relatively few eggs.
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This copepod has been recorded in Thailand in Anabus testudineus,
Ophicephalus. striatus, Pantius gonionotus. It does not seem to form abundant
population only found 1 or 2 in each fish. Damage of the parasite is very minor
compare to other crustacean parasites.
Pathogenticity
Can caused connective tissue hypertrophy and local degeneration of the
capillaries of the gill filament around the head of the copepod, resulting from irritation
set up by the cephalothoracic appendages. Feeding activities cause severe damage to
gill tissue. Tissue hyperthrophy, resulting primarily from the reaction of the
respiratory epithelium, causes some reduction some reduction of sea respiratory
surface. The seriousness of injury depends on the number of copepods present.
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Branchiura
There are about 150 species of Branchiura, as many as 100 of them belonging
to the genus Argulus.
Argulus
Argulus has world wide distribution with species in both marine and freshwater
habitats but commonly found in freshwater.
It is called fish lice. It is a skin, gill or fin parasite. Mostly found on the skin.
The body is divided into three regions cephalothorax, thorax and abdomen. The
most conspicuous appendage is the sucker, modified from its maxilla. It is a hard,
sclerotized, organ with a rim supported by a ring of complex sclerites and with a
flexible extensible stalk.
Life clycle
Argulus cannot survive for prolonged periods without host. It is quite able to
leave it and swim freely in search of another. Unlike other crustacean parasites, it also
leaves its host to deposit it eggs on suitable submerged objects. Eggs are produced in
clusters, each consisting of serveral egg strips arranged in parallel rows. The
emerging larvae are at the copepodid stage. There are six larval stages, separated by
moults and characterized by progressing development of the dorsal shield and
abdomen, the formation of the maxillary suckers and the gradual development of the
natatory appendages and reproductive organs.
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Fertilized female
mating
leave the fish to the water to
lay eggs
adult
molt several times
14-16 days
nauplii, metanauplii
nnd 1st copepodid develop
in the egg
sub adult
7th
2nd
 14 days 
The life cycle needs 40-100 days to complete
Pathogenicity
Injuries are caused by attachment and feeding. Prolong attachment cause
extensive pathological changes in the skin.
The mode of feeding involves secretion and injection of relatively large
quantities of digestive fluids. The highly toxic secretion of the buccal glands can
cause a severe inflammatory response. Weight loss is common, it may lead to
retarded growth, and can also act as a vector for various viruses, bacteria and
flagellates.
Treatment
- Dipterex 0.25 ppm. in pond repeat twice weekly until no parasite is observed.
- Limes pond bottom and left dry for 1-2 days.
- Argulus cannot servive for long period without host so leave pond empty for
sometimes.
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Isopod
There are about 400 species which are parasitic on fish. Many of them are
facultatively parasitic. Some are intermediate type of parasitism. Some feed on host
blood and when sexually mature leave the fish to lead sheltered, demersal lives.
Many isopods are only facultatively parasitic, capable of leading either free or
parasitic existences. Isopods associated with the external surfaces of fish sometimes
produce gall-like depressions in the skin and muscle of the body wall, other line in the
buccal or branchial cavities.
The body consists of three regions. The first of them, the head (or cephalon) is
unsegmented and bears two pairs of antennae and a mouth. The most external mouth
appendage is the maxilliped, covering the other mouth parts. Sessile eyes can be large,
small or absent. The second region, the peraeon, consists of seven segments. Each
segments carries a pair of appendages the peraeopods. These can be prehensile or
ambulatory. The third region, the pleon, consists of six segments. Each of the first
five segments carries a pari of biramous natatory limbs, the pleopods. The sixth
segment, the pleotelson, is in the shape of a horizontal, fin-like plate, flanked by the
biramous ceropods.
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Pathogenicity
Blood feeding isopod give the most severe effect to fish especially small fish.
Mortality can occur with 15-30 minutes in fry with 5-6 isopods. Other effect due to
destruction of host tissue resulting from the pressure of the parasite’s body. When
present in the gill cavity it reduces the respiratory surface by causing atrophy of the
gills.
Treatment
No specific control or therapeutic measures against isopods. If necessary,
measures used against other crustacean parasites could be adapted.
Glochidia
It is a larva of freshwater bivalve molluscs. Hatching out from eggs incubated
between the gill lamellae of the parents. Glochidia are expelled into the surrounding
water. It is miniature bivalves, the margins of their shrills equipped with sharp teeth.
To survive the glochidium must find a fish. When it contact, the gill, the valves clamp
shut on a gill filament. The enclosed part becomes the source of food for larva. This
cause vigorous proliferation of the branchial epithelium a process soon causes
complete enclosure of the glochidium in the host tissue. Development of glochidia to
juvenile will take about 7-10 days depends on temperature. Juvenile will leave the
fish.
Pathogenicity
Proliferative reaction effectively destroyd the respiratory function of the gill
epithelium. Severity depends on number infected. Escape of juvenile leaves open
would that are subjected to microbial infection.
Treatment
No specific treatment
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Mycotic Disease
The word mycosis (or mycotic) is derived from Greek, word mykes means
mushroom.The word fungi is derived from latin and also means mushroom.
There are two major types of fungi saprobes and parasite. Saprobes utilize dead
organic matter, but parasite obtain nutrient from infecting living organisms. Many
saprobes are facultative parasites and many parasites are also facultative saprobes.
All fungi are heterotrophic. It requires organic matter for growth and
reproduction. Fungi are incapable of synthesizing their own nutrients.
Structure
Can be one cell or many cells joined together into long filament or hyphae
which branch in all direction and the tangled mass of hyphae is called a mycelium or
thallus. Each cell of a hyphae is seperated by septa and called septate hyphae. If not
visible called aseptate or non-septate. Reproduce sexually or asexually. Most fungi
produce spores, usually zoospores because of flagellation, at some stage of the life
cycle. Spores are the primary unit of transmission. Sexual reproduction involves the
union of the nuclei of two cells
Asexual does not involves the union of other
cells, reproduce from a fragment of mycelium seperate from the main fungal mass.
Fungal spore is resistant to heat, drying, disinfectants and the defense
mechanism of the host.
Relatively few genera and species of fungi are known to cause disease in
fishes. The most known disease by fungi is Saprolegniasis causes by Saprolegnia,
Achlya, Dictyuchus, Aphanomyces.
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Saprolegniasis
Saprolegniasis is a fungal disease of fishes and fish eggs caused by a member
of the family Saprolegniaceae. It has other names, fish fungal disease or fungal
disease. All freshwater, brackishwater fishes and fish eggs are susceptible to
saprolegniasis. Dead fish eggs are growth medium for the fungi. The fungal growth
on dead eggs may be responsible to kill normal eggs by suffocation and invasion.
One distinctive feature of the genus Saprolegnia is the zoospore. Zoospore are
pear-shaped and have subapical biflagellate form in many rows inside the sporangium.
Movement stops soon after the zoopore leaves the sporangium.
Saprolegniasis has been called by other names. Fish fungus disease or fungus
disease is broadly used because of its common occurrence.
Epizootiology
saprolegniasis
(secondary infection)
water quality, malnutrition,
damage skin, fins, gills, physical stress.
bacterial infection
digestive enzyme
spreading
destroy surrounding area
mycelium
dead cell
mycelium spread
produce hyphae
germinate
stimulate reproduce
zoospore
Member of the family are primarily in freshwater, but some species can grow
in brackish water to a salinity of above 2.8 ppm.
Saprolegnia parasitica, Achlya hoferi and Dictyuchus spp. are the major
etiological agents of saprolegniasis.
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Life cycle
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Epizootiology
There apparently are no primary cases of saprolegniasis among fishes.
Malnutrition has been and continues to be a primary cause. Damage to the skin, fin or
gills leads to secondary invasion Physical stresses, water quality, temperature, pH may
be responsible for secondary invasion.
Dead fishes are a fertile medium for more fungal growth and production of
zoospores.
Optimum growth is about 18-20oC and reduce at higher temperature.
Diagnosis
Appearance of cotton-like, white to gray-white or gray-brown growth on
exterior surface of fish or on dead eggs.
