PARASITOLOGY

HONOURS
Parasitic Diseases
 LYMPHOCYSTIS

Species affected:
• Tilapia spp.

Gross signs:
• External lesions on skin consist of:
• focal clusters of rounded pustules or
• growths of wart-like or nodular tissue.
• Lymphocystis is a common irido-virus disease on most aquarium
fish (marine angelfish and butterfly fish).
• Classic sign = white cottony looking patches normally at the
edges of the fins, but can also appear on the body.

Cause:
• Viral infection of lymphocytes.
Diagnosis:
• Histological examination.
• Electron microscopical examination.
• Lesions consist of clusters of:
 greatly enlarged dermal cells,
 with thick hyaline eosinophilic cell wall and
 extremely large nucleus with large nucleolus.

Morphology:
Life history:
• Virus particles released into water when infected cells
burst and disintegrate.
• Fish become infected when exposed to water containing
emulsified lymphocystis cells.
• Virus is spread by physical contact.
• Incubation period is temperature dependent.
• Host specificity is strong but not absolute.
• Cross infection is possible among fish of the same genus.
• Re-infection also possible.

Pathology:
• Clusters of lymphocystis warts up to 5 mm in diameter on
tip and base of caudal fin.
• Cells in the cluster consist of:
 vacuolated cytoplasm and inclusion bodies with granular
or reticular basophilic material,
 large nucleus and
 distinct nucleolus.
Later stage of infection:
• nuclei disintegrate,
• cell wall collapse, and
• phagocytic cells invade cell.

In other fish lymphocystis may:

• proliferate (multiply, increase);
• cover entire skin, and
• extend to gills and internal organs.

Control:
• No treatment for the disease.
• Infected fish should be removed from water and destroyed.
• Disease is rarely fatal, normally white tuffs of enlarged cells
will disappear on their own in time.
 BACTERIAL INFECTIONS

Species affected:
• All fish species.

Gross signs:
External signs:
• Scattered haemorrhages on skin.
• Haemorrhages on vents and base of fins.
• Ulcerating and necrotic lesions on skin.
• Loose scales.
• Abdominal bulging into dropsy.
• In fin and gill rot condition:
 signs indicate progressive erosion and necrosis of fins and
 extensive lesions on gills,
 often with whitish patches covering gills.
A typical bacterial infection show:
 Large area of ulceration just behind operculum (gill cover).
 Pectoral fin has totally eroded.
 Both pelvic and anal fins very red and inflamed.
 Caudal (tail) fin has advanced fin rot.
Koi carp with bacterial infection:
 Raised scales, with extensive inflammation and
swelling.
 If left untreated the infected area is liable to
ulcerate.
Internal signs:
• Oedematous change (swelling) in visceral organs;
• Scattered haemorrhages in muscles and internal serosa;
• In dropsy: extensive peritonitis with serous, purulent or
haemorrhagic exudates.
• In chronic condition, focal lesions may occur in
kidneys, spleen and liver.
• Bacterial infection in testis of a koi carp. No external
signs of disease.
Normal gills at low magnification showing primary gill
filaments with secondary lamellae branching out from each
side. The viability of secondary lamellae is crucial to fish
health.
High magnification of healthy gill tissue. Red blood cells pass
in single column through secondary lamellae where they pick
up oxygen and dump carbon dioxide and ammonia.

Hyperplasia (excessive growth); chemical or physical

irritation cause addition cells to grow as a form of
protection. Secondary lamellae clump together affecting
gaseous exchange and respiration.
Effects of hyperplasia - higher magnification. Gills are
swollen and clumped.

Extreme hyperplasia where both the secondary lamellae and

primary filaments are clumped together in a mass of tissue.
No gaseous exchange can take place and the fish literally
suffocates.
Severe infection of caudal fin of a koi. Extensive
inflammation around lesion extending into body of
fish. This fish recovered and surprisingly the fin did
partially re-grow, with the two halves knitting back
together.

Typical fin rot affecting dorsal fin of a koi. On the

leading edge of the lesion is an area of white necrotic
tissue. Surrounding this is a large area of inflamed,
infected tissue. The front fin ray has been exposed
and destroyed. The infection has reached the fish's
body.
• Extreme example of fin rot of caudal fin. White necrotic
region of fin edge is clearly visible. Whole of fin is very
red and inflamed. Infection has entered body of fish
resulting in raised scales and a large area of
inflammation.
• Typical cases of ulcers on koi carp. Area of erosion in both
cases is quite extensive. Lesions are deep, exposing the
muscle underneath. Margin of inflammation can be clearly
seen around the lesion.

• Severe ulceration on the body of a koi. A close view of the

photo shows many infected scales around the lesion.
Cause:
• Gram-negative bacteria of the genera Aeromonas,
Pseudomonas and Vibrio.
• Gram-positive bacteria (Streptococci and Micrococci) cause
fish septicaemia.
• Fin and gill rot are caused predominantly by Myxobacteria.
• Bacteria of these genera are facultative pathogens, and stress
condition in fish:
 due to handling injuries or
 deteriorating of environmental quality, is generally the
predisposing factor in the outbreak of diseases caused by
these bacteria.
Diagnosis:

• No bacteriological base-line data and type cultures are

available from Africa = making identification extremely
difficult.
• Bacterial infections are identified through culturing on
routine media.
• Myxobacteria are elongated rods, or filaments, gram-
negative and motile.
• For bacterial diagnosis the fish surface is disinfected (by
70% alcohol) and samples are taken from the blood, the
peritoneal exudates and the kidney, streaked on the
media in a petri dish and incubated for 24-48 hr at room
temperature (22-28 °C). If several types of bacterial
colonies appear on the agar medium, different types
are further isolated through sub-cultures.
Morphology:

Tail rot and dermal ulcers caused Gill rot caused by Myxobacteria
by bacteria
Epizootology:
• Although bacteria potentially pathogenic to fish are continuously
present in most water habitats, epizootics seldom occur unless fish
are exposed to:
 adverse environmental conditions (oxygen depletion or super-
saturation, extreme temperatures or salinities), or
 kept overcrowded,
 undernourished,
 or injured during hauling or handling.
• In fish stressed due to above-mentioned factors, the host defence
system deteriorates.
• In injured fish, damage to skin disrupts osmoregulatory system of
fish and causes physiological stress to fish.
• Direct damage to skin facilitates entrance of bacteria to the fish’s
internal system; therefore septicaemia conditions often follow skin
injuries.
• In warm-water environments higher temperatures accelerate
reproduction of bacteria and hence their invasion and
pathogenicity.
Pathology:
• Bacterial infections cause haemorrhages, epidermal hyperplasia,
spongiosis in peripheral tissue and extensive necrosis with a
superficial stroma of bacterial mass overlying the necrotic area.
• Skin lesions contaminated by Aeromonas, Pseudomonas or Vibrio
spp. often develop into wide and deep haemorrhagic ulcers of
extensive necrosis which result from complete erosion of
epidermal and dermal layers, exposing underlying muscular
layer.
• Degenerative and necrotic changes often extend into muscle
layer as well.
• Septicaemia may result in muscle, intestine and intestinal
mucosal.
• Acute septicaemia may result in dropsy - accumulating serous
liquid build up in abdominal cavity.
• In chronic bacterial infections encapsulated or diffuse foci of
necrosis (abscesses) may occur in various organs – kidneys,
spleen and the dermal and sub-dermal layers.
Control:
Routine application of suitable antibiotics or disinfectants
to fish.
 EPITHELIOCYSTIS

Species affected:
Tilapia spp. and carp.

Gross signs:
Transparent cysts of variable size attached to or embedded in gill
filaments.
In heavy infections gill filaments lose their lamellar structure, swell
and adhere to one another.
Diagnosis:
• Microscopic examination of fresh gill filaments reveals
transparent cysts with homogenous granular substance.

Morphology:
Life history:

• Route of infection unknown.

• Earliest stage of infection in superficial epithelial cells
lining gill lamellae.
• Infections only occur in gill cells.
• Infection results in granular hypertrophy (hyperplasia) of
infected cells, which is also encapsulated by a layer of
epithelial cells.
• Maturing cyst eventually detaches and washes away
from gills.
• Epitheliocystis organism develops through a succession
of generations through initial, giant and elementary
bodies.
Epizootology:
• Infection is transmitted directly from fish to fish.
• Infective stages are apparently resistant to adverse conditions.
• Overcrowding and poor growth promote development of hyper-
infection and proliferative changes in gill tissue.

Pathology:
• Epithelial cells adjust to cyst proliferation and enclose the cyst.
• In hyper-infections entire gill filament proliferates, embedding
completely the capillary network of gill lamellae in a mass of
hyperplastic epithelial.
• If small fish survive hyper-infections, epitheliocystis cysts
degenerate and are eliminated by infiltrating macrophages. Gill
epithelium becomes normal.

Control:
• No effective means of treatment.
 FUNGAL INFECTIONS
Saprolegnia spp.

Species affected:
• Tilapia spp., Clarias spp.

Gross signs:
• Patchy or extensive lesions on skin and mouth covered by
cottony growth, which consists of a mass (mycelium) of fungal
filaments (hyphae).
Cause:
• Infection by fungi, predominately of the Class Phycomycetes.

Diagnosis:
• A mycology specialist should make generic and specific
identification.

Morphology:
• Fungi of the genus Saprolegnia consist of a branched non-
septate multinucleated mycelium.
• Reproductive organs oval-elongated sporangia containing bi-
flagellated zoospores are born on the tips of hyphae.
• Sex organs, rounded oogonia, develop in tips of hyphae.
Male organs – antheridia are less distinct.
Sporangia of Saprolegnia
Life history:

• Asexual reproduction by production of zoospores

(sporangiospores) in sporangia.
• Released flagellated zoospores settle and produce new hyphae.

• Sexual reproduction by female oogonia fertilized by male

antheridia.
• Antheridia penetrate into oogonium and fertilize it. Zygote
form and develop into 1-20 zygospores.
• Fertilized zygote develops into resting spores. Germinating
spores undergo meiotic division followed by several mitotic
divisions sending out un-branched hyphae, which form
sporangia containing zoospores.
• Saprolegnia is considered secondary invaders and will invade
skin already damaged through handling, netting and transfer,
or other ectoparasites.
• Saprolegnia often occur on incubated eggs and fry.
Pathology:

• Erodes dermis.
• In acute infections it may also penetrate into the muscle.
• Results in extensive necrosis of invaded tissue, oedema
and haemorrhage.
• Infiltration is often associated with bacterial
contamination of the lesion.
• Causes complete destruction of caudal fin and peduncle.

Control:

• Malachite green.
• Saline dip or seawater dip after handling fish.
The End