The organisms have branched, non septate hyphae.
Therapy and Control
- remove dead fish and eggs
- used malachite green on non food fish bath at 5 mg/l. for 1 hr.
- 5% salt at 1-2 minutes
- Formalin at 1 : 4000 for 1 hr.
Branchiomyces
It is a gill mycose. They grow in gill epithelium, infitrate the tissue and
obstruct circulation. The affected gill filaments die, decompose and fall off. Fish
become lethargic, gasp for air breathe with difficulty and finally suffocate.
The disease has been of great importance among cultured fishes of Europe.
It is an opportunistic parasite. The disease is primarily environmental induced.
Etiological agents
Branchiomyces sanguinis and B. demigrans are found in common. Both
produce branched, nonseptate hyphae. Grow in temperature between 25-32oC
Epizootiology
Branchiomycosis is transmitted from water to gill tissue. Fungal spores attach
to the gills, germinate and preduce hyphae. The hyphae penetrate gill epithelium and
locate in the gill epithelium or within capillaries.
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Disease signs
Gills appear bright red or white to brown depending on the stage of necrosis.
The gills become ragged and corroded.
Diagnosis
Squash preparations of the gill tissue examined under subdued light through
the microscope or by phase microscopy may reveal fungal hyphae and spores.
Therapy and Control
See saprolegniasis
Epizootic Ulcerative Syndrome
(EUS)
It is a seasonal epizootic condition of freshwater and estaurine warm water fish
of complex infectious etiological characterised by the presence of invasive
Aphanomyces infection and necrotising ulcerative lesions typically leading to a
granulomatous response.
History
The first report on an EUS-like condition came in summer 1971. in Japan and
named mycotic granulomatosis (MG) In 1972, outbreaks of a cutaneous ulcerative
condition called red spot disease (RSD). The disease was spread westwards across
Asia. In 1998 it was confirmed to affect fish in Pakistan.
Characteristicsd
A slow growing with wide aseptate mycelia. Grow best between 24oC and
30oC will grow at 31oC but die at 37oC
The isolates from various places were conspecific and probably constitute a
single clonal genotype spread throughout the Indo Pacific area.
Etiological agent
Aphanomyces invadans is a necessary cause of EUS. It is in the family
Saprolegniaceae. EUS has complex infection aetiology. There is strong evidence that
many EUS affected fish die as a result of septicaemia caused by opportunistic
bacterial pathogens particularly Aeromonas hydrophila. No evidents to prove that
isolated virus alone can cause severe ulcerated fish or even consistent lesion.
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A. invadans is in the family Saprolegniaceae. It has been named variously as A.
picicida, A. invaderis, Aphanomyces sp. and A. invadans.
Disease signs
Affected fish typically show necrotic dermal ulcers which are characterised
histologically by the presence of distinctive mycotic granulomas in underlying tissue.
Diagnosis
Squash preparation showing aseptate hyphae (12-30  in diameter) in the
muscle underlying the visible lesion. Requires histological demonstration of typical
granulomas and invasive hyphae.
Epizootiology
It is known to grow fast at temperature 26-30oC. Aphanomyces produces
zoospore. However, there is strong evidence that outbreak occur only when a number
of causal facter combine.
Therapy and Control
The most effective means of control would be to prevent the disease entering
the country.
Affected fish must be removed and burried or burned.
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Aphanomyces in USA
History
During summer and fall 1997. Unusally high prevalence of skin lesions in
fishes from Chesapeake Bay and Pocomoke River. Stimulated significant public
concern. Associated cause also found Pfiesteria piscicida (dinoflagellate) which
produce Pfiesteria toxin causing skin ulcer.
Susceptible species - Atlantic menhaden (Brevoortia tyrannus)
Disease signs
Deeply ulcers or raised lesions
Diagnosis
Characterized by deeply penetrating fungal hyphae surrounded by chronic,
granulomatous inflammation
- Aphanomyces of this disease is similar or identical to A. invadans
Ichthyophonus Disease
This disease is caused by Ichthyophonus hoferi which is an obligate parasite
with a complicated life cycle. It is sometimes called tumbling disease because affected
fish rocked or swayed as they swam.
It occurs throughout the world, in fresh and salt water, mostly in Europe and
North Atlantic Ocean. They were reported in many species of aquarium fishes and
among cold and warmwater species also in amphibian and copepods.
Epizootiology
The primary route of transmission for I. hoferi is oral. Raw fish, fish products
or other food containing mature amaeboblasts taken by the fish enter the intestine,
ruptured and amoeboid bodies released. The heart, liver, kidney and spleen are the
major target organs but the brain, gills, muscle and other tissues are also common
infected.
Diagnosis
Squash preparation and examined under the microscope. Presence of spherical
bodies with double refractive walls and external signs of disease are presumptive
positive.
Therapy and Control
No therapeutic procedures. Fishes with I. hoteri infections will carry the
infection for life.
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Microbial diseases
Microbial disease mean diseases cause by bacteria or virus.
In the popular view, microorganisms are responsible for more diseases than
any other type of pathogens. In the field of fish health studies, knowledge of
infectious diseases had tended to lag behind the understanding of other health
problems. Even in country where aquaculture has long been done.
Bacterial diseases
Bacterium is a single cell organism which reproduce by binary fission, occur in
three shapes.
rod (bacillus)
spherical (cocci)
helical (spirillum)
Most bacteria pathogenic to fish are rod shaped. Only few are spherical, no
known helical forms. Bacteria have cell wall which maintains cellular shape and an
inner membrane which allows diffusion of nutrients and metabolite into and out of the
cell.
Some bacterial pathogens of fish develop a capsule outside of the cell wall
which is usually associated with the virulence of the organism. None form spores,
although some may form microcysts. Many of bacterial pathogens of fishes are
flagellated but a few have no flagella for locomotion. Some move by body flexing or
gliding.
o
Many pathogenic bacteria of fish are psychrophilic. Only few grow above 35 C
o
and many have maximum growth temperature at 35 C or less. Many of psychrophilic
species have an optimum growth temperature of 10oC and continue to replicate at 4oC.
Some are halophilic with optimum sodium chloride tolerance of 3.5% but can
not replicate at salt concentrations above 7.0%. All reproduce better if at least 0.5%
salt is present.
Opportunistic or secondary bacterial pathogens of fishes can replicate at a pH
range from 5.5 to 10.0. The primary pathogens of fishes usually have a more narrow
pH tolerance; generally 6.0-9.0. Nearly all of the bacteria infecting fishes are aerobic
or facultative anaerobic. Rarely are strictly anaerobic.
Some of them are chromogenic with wide variety of pigments produced such
as brown, yellow, orange or red and some are fluorescent.
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Many of the bacteria capable of causing disease in fishes are saprophytic. They
become pathogens where fishes are physiologically unbalanced, nutritionally deficient
or other abnormalities which allow opportunistic organisms to invade.
Some bacterial pathogens are fastidious and require special growth media.
Classification of Bacteria Pathogenic to Fishes
There are members of the true bacteria (Eubacteriales) the ray bacteria
(Actinomycetales) and the glinding bacteria (Cytophagales). Associated with disease
in fishes.
Classification of bacterial pathogens of fishes
Order
Family
Genus
Eubacteriales
(Gram-negative, rod-shaped)
Enterobacteriaceae
Edwardsiella
Yersinia
Pseudomonadaceae
Pseudomonas
Vibrionaceae
Aeromonas
Plesiomonas
Vibrio
Uncertain
Flavobacterium
Haemophilus
Actinomycetes
(Gram-positive, rod and
spherical-shaped)
Coryneform Group
Renibacterium
Nocardiaceae
Rod Mycobacteriaceae
Sphere Streptococcaceae
Nocardia
Mycobacterium
Streptococcus
Cytophagales
(Gram-negative, long rod-shaped)
Cytophagaceae
Cytophaga
Flexibacter
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Motile Aeromonad Disease
The name motile aeromonad disease was accepted in 1974 for a disease
previously reported under several synonymous names: hemorrhagic septicemia, red
sore disease, redmouth disease, red leg disease of frogs and bacterial septicemia. It
occurs as an acute, subacute, chronic or latent disease. Fish with susceptibility to
motile aeromonads are limited to freshwater.
The taxonomy of motile aeromonads has not been fully settled. However, there
are two recognized species. Aeromonas hydrophila and Aeromonas punctata. These
are primary pathogens of many cultured freshwater fishes. There is evidence to
indicate that unsatisfactory environmental conditions or debilitations of the fish are
conductive to epizootics caused by any of the motile aeromonads.
Motile aeromonads have been described as primary or secondary pathogens of
fishes throughout the world. Thus, the etiological agent of motile aeromonad disease
may be found under various synonyms. Aerobacter liquefaciens, Pseudomonas
hydrophila, Bacillus hydrophilus. A. punctata, A. hydrophila, A. liquifaciens.
The etiological agents of motile aeromonad disease are rod-shaped bacteria
motile by polar flagella and generally monotrichous. All are gram-negative and nonacid-fast. None are spore-forming. All cells are usually not capsulated. All are aerobic
and facultatively anaerobic. Some produce brown to red-brown water soluble
pigment.
Aeromonad disease
This disease causes by Aeromanas hydrophila. It is a short rods, almost
coccobacilli, 0.7-0.8 x 1.0-1.5 m, motile, with single polar flagellum. Gramnegative, oxidative and fermentative. Facultative aerobes producing colonies on
relatively simple media. The normal habitat is water, particularly when it contains
high organic loads. It may also become a non-pathogenic resident of the intestine of
fish.
Aeromonas hydrophila is the most common cause of bacterial haemorrhagic
septicaemia. The disease occurs in three distinct forms:
(a) abdominal dropsy, characterized by distension of the visceral cavity with
fluid
(b) ulcerative, characterized by skin and muscle lesions; and
(c) generalized bacterial haemorrhagic septicaemia.
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The disease is world-wide, affecting pond fish. It is commonly associated with
fish populations suffering from stress. Fish are abnormally dark, show large
subcutaneous haemorrhages and have distended abdomen. Haemorrhages are present
in internal organs. Kidney and spleen are internally liquefied.
FHS/AFS has adopted the name “Motile Aeromonas Septicemia” for the
disease causes by Aeromonas hydrophila.
Epizootiology
The organisms are usually transmitted orally except in those instances when
fish have skin or gill abrasions and the organism may enter through these routes. The
organisms multiply in the intestine or at the site of invasion and are spread throughout
the body by the blood stream. The incubation period between initial infection and
appearance of disease signs is dependent upon the temperature of the environment.
Acute cases may appear within four to ten days after infection.
Transportation of fishes and fish eggs is a part of the epizootiology of motile
aeromonad disease.
Disease signs:
External signs of motile aeromonad disease include erythema (redness) at the
base of fins, in the mouth, in the grooves under the lower jaw, within the opercula and
around the anus. Internal signs include erythema and petechial hemorrhages in the
peritoneum and most of the visceral organs. Slicing through the muscle may reveal
petechia. The intestine is usually erythemic and there may be bloody mucus and fluid
in the lumen.
Therapy and Control
- Improve water quality is the best prevention method. Liming is a common
method to improve water quality.
- Antibiotic treatment become more practice in bacterial treatment in fish.
However, to date, there are only few antibiotics approved to be used in food fish.
- Oxytetracycline (OTC) treatment used in the food at the rate of 50 mg per kg
of fish per day for 10 days. OTC has been known to be poor in seawater.
- Buffodine 20 ppm could be used safely for A. hydrophila disinfection in C.
bactrachus eggs.
- Control of motile aeromonad disease by immunization has not been
successful. This is because of the large number of serotypes.
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Pseudomonas disease
This disease causes by Pseudomonas fluorescens, which is a gram-negative
rods, rounded at both ends 0.5-0.8 x 1.0-2.8 m. single or in pair, motile with, may be
3 polar filaments (occasionally non motile). Usually obligate aerobes. Optimum
o
temperature is 20-35 C., grow in ordinary media. Fluorescen pigment occurs within 2
days but some strains may take 10 days. Incubation period varies with species.
It is a common disease of freshwater fishes. In each disease may be more than
one species of Pseudomonas are found.
This bacterium is often found in superficial lesions or infecting mechanical
injuries. It is a secondary infection where fish weak due to environmental problems
such as polluted water, high pH.
Disease signs:
Mouth, lower jaw, and area around anus shows hemorrhage as well as in
messentaries or sometimes in internal organs and muscles, more fluid in intestine,
opaque cornea.
Pseudomonad diseases are primarily found in cultured or aquarium fishes. It
can occurs as single fish case or as epizootic. Secondary infection occurs when
defenses of the fish are disturbed in someway physical stress, mulnutrition,
physiological alteration.
Epizootiology
Bacteria in the water get into fish through mouth or skin (when skin damages)
then spread through blood circulation to various parts of the body. Toxin secrete by
this bacteria may effect fish tissue causes tissue disfunction. Fish release bacteria
through fecies into water and may infect other fish.
As mention earlier, P. fluorescens was identified together with other
Pseudomonas spp. in fish pox disease in Osphronemus gouramy also in red spot
disease in several species of fish., Cyprinus carpio, Leptobarbus harveni and Chinese
carp.
In Philippines it was reported in Amphiprion opercular which causes red spot
on abdominal wall and abdominal distension.
In Singapore it was reported in various sp. of ornamental fish cause abdominal
distension, skin lesions, bristing of scales or fin rot.
Therapy and Control
See aeromonad disease
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Columnaris disease
This disease causes by Flexibacter columnaris. It is in order Cytophagales.
Bacteria in this order have been called Myxobacteria. The Cytophagales are long,
slender or filamentous, rod-shaped bacteria, All are motile by gliding. (achieved by
flexing). All bacteria of the family Cytophagaceas involved as fish pathogens are
fastidious. Most will grow on only specially prepared media. This disease has been
called cotton-wool, mouth fungus. The name mouth fungus is quite wrong because it
does not cause by fungus.
Columnaris is a chronic to subacute disease and mostly in freshwater fishes,
o
effect external fish body. Generally outbreak occur when water temp reach 15 C and
above. Inhibit by as little as 0.1% salt and will not grow at all in media which contains
0.5 to 1% salt. Flexibacter maritimus causes salt water columnaris disease. It requires
salt in media to grow.
o
This organism grows in wide range of temperature 4-30 C. It is seldom caused
o
disease when temperature below 15 C. The bacterium grows on the surfaces or fish
will produce colume-like structure. This organism produces a yellow-green pigment.
The cells are gram-negative, slender and rather long bacilli (3-8  long). F.
columnaris could persist for long periods in water of high hardness and organic matter
content but survive time was reduced significantly in water with pH 6.0.
It is an annoying disease of cultured and aquarium fish.
Disease signs:
On body, thickening of the mucus at various spots on the head, along the body
opercula, fins and around injuries. The mucus continues to become thicker until
definite areas of skin involvement appear as circular areas of fluffy grayish opalescent
growth.
- In gill, light-colored at the tip of the gill filament followed by overgrowth of
the outer part of filament.
- In fin, causing necrotic lesion on the outer edges.
- The bacteria are not usually found systemically until relatively large amount
of external skin or gill damage has taken place.
Therapy and Control
Control procedures
- immunization may be possible as research has demonstrated that fish produce
a high antibody titer against the bacterium when inject either subcutaneously or
intramuscularly.
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- management
- overcrowded fishes become more susceptible to columnaris disease
- nutrition (complete diet)
- external disinfection before handing
Treatments
-Furanace (Nitrofuran derivative) found to be the most effective
chemotherapeutic agent. Furanace 1.5 mg/l for 1 hr one day or up to three
consecutive days, depending on the progress of the disease.
Ideal for Furanace
1. It acceptable to use for fish disease control for non food fish.
2. absorbed rapidly from water and also leave tissue rapidly (few hours).
- Oxy-tetracycline 50 mg/kg of fish/day for 10 days.
- Benzalkonium chloride (Roccal, Cyncal and Hyamine) have been used
extensively in United States.
- Oxolinic 1 mg/l for 24 hrs.
- Salt 0.5-1% for freshwater fish
Vibriosis
It is a disease of many marine brackish and freshwater. It has been called red
pest of eels, red sore, red boil and pike pest. Vibriosis was given in 1974.
Vibrios as with marine environment like aeromonads in
freshwater
environment. They are ubiquitous especially where organic loads are high. Vibrios are
primary pathogen and also opportunistic.
The common ones in our region are:V. harvyi
V. parahaemolyticus
V. anguillarum.
V. anguillarum was the first Vibrio to be isolated and it is very common in US.
Vibrio consists of Gram-negative, straight or slightly curved rods -0.5 
x 1.4-2.6  (comma shape). They are non spore forming and motile by monotrichous
or multitrichous sheathed polar flagella. All are facultative anaerobes and chemoorganotrophs and most are oxidase positive. Most species grow well in media with a
sea water base sodium ions stimulate the growth of all species. The outstanding
feature of clinical vibriosis is the level of anaemia which results in all but the most
acute cases.
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Vibrio harvyi causes mortality in shrimp including shrimp larva and
seems to cause more problem in pond with high organic material.
V. harveyi has biofilm on their cells therefore, antibiotic as high as 50
ppm can effect them.
One research found that phytoplankton such as Chlorella, Skeletonema and V.
alginolyticus can inhibit the growth of V. harveyi.
Epizootiology
Vibrio transmission is likely through the oral routs. Those pathogens in the gut
may be capable in invasion of the host under any condition of stress. Also evidence of
entering through external injuries. Dermal route may to due to parasite
Incubation period may as short as three days, depend on the virulence of
pathogen.
This bacteria becomes septicemic after invasion and can be demonstrated in
blood, kidney, liver and other organs. They can be transmitted to water in feces. Dead
fishes become a source of infection. Another route of transmission through feeding of
infected. No evidence of transmission with eggs
Disease signs
External signs similar to aeromonads; erythema at the base of fins, in the
mouth, operculum and around anus, boil-like lesion under the skin and in muscles.
Internal signs are petechia and erythemia in the peritoneum and visceral organs. The
intestine is usually erythemia and filled with fluid.
Prevention
Prevention is the best achievement by
- maintenance of good water quality, good husbandry and lows stocking
density.
- No movement of fish from infected area.
- Eggs from suspected brood fish should be treated prior to move to other area.
- Using raw fish or viscera of marine species to feed the fish is prohibited.
Therapy and Control
- Oxytetracycline, nitrofurazone, sulfamerazine are the drug of choice.
- Sulfamerazine 250 mg/kg of fish per day for 3 days and 150 mg/kg fish per
day for 10 days.
- Oxytetracycline 50 mg/kg of fish per day for 10 days.
- Nitrofurazone (furacin) 50 mg/kg fish per day for 10 days.
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- Chlorine is a choice of disinfectant for the hatcheries
Control by immunization is possible. Effective bacterins have been developed.
Immersion route appears to be the more practical. But the intra peritoneal injection
(IP) is more effective.
Vibrio vaccine is now in the market
Vibriosis in shrimp
Vibrio spp. infections of one sort or another are probably the most common
form of disease in cultured shrimp. It is not possible to say which species of Vibrio are
more or less pathogenic since the ability to cause disease varies dramatically within
species. In all cases, the shrimp have to be harmed to some extent before they develop
vibriosis, however, some strains of Vibrio will cause disease in the presence of only
slight adverse environmental conditions. Other strains can only infect the shrimp
when they severely damage.
Disease signs
There are a number of recognised forms of Vibriosis including.
- acute localised or systemic
- chronic localised or systemic
There are also given specific names as follow:
1. One month mortality syndrome
This disease refers to a Vibrio spp. and other types of infection associated with
deterioration in the pond environment. Exposing the shrimp to adverse environmental
condition and large numbers of bacteria, resulting in a large proportion of the shrimp
developing shell lesions and systemic bacterial infection around one month after
stocking.
2. Black splinter is a chronic melanized lesion confined to the muscle of the
abdomen.
3. Luminescent bacterial syndrome causes by luminescent bacterial (Vibrio
spp.). Affected shows luminescent in dark. This type of infection is more common in
hatcheries but has become more of a problem in growout ponds.
4. Septic hepatopancreatic necrosis. This disease is a result in distruction of
large areas of the hepatopancreas reducing it in size and marking it dark in color. In
some cases they would appear to be a form of chronic vibriosis but some reports as
the result of toxin (aflatoxin) in food or presence of other types of bacteria.
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5. Systemic infection. It is relatively uncommon and often associated with poor
water quality or with other diseases. In acute form the signs are
- abnormal beheaviour
- lethargy
- inappetence and
- descoloralion either blue or red
6. Gill disease
Vibrio spp. may affects the internal tissue of the gill causing inflammatory
response resulting in black gill lesions.
Treatment
Treatment of vibriosis must always involve improving the environment,
sometimes combined with antibiotic therapy.
If antibiotic is applied, it has to be used with great care to avoid.
- risk to farm workers
- residues in the shrimp which may cause rejection by buyers
- development of resistant strains of bacteria.
Chemical treatments
The following are chemicals recommended as pond disinfectants.
- quaternary ammonium compounds e.g. benzakonium chloride
- buffered iodophores e.g. povidine iodine
- calcium hypophlorite
- lime
Furunculosis
Bacteria causing this disease is Gram-negative, rod with round end without
flagella, lacking motility, spores and capsules. It is a facultatively anaerobic.
Etiological agent of this disease is Aeromonas salmonicida. It prefers low
o
temperature and has an optimum growth temperature of 20-22 C and never been
reported in SEA.
Disease signs
This disease is very important in Europe and US in salmon and trout. It is a
systemic infection, may be acute or chronic with development of furuncles, necrotic.
swelling in the muscle. The typical sign of furunculosis is the appearance of swollen
diseased regions usually in one place on the trunk, and occationally in several places.
The muscle tissue fused with bacterial propagation following by softening of the
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diseased region due to hemorrhaging, exudature of serum and infiltration of
phagocytes.
Prevention
To prevent the invasion of bacteria in fish farms, eggs should be disinfected
during transfer of eggs in the eyed stage.
Facilities are kept free of contamination.
Treatment
- Wescodyne and Betadine are extensively used in the United States. Eggs are
immersed for 10-15 min. in 100 ppm.
- OTC 55 mg/kg of fish perday for 10 days
- Immunization have been made but very low level of protection was received.
Mycobacteriosis
Fish mycobacteriosis is a chronic to subacute disease of many fishes. The
disease is found among fishes in fresh, brackish and salt water. It is also called a fish
tuberculosis.
Etiological agent
The etiological agents of mycobacteriosis are Mycobacterium marinum in
marine fishes and Mycobacterium fortuitum in freshwater and brackish water fishes.
M. chelonae
Mycobacterium are Gram-positive bacilli. Growth often does not take place at
o
37 C. The bacteria are aerobic, non-motile and acid fast.
Epizootiology
The most probable route of transmission for these bacteria is orally. The
feeding of fish viscera or fish products contaminated with the organisms has served to
transmit the disease.
Mycobacteriosis in other aquatic vertebrates is a source of infection to fishes,
frogs, snakes and turtles may become involved in the transmission cycle.
The 3 species are capable of infecting warm blooded vertebrates including
man. M. marinum is the most frequently encountered of the three species and causes
cutaneous granulomatious in man usually of the elbow but also of the knee, fingers
and feet.
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Disease signs
There may or may not be external signs of mycobacteriosis. They may be
listless and lethargic, refuse to eat and become emaciated. Some fishes may have skin
ulcerations where lesions lying in the muscle directly below the skin rupture to the
outside. It is a chronic systemic disease with granulomas forming both externally and
scattered throughout the internal organs.
Gross internal pathology of mycobacteriosis is generally similar in all fishes,
with white nodules scatter in kidney, liver and spleen.
Transmission
Transmission is by ingestion of contaminated food or aquatic detritus, although
bacteria invasion through damage skin or gill tissue may also possible.
Therapy and Control
Sanitation, disinfection and destruction of carrier fishes are the primary
methods of controlling mycobacteriosis. Kanamycin will give limited control when
used at 100 mg per kg. fish per day for five to ten days.
Bacterial gill disease
Actually it should be called environmental gill disease because epizootics of
this disease are caused by an environmental irritant which damage to gill epithelium
and later bacteria infection.
The products of fish metabolism, particularly ammonia are the primary
environmental factors predisposing fish to bacterial gill disease.
The involved bacteria are all gram-negative and rod-shaped, such as
Flexibacter, Pseudomonas, Flavobacterium, or Aeromonas, often a single species or
strain of bacteria is involved.
All species of fishes are susceptible to environmental or bacterial gill disease.
Fish which have involved in water supplies rich in detritus and organic material seem
to be more resistant.
Disease signs
- gill swollen, opercula may not close normally
- red gill tissue may protude
- loss of appetite
- lethargic and anorexic
- tend to remain near the surface or inlet
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Therapy and Control
This disease is usually the result of mismanagement.
The best therapeutic method is to improve water quality, use proper stocking
rate, regulary changing water.
Shell disease
There are number of infections that start on the outside of the shrimp and
invade through the carapace. The most common externally invasive conditions are
bacterial shell lesions. These often occur when the carapace is either damaged or fail
to harden, allowing superficial infections to establish. Many of the bacteria involved
can digest the chitin in the shell, causing erosions or small depressions, giving the
carapace and roughened appearance. As with any injury, if they persist long enough,
they will become melanized, resulting in the typical brown or black spots.
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Antibiotic Treatment
The use of antibiotic substances is the cause of much controversy. There is no
doubt that these compounds are widely abused in aquacultrue at present. They do,
however, have a role to play health management, if they are used responsibly and it is
in everyone’s interest to ensure that this is the case. Their abuse may have serious
consequences; putting workers handing the substances at risk, leading to the
accumulation of residues in animal for human consumption and resulting in bacterial
strains which are resistant to available antibiotics.
Development of antibiotic resistance has to implications, it reduces the efficacy
of treatments and may also lead to drug resistance in human pathogens. The improper
use of antibiotics will encourage resistance very rapidly, but any use of antibiotics has
the potential to encourage development of resistance.
There are several rules that should be followed when considering the use of
antibiotics:
- always improve the pond environment
- only use antibiotics when it is essential
- only use antibiotics for bacterial infections, they are not effective against
viruses, fungi or protozoa
- use an antibiotics to which the bacteria are sensitive
- use fresh antibiotics from a reliable source
- take care when handling antibiotics they can be dangerous to some people
- make up the medicated feed fresh and do not store it for prolonged periods
- use the correct dose
- use for a sufficient duration and
- apply an adequate withdrawal period.
The sensitivity of different strains of bacteris to antibiotics has to be
determined by laboratory tests. Unfortunately, antibiotics may have to be used before
the results of the laboratory tests are available. In most cases an antibiotic which has
been effective against previous bacterial isolates from the farm should be used. If the
laboratory analysis subsequently indicates that the bacteria involved are not sensitive
to the antibiotics being used, the antibiotic should be changed or the necessity for
treatment re-evaluated.
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Viral Diseases
Fish virus received intensive study since about 1960 while plants and higher
vertebrate since 1892.
Virus is a smallest organisms. Without electron microscope it is not possible to
look into the unique world of viruses. The most important feature of viral biology is it
only reproduce inside living cell. They can remain outside of a cell for long period in
a biologically state but to reproduce they must enter a suitable cell. The reproduction
will disrupts the normal activities of the invaded cell causing structure or functional
abnormalities, damage to the nucleoli, fragmentation of chromosomes and release of
autolytic enzyme by lysosomes causing damage known as the cytopathic effect (CPE)
The single viral particle (virion) has no metabolic apparatus for maintenance or
reproduction. The virion depends on the synthisizing structures of the host cell for
replication. Viruses, therefore, are obligate parasites in the truest sense.
Transmission of virus
1. Virus emerge from the infected cell. The new virions attaching themselves
to neighbouring cells and being engulfed by those cells. They are transported via the
blood or lymph of the host.
2. Virus can be transmitted through eggs. Egg is contaminated by adhering
virions and the embryo become infected during hatching.
3. Infected fish shed the virus into the water with urine, faeces and
reproductive secretions. Direct contact is not the only way to spread the virus. Water
is an excellent mechanical vector.
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Viral diseases of fish
Infectious Pancreatic Necrosis (IPN)
It is an acute to subacute highly contagious disease of young salmonid fish. It
was first identified in the northeastern part of the US. It was later found in Canada.
Europe and in Japan. Not yet report in SEA
Etiological agent
This disease causes by Reovirus or a reo-like virus which is icosahedral 57-74
o
nm. The virus is resistant to heating at 60 C for 15 minutes and retains slight activity
o
in physiological solutions held at 60 C for one hour.
Epizootiology
The most important source of IPN are ovarian fluid of infected (carrier) female
fishes and feces or intestinal discharge from clinical cases of the disease.
Transmission is directly from gravid females to developing eggs.
There is
no evidence on the exact route. IPNV is probably passed by water from infected to
non infected fry.
Disease signs
External signs include a reluctance to take food gradual loss of equilibrium,
swimming in spirals. Sometimes violent flexing of the body as if in abdomeminal
distress and lethargy. The usual lethargic or spiral swimming activity of young
salmonid fishes is suggestive of this disease. Diseased fish demonstrate the opalescent
to white color of the intestine.
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Therapy and Control
There is no direct therapy. Reduction in water temperature may decrease
rapidly of viral replication. The best control of IPN is prevention. Eggs should be
obtained from known IPN-free brood fishes.
Infectious Hematopoietic Necrosis (IHN)
IHNV is an acute to subacute hemorrhagic disease of several salmonids
species. Susceptible species are chinook salmon, sockeye salmon and rainbow trout.
The hematopoietic tissue of the spleen an anterior kidney is the primary topic tissue.
The major route of natural transmission have been demonstrated to by oral, by
contact and from parents to offspring through eggs.
Etiological agent
This disease causes by Rhabdovirus, which replicates in the cytoplasm of the
infected cell. Signs of the disease can be halted in fishes by raising the water
o
temperature to above 15 C.
Disease signs
IHNV is present in many tissues during acute and subacute stages of the
disease. Kidney and spleen are the best sources of the virus in fingering sized fished
and ovarian fluid or milk from ripening or ripe adult fishes.
Fish become lethargic, usually are dark in color and swim cratically. Some
cases, fish develop exopthalmas and a distended abdomen . Serous fluid in the
abdomen. Liver may be pale. The intestive can be filled with bile-stained mucus and
with little or no food or feces. Kidney may be swollen and edematous.
Therapy and Control
No Therapy, prevention is the best method IHNV has been eliminated from
some fish culture facilities by removing all fishes and disinfecting the entire facility as
well as utensils used around fishes.
Control by immunization has not been possible.
Channel catfish virus disease (CCVD)
It is an acute to chronic disease of channel catfish. Large numbers of fry and
fingering were dying during the summer in 1968. Epizootics were gradually increased
is a Herpesvirus, enveloped and about 175-200 nm. CCV is extremely host specific.
Fry and fingerling are most susceptible.
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Disease signs
Infected fish may swim erratically, sometimes rotating longitudinally as if
attempting to maintain balance. They may remain motionless in the water with the
body in a vertical position.
External signs include petechial hemorrhages at the bases of fins and
occasionally over much of the skin, more pronounced on the ventral surface. Gills
may be pale and hemorrhagic. The abdomen is distended and there is exopthalmos.
The most striking internal signs is the general hemorrhagic appearance of
peritoneum, muscle liver, kidney, spleen and other visceral organs. The abdominal
cavity is usually filled with yellowish edematous fluid. The alimentary tract is free of
food. The intestinal tract is filled with yellowish mucus. The stomach is distended
with mucus secretions.
Diagnosis
The kidney, being a primary target for the virus, is damaged most rapidly
follow infection. Necrosis is also present in pancreatic tissue. The liver is congested
and with foci of necrosis.
Therapy and Control
There is no therapy for CCVD. However, the virus is usually not a single entity
in epizootics. Bacteria, fungi and animal parasites are usually opportunistic adjuncts
to the epizootics. Careful selection of a channel catfish supplier to be relatively sure
the brood fish are free of CCV.
Lymphocystis disease
It is a chronic slowly developing viral disease of connective tissue cells. Only
infected cells become hypertrophic enlarged about 500 times. Other near or attached
to affected cells remaining unaffected. The tumorous growths are not malignant. The
disease usually is no fatal to infected fishes. Incubation period about 2 weeks.
LDV is very easy recognized because it occurs on the surface of the body. It is
a warty like on skin and fins, white or gray-white in color. If the entire lession
ruptured, the lesion will heal usually leaving a light colored scar but no other effect.
This disease is wide spreaded in Europe and America. It was first reported in
Thailand in 1983.
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Etiological agent
It causes by virus in family Iridovirus. LDV is a large, complex, naked virus
with a deoxyribonucleic acid genome. The nucleocapsid is icosahedral-shaped. It’s
diameter is about 250 nm.
Transmission
Virus is shed from infected cells and reinfect fish through injuries and fins.
The infection route is from contaminated water and bottom detritus into epithelial
connective tissue cells and replicate causing a hypertrophic warty growth.
Oral route is also possible. The large, heavy lymphocystis cells fall to the
bottom and cells may be ingested by bottom feeding fish. Lymphocystis cell have
been reported along the gut, heart, and other internal organs. No transmission by egg.
Therapy and Control
LDV is self limiting. Within few months will fall of. The disease infected cells
spontaneously slough off, The warty growth is gradually disappear.
Viral Diseases of Shrimps
Hepatopancreatic viruses
There are a number of viruses that affect the shrimp hepatopancreas including:
- Monodon baculovirus (MBV)
- Hepatopancreatic parvo-like virus (HPV)
- Type C baculovirus
- Baculovirus penaei (BP)
Thess viruses damage the cells of the hepatopancreas and make the shrimp
more susceptible to adverse environmental conditions or other diseases. The severity
of their effect and the age at which infected shrimp are most sensitive vary with the
different viruses. It has proved difficult to demonstrate conclusively the effect of these
viruses on the health of shrimp poulations, but it would seem that they reduce growth
rate.
Etiological agents
These viruses are detected by their effects within the cells of the
hepatopancreas. With the exception of the type C baculoviruses they cause inclusion
bodies in the nuclei of affected cells. MBV and BP produce specialised forms of
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inclusion known as occlusions, which contain or hide virus particles. The occlusions
are thought to protect the viruses when they are excreted in the faeces, and make them
more likely to be picked up by another shrimp.
Transmission
All these viruses are spread by excretion in the faeces and subsequent ingestion
by other shrimp. The infection may spread between the broodstock and larvae by this
route.
Diagnosis
Inclusion bodies can be detected in fresh smears or in histological sections. In
theory, every effort should be made to avoid stocking with infected shrimp, however,
MBV would appear to be very widespread in South East Asia, making it difficult, or
impossible, to find larvae free from infection.
Therapy and Control
It is possible to reduce the prevalence of MBV in post larvae by using
disinfectants to prevent its spread from the broodstock. Despite these precautions,
most uninfected post larvae will subsequently become infected with the virus during
the production cycle.
Acutely fatal viruses
Since the early 1990’s, three acutely fatalvirus conditions have appeared in
cultured shrimp. The first was Yellow Head Disease in Thailand and, subsequently, a
condition known as Taura syndrome occurred in Ecuador. The third condition has
been reported from Japan to India and has been referred to as White Spot Disease,
Red Body or by more detailed names including Systemic Ectodermal and Mesodermal
Baculovirus (SEMBV) and PJ-RV. The infection will be referred to here as White
Sopt Disease since this is the most noticeable of the chlinical features.
When they first appeared these viruses were all associated with extremely
severe losses, and all appeared to be highly pathogenic. If shrimp were exposed to
enough of the virus they would die regardless of environmental conditions. Now,
however, all of the infections appear only to cause severe losses if the shrimp are also
suffering from poor environmental conditions. It is still not clear if this change has
been due to alternations in the viruses.
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Yellow Head Disease
This condition was initially confirmed in P. monodon from Thailand, but has
now been confirmed in other parts of Asia and the Americas. It caused very severe
mortalities, up to 100% within 3 to 5 days of the first clinical signs appearing, and it
occurred from 20 days post stocking onwards.
Etiological agent
This disease is caused by a monodon baculovirus (MBV)
Disease signs
The disease is characterised by pale body colour with yellowish gills and
hepatopancreas, although these signs can also be seen in other diseases.
Histologically, there is necrosis in a number of organs and prominent basophilic
inclusions in the cytoplasm of various cells.
Epizootiology
Outbreaks of this disease often occurred in ponds with poor environmental
conditions and in areas with a high density of farms. The presence of the virus is no
longer strongly associated with severe disease outbreaks and the appearance of
outbreaks on farms can be very confusing. In cases where outbreaks of Yellow Head
Disease have been associated with very poor environmental conditions it is difficult to
determine if the virus or the environmental deterioration is responsible for the
mortalities.
Diagnosis
A presumptive diagnosis can be made by examining smears of haemolymph. In
cases of Yellow Head Disease, abnormalities should be observed in the haemocytes.
The most important of these is the presence of inclusions in the cytoplasm. Other
changes such as shrinking of the nuclei (pyknosis), breakdown of the nuclei
(karyorhexis) can be associated with other conditions and may aslo be seen in shrimp
that were dead prior to sampling. The diagnosis can subsequently be confirmed by
histology.
Therapy and Control
It is important to keep predators and competitors out of the pond. Initially this
means that the pond should be filled and the water treated with calcium hypochlorite
at 15 to 20 ppm active chlorine. After the pond is filled, water exchange should be
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reduced to a minimum for at least the first month after stocking. Water should only be
exchanged when it is necessary, not as a routine procedure. It is also important to
ensure that incoming water is free from animals and has not been contaminated by the
waste from other farms. A reservoir is essential for such treatment of incoming water.
If water exchange is reduced it is necessary to reduce stocking density and
ensure that water and feed are managed very effectively. Pond preparation also has to
be as through as possible. It is impossible to run a reduced water exchange system
unless the ponds are adequately cleaned.
White Spot Disease
This condition was first reported in Japan in 1993. in shrimp that had been
imported from China. Since then there have been a number of reports of the infection
in countries from China to India and several species of Penaeid have been affected,
including P. monodon, P. merguiensis, P. chinensis, P. indicus and P. japonicus. It is
possible that White Spot Disease may be associated with slightly different viruses in
different areas (e.g. SEMBV and PJ-RV) (Takahasi et al, 1994). Outbreaks spread
rapidly through areas, but there is an association between poor environmental
conditions and outbreaks of White Spot Disease.
Disease signs
The characteristic feature of the infecion is white spots or patches under the
carapace. This may be associated with a red discoloration and many other non-specific
signs of ill including damaged appendages and external fouling. Initially, the shrimp
are often observed near the surface of the water and they stop feeding. The typical
white spots appear in some, but not all, of the shrimp soon after the first signs of ill
health and up to 100% mortalities can occur in less than 7 days. The problem has
occurred in post larvae 15, throuth to 40g shrimp, and has been reported in all types of
farm, from high yield to lower yield traditional systems.
Diagnosis
Histologically, distension of the nuclei and eosinophilic to basophilic
inclusions are seen in the cells in the tissue under the carapace and gut.
Therapy and Control
Infections can move between ponds on a single farm, but when more than one
pond is affected with White Spot Disease it is usually due to a common source of
infected post larvae. None the less, equipment should not be used in more than one
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pond, unless it is absolutely unavoidable. If equipment is moved between ponds it
must be first thoroughly cleaned and disinfected.
If the infection does get into the population and an emergency harvest is not
appropriate, it has been suggested that removing the affected shrimp may limit the
spread of the infection within the pond. The affected shrimp will usually be seen on
the surface of the pond, especially in the morning and evening.
Some general recommendations are available for preventing the spread of
these, or other, serious viral infections.
Moving shrimp between countries, or between distinct areas within a country,
should be avoided wherever possible. Moving stocks of shrimp not only carries the
risk of introducing disease to farms, but may also have adverse effects on the local
population of wild shrimp. This practice is still occurring and should be discouraged
wherever possible.
Early detection of the problem is extremely important. The shrimp should be
examined regularly for signs of disease, expecially if there is an increased risk on
infection.
If a new infection occurs, it is important that it is not allowed to spread to
neighbouring farms. The dead shrimp should be removed from the pond and disposed
of in a manner that does not contaminate the water supply. They can either be buried
with quick lime or they can be burned. The water from the affected pond should not
be discharged from the farm. Once the infection is detected in the shrimp it may be
possible to conduct and emergency harvest. The water from an emergency harvest
should be retained in a settling pond and treated with calcium hypochlorite at least 20
ppm active chlorine. In some cases it may not be worth conducting an emergency
harvest, for example, if the shrimp are too small or if most have already died. In such
a case the water should be treated in the pond, prior to discharge. Every effort should
be made to avoid the water from the affected pond coming into contact with the inlet
water for the affected farm or any neighbouring farms.
Taura Syndrome
This condition was initially thought to be associated with fungicides used in
banana plantaions. It has now been demonstrated that it is associated with a virus. It
was first recorded in June 1992 in the Taura river region of the Gulf of Guayaquil,
Ecuador. Taura syndrome has been report in several other South and Central
American Countries and in Hawaii, but not yet in Asia.
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Disease signs
The condition typically occurs in P. vannamei between 14 and 40 days after
stocking. In the acute phase, shrimp have a red appearance and affected animals
usually die during the moulting process. If the shrimp survive the acute phase, they
develop multiple superficial brown or black melanised lesions.
Diagnosis
The histopathology of the condition is very ditinctive, with patches of cell
death (necrosis), and basophilic and eosinophilic inclusions in the cells under the
surface of the cuticle or in the gut.
Infectious hypodermal and haematiopoietic necrosis virus (IHHNV)
This virus has been detected in P. monodon in South East Asia but is not
thought to be a serious pathogen. It appears to be more of a problem in P. stylorostris
and to a lesser extent in P. vannamei. The virus causes characteristic Cowdrie type A
inclusion bodies in the nuclei of various types of cell.
Other viruses
There have been other viruses, including reoviruses, togaviruses and
rhabdoviruses observed in, or isolated from, shrimp, however, they do not appear to
be associated with significant disease problems.
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Prevention of the diseases
Prevention of these diseases is a good management. It is the best preventive
medicine. Management begins with MAN., therefore the hatchery or farm manager is
the focal point in the successful production of healthy fish.
To be a good farm manager, fish culturist or fish disease researchers must have
the knowledge on the normal condition of fish then can recognize the fish
abnormalities. To be able to identify abnormal from normal you have to make
frequent and regular visits to your fish pond. With this practice, you are not only
obtain the baseline information but the probability of early detection of fish health
problems.
When you make the visit, you must observe
1. Fish behavior If possible, you should feed the fish yourself and observe fish
behavior, movement, distribution, scraping against the submerged objects, rapid
respiration.
2. How do they feed ? (eagerly, sluggish or refuse to eat)
3. Do they show any abnormal appearance? (discoloration, frayed eroded fin
or operculum). This may be difficult for pond fish but aquarium fish you can easily
observed.
4.You should also observed environmental condition, water color, and measure
the water quality.
Control of Fish Diseases
There are at least six general methods of disease control in fishes.
1. Test and slaughter
2. Quarantine and restriction of movement
3. Drug therapy and sanitation
4. Immunization and disease resistance
5. Destruction or reduction of a link in the transmission cycle and
6. Limitation or control of the release of toxic substances.
1. Test and slaughter
Test and slaughter means that fish are examined and if infectious organism
which has no known control is found the entire population will be killed and the
carcasses disposed (burn and deep buried). This method is necessary when absolute
control is needed.
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2. Quarantine and restriction of movement
This method means that
1. fish which are to be removed from a suspected or infected geographical area
to a noninfected geographical area must be held in detention for a period of time at
least as long as the incubation period of the suspected disease then moved if the
suspected disease does not develop.
2. all movement of fishes is restricted between two geographical areas.
3. Drug therapy and sanitation
There are extremely large number of therapeutic compounds available which
have not been applied to the control of fish diseases. FDA must approved first which
take time. FDA control of all therapuetic substances including external disinfectants.
4. Immunization and disease resistance
This method is very limited to fish because
1. fishes are not an immunologically competent as higher animals especially at
lower temperature.
2. there are limitated methods for mass immunization of cultured fishes.
However, attempt have been made in immunize fish and it hold promise but
requires much more research.
5. Destruction or reduction of a link in the transmission cycle.
This method can be used when involving animal parasites. Many parasites
require one or more other animal host species to complete the live cycle for example
bird. Then this method become difficult.
6. Limitation or control of the release of toxic substances
This method has been one of the most effective methods of disease control in
the more technologically oriented countries of the world.
There are several disinfectants known. At the same time, there are many
disinfectants use today which have not been examined for potential use as external
disinfectants for fish.
Must control the release of toxic substances from industries agriculture and
domestic wastes.
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Treatment
If the control and prevention is failed then come to the treatment
Treatment with various medications and chemotherapeutic agents is only for
the purpose of buying time, not for killing 100% of the disease organisms.
There are several questions to ask yourself before you make a decision whether
or not to treat:
1. What is the prognosis? Is the disease treatable? and what is the probability of
a successful treatment ?
2. It is economically feasible to treat the fish when you consider cost.
3. Can the fish in their condition withstand the treatment.
4. Does the loss rate and the present disease justify treatment ?
After consider then treat
External treatment
External chemical disinfectants must be :1. mixible with water or capable of being suspended in water at a therapeutic
concentration.
2. must destroy the target organism at a concentration below the lethal level for
the fish being treated.
3. should resist absorption by the fish
4. should be capable of being used for multiple treatments without harm to fish.
etc Ich, Lerneae
5. should be ecconomically acceptable for use in the fish culture facilities.
The success of any disinfectant is a time-concentration ratio.
External disinfection
1. Dip Use for small numbers of fish and for those disinfectants, which can be
used for a short treatment time.
2. Flush similar to dip but fish are not handled. Flush treatments are used in
troughs, tanks raceways and ponds where direct water flow.
3. Bath or static procedure. (also with long period calls prolong treatment)
Advantage of the bath procedure is that a more precise treatment can be given
to fish. An exact quantity of disinfectant can be added to a more exact quantity of
water. Fish are held in the more precise disinfecting bath for a more carefully
regulated length of time.
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Disadvantage, if used in trough, tanks or race ways or ponds require that inflow
water be shut off during the treatment time. Fish may become anoxic during the
treatment period.
Disinfectant/water mixture be removed at the end of the treatment time. It is
not easy with large pond.
4. Dynamic or flow-through treatment. This method can only be used in fish
holding facilities which have inflow and outflow water. Disinfectant is added at a
constant rate. A requirement for the dynamic treatment procedure is that the inflow
water can be measured and the volume of inflow remains constant during the
treatment period. Water does not need to shut off during treatment period.
5. Systemic treatment
In general, through oral route, mix with food. Therapeutic drugs used must be
1. capable of controlling reproducting of the pathogen under conditions found
in the fishes.
2. dose level must be safety below the toxic level of the drug.
3. be economically acceptable for use in cultured fishes.
Constraints in using systemic therapeutic drugs.
1. Must be mixed evenly and thoroughly
2. The medicated food must be fed so each fish receives the required amount of
drug.
3. The mixture must be fed over a long enough period of time to be effected in
controlling the pathogen.
4. System drugs must be absorbed from the alimentary tract of the fish and
produce a therapeutic concentration of the drug in all tissue without reaching a toxic
concentration.
5. There are limited number of drugs.
6. The drugs for alimentary pathogens should remain in the alimentary tract
long enough to kill the pathogen.
7. The drugs should kill the pathogens in situ or render them incapable of
remaining in place.
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SHRIMP DISEASES
Disease problems have resulted in massive financial losses to the shrimp
farming industry, therefore, the control of disease is essential and, order to control it,
the nature of shrimp diseases must be understood.
Identifying the pathogen also helps in the understanding the general health of
the population. Laboratory study of the pathogen can have other uses, if a bacterial
infection is identified, the antibiotic sensitivity can be checked to determine the most
effective drug for treatment, however, by the time this information is available it is
usually too late for the current crop but it can be used to select a more effective
treatment in other ponds, or in subsequent production cycles.
One of the most important uses of pathogen identification, is that it produces
data relating to the disease status of populations, either within a farm or within a
larger area. This can help to reduce the spread of infections and is essential
information if a new infection occurs.
TYPES OF DISEASE PROBLEMS
Diseases in shrimps can be grouped into four main types :
- Disease can be the direct result of poor environmental conditions e.g. low
dissolved oxygen or high ammonia.
- The shrimp can be stressed by poor environmental conditions and then
become infected by an opportunist pathogens (organisms that can only attack
stressed or damaged animals) e.g. poor pond bottom conditions may lead to
vibriosis.
- The shrimp may have organisms within its tissue which only causes damage
when the shrimp is stressed by poor environmental conditions e.g. monodon
baculovirus (MBV)
- In humans and other terrestrial animals there are some primary pathogens
which spread through a population causing disease regardless of
environmental stress. There are relatively few examples of such pathogens in
shrimp but some of the recently emerged viral infections may fall into this
category e.g. yellow head baculovirus.
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DISEASE SYNDROMES
The disease organisms have been grouped together into a small number of
syndromes.
1. EXTERNAL FOULING
External fouling is the growth of organisms and the accumulation of inorganic
debris on the surface of the shrimp.
There are a large number of organisms which may attach to the surface of the
shrimp including :
- macro-invertebrates e.g. barnacles
- algae
- protozoa e.g. Zoothamnium. spp., Vorticella. spp., Suctoria. spp.
- Bacteria e.g. Leucothrix. spp.,
- fungi and others.
The appearance of shrimp with external fouling depends not only on the type
of organism involved but also on any additional debris which become attached.
Fouling on the gill frequently causes a dark discoloration and can even result in the
gills appearing black.
The main affect of fouling is to interfere with movement
and respiration.
P. monodon are thought to be susceptible only in the early stages of growth.
There is also some evidence that levels of infection are increasing in wild stocks. The
most commonly used compound for this purpose is formalin (37 to 40%
formaldehyde). The dose of formalin used to treat external fouling in shrimp ponds is
much lower than that used for finfish or shrimp hatcheries. It has been found through
practical experience that a lower dose can alleviate fouling without seriously
damaging the environment within the pond.
The recommended dose of formalin is 25 to 30 ppm.
2. EXTERNALLY INVASIVE CONDITIONS
There are a number of infections which start on the outside of the shrimp and
invade through the carapace. The most common externally invasive conditions are
bacterial shell lesions. Many of the bacteria involved can digest the chitin in the shell,
causing erosions or small depressions.
Any condition which affects the internal tissue of the gill enough to produce an
inflammatory response can produce black gill lesions
Areas of the carapace other than the gill can be affected by localised damage.
In ponds where the shrimp cannot avoid the accumulated waste, cases of swollen tail
may be seen.
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3. VIBRIOSIS
The term vibriosis is used to refer to all types of infections caused by bacteria
of the genus Vibrio, including bacterial shell disease and ‘black gill’. Vibrio spp.
infections of one sort or another are probably the most common form of disease in
cultured shrimp.
There are a number of recognised forms of vibriosis, including :
- acute localised or systemic and
- chronic localised or systemic.
Some forms or outbreak have been given specific names. For example ‘one
month mortality syndrome’ refers to a Vibrio spp. and other types of infection
associated with deterioration in the pond environment.
‘Black splinter’ is used to describe a chronic melanized lesion confined to the muscle
of the abdomen.
Some Vibrio spp. are luminescent, if these are present in large numbers, they
may cause the affected animals to glow in the dark.
Systemic infections, where the bacteria are present throughout the body of the
shrimp, appear to be relatively uncommon.
If the shrimp are severely stressed, or the bacteria are highly pathogenic, a
large number of shrimp may die within a short period of time.
Vibriosis is found so often in association with other problems that it is almost
true to say that any dead or dying shrimp will have some form of vibriosis.
Treatment of vibriosis must always involve improving the environment,
sometimes combined with antibiotic therapy. Antibiotics can be valuable in the
treatment of vibriosis but they have to be used with great care so as to avoid :
- risk to farm workers
- residues in the shrimp which may cause rejection by buyers and
- the development of resistant strains of bacteria.
4. HEPATOPANCREATIC VIRUSES
There are a number of viruses which affect the hepatopancreas including :
- Monodon baculovirus (MBV)
- Baculovirus penaei (BP)
- Type C baculovirus and
- Hepatopancreatic parvo-like virus (HPV)
These viruses are thought to damage the cells of the hepatopancreas and make
the shrimp more susceptible to stress or other diseases. The severity of their effect and
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the age at which infected shrimp are most sensitive vary with the different viruses. It
has proved to be difficult to demonstrate conclusively the effect of these viruses on
the health of shrimp populations.
The viruses are detected by their effect within the cells of the hepatopancreas.
MBV and BP produce a specialised form of inclusion known as an occlusion which
contains virus particles. All these viruses are thought to be spread by excretion in the
faeces and subsequent ingestion by other shrimp. The infection may spread between
the broodstock and the larvae by this route.
5. ACUTELY FATAL VIRUSES
The first was yellow head baculovirus in Thailand and subsequently a
condition known as Taura syndrome occurred in Ecuador. The third condition referred
to as white patch disease, red body or by more detailed names including.
YELLOW HEAD BACULOVIRUS
The disease is characterised by pale body colour with yellowish gills and
hepatopancreas.
Outbreaks of this disease often occur in ponds with poor environmental
conditions and in areas with a high density of farms. (It causes very severe mortalities,
up to 100% within 3 to 5 days of the first clinical signs appearing, and can occur from
20 days post stocking onwards).
The best course of action if yellow head is identified is to conduct an
emergency harvest, regardless of the stage of production.
WHITE PATCH DISEASE
The characteristic feature of the infection is white spots or patches under the
carapace. This may be associated with a red discoloration. Initially the shrimp are
often observed near the surface of the water and stop feeding. The typical white
patches appear soon after the first signs of ill health and up to 100% can occur in less
than 7 days. The problem has occurred in pl 15 through to 40g shrimp and has been
reported in all types of farm from intensive to extensive.
TAURA SYNDROME
Is was first recorded in June 1992 in the Taura river region of the Gulf of
Guayaquil, Ecuador. The condition typically occurs in P.vannamei between 14 and 40
days after stocking. In the acute phase shrimp have a red appearance and affected
animals usually die during the moulting process.
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6. INFECTIOUS HYPODERMAL AND HAEMATOPOIETIC NECROSIS
VIRUS (IHHNV)
This virus has been detected in P. monodon in South East Asia but is not
thought to be a serious pathogen. It appears to be more of a problem in P. stylorostris
and to a lesser extent in P. vanamei. The virus causes characteristic Cowdrie type A
inclusion bodies in the nuclei of various types of cell.
7. MICROSPORIDEANS
There are a number of different species of microsporidean that affect shrimp.
In Thailand reports refer to an Agmasoma (formerly Thelohania) spp. which infects
the muscle of the abdomen causing it to turn opaque and white. The appearance of the
muscle has led to the condition being called ‘cotton shrimp’ or ‘milk shrimp’ . These
organisms can affect a wide range of shrimp species including P. merguiensis and
Acetes spp. and have been associated with significant losses in P. monodon .
Their abuse of antibiotic may have serious consequences, it leads to the
accumulation of residues in shrimp for human consumption and it results in bacterial
strains which are resistant to available antibiotics.
The duration of the treatment should be not less than 5 days. The shrimp should
not be harvested until at least 14 days after the end of a course of antibiotics.
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