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PARASITOLOGY

HONOURS
Cestoda
CESTODES
Species affected:
• Larval forms in many Cyprinidae and Cichlidae.
• Adult cestodes in intestine of Clariidae & Polypteridae.

Gross signs:
• Larval cestodes (pseudophyllidean pleurocercoid and dilepoid
cysticercoids) occur in a wide range of Cyprinidae & Cichlidae fishes.
Ligula intestinalis Bothriocephalus sp.
Cause:
• Five families have been reported in Africa:
Amphilinidae; Caryophyllaeidae; Bothriocephalidae;
Ptychobothriidae and Proteocephalidae.
• Pleurocercoid of Ligula intestinalis establish themselves
in abdominal cavity of small fish (100-150 mm long
cichlids & cyprinids), where they rich length of 100 mm
& width of 10 mm.

Diagnosis:
• Cysticerci on visceral organs.
embryonated egg coracidium

onchosphere

procercoid

procercoid cysticercus
Morphology:

Ligula intestinalis
in body cavity of cysticercoid
Barbus sp.

pleurocercoid

Ligula pleurocercoid

Bothriocephalus
aegypticus scolex
Life history in general:

• Larval cestodes demonstrate a low degree of host specificity


and will infect a wide range of hosts.
• All cestodes develop via intermediate hosts.
• First host of polyzoic cestodes are copepods.
• The definitive hosts of cestodes are piscivorous birds,
mammals and reptiles.

• Eggs released with faeces into water are either ingested by an


intermediate host, or hatch and a ciliated larva (coracidium) is
ingested by copepod host.
• Life cycle of fish cestodes: From egg, a coracidium hatches
and is eaten by a copepod. In gut of copepod larva –
oncosphere emerges and enters through gut wall into body
cavity where it develops into procercoid.
Bothriocephalus

Bothriocephalus acheilognathi heads


Life cycle of Bothriocephalus
The life cycle of B. acheilognathi involves a definitive host, a fish, and an
intermediate host, a copepod. The adult tapeworm is hermaphroditic; each
proglottid has a complete set of both male and female reproductive organs and
produces eggs via self-fertilization. The tapeworm is sensitive to temperature, in
addition the species is thermophilic; lower temperatures interfere and delay
development and completion of the life cycle.

The eggs are released into the water through the fish fecal material, where they
hatch into free-swimming hexacanth (six-hooked) larvae (coracidium). Between 1–
28 days, the eggs will hatch according to the water temperature range it is in. Eggs
that hatch within 1–5 days occur at temperatures between 28-30 °C and eggs that
hatch within 10–28 days occur at temperatures between 14- 15 °C.

When the free-swimming larvae, called coracidia, are eaten by copepods


(intermediate host), it penetrates into the gut wall, travels to the coelom, and
develops into a second larval stage called a procercoid (infective form) all within 6–
10 days. Once the infected copepods are eaten by the fish hosts, the procercoid
rapidly transform into the plerocercoid stage and attaches to the intestinal gut wall,
where it develops into the adult parasite over the course of 21–23 days.
Life cycle of Bothriocephalus aegypticus:

• Adults in fish as definitive hosts,


• Eggs released via faeces,
• From egg a coracidium hatches,
• is eaten by a copepod.
• In gut of copepod larva – oncosphere emerges,
• enters through gut wall into body cavity where it develops into a
procercoid.
• Fish eats infected copepods and cestode develops to pleurocercoid,
then to maturity, producing eggs via all segments.
Ligula intestinalis
Ligula intestinalis
Ligula: cycle starts in body of birds. Life expectancy in major host is
maximum of 5 days, but in this time they will lay a multitude of eggs.
• Eggs are passed into water via faeces of bird.
• Once in aquatic medium they hatch as a coracidium.
• Eggs/coracidia are eaten by a wide range of copepod zooplankton.
• In gut of copepod larva – oncosphere emerges and enters through gut
wall into body cavity where it develops into a procercoid.
• Copepod is eaten by fish.
• Pleurocercoid of Ligula intestinalis establish themselves in abdominal
cavity of small fish.
• Cycle is complete when a bird eats tapeworm hosting fish.
Pathology:

• No pathogenic effect in most hosts.


• Haemorrhagic enteritis, destruction of intestinal epithelium
causing swelling of abdomen, emaciation and cessation of
feeding.
• Encysted pleurocercoids and cysticercoids in peritoneum
and mesenteries or in visceral organs will induce a low
tissue response. Heavy infections may result in irritation,
inflammation and abdominal adhesions of mesenteries and
peritoneum and fibrotic changes in heavily infected visceral
organs.
• Pressure by these encysted larval stages on gonad
development may cause sterilization of fish.
NEMATODA
NEMATODES
Species affected:
• All species of fish.

Gross signs:
• Round worms are found within encapsulations in tissues.
• Necrotic lesions in dermis, sub-dermis and visceral organs.
• Free, non-encapsulated worms also in abdominal and pericardial
cavities.

Cause:
Infection by larval nematodes most commonly of Families
Heterocheilidae (genera Contracaecum and Amplicaecum) and
Dioctophymidae (Genus Eustrongylides).
Diagnosis:
• Identification of larval nematodes difficult and often not
feasible.
• Heterocheilidae differ from Dioctophymidae as follow:

➢ Heterocheilidae:
Oesophagus short, structurally very distinct from
intestine and terminates distally by a posterior
ventriculum (muscular bulb).

➢ Dioctophymidae:
Oesophagus very long and almost indistinct from
intestine, posterior ventriculum absent.
• Generic level Heterocheilidae have the following
characteristics:
❖Genus: Contracaecum

Posterior ventriculum present, from which an appendix


is extending; intestinal caecum present.

o = oesophagus
i = intestine
g = glandular ventriculum
❖Genus: Porrocaecum

Ventriculum present, ventricular appendix absent;


intestinal caecum present.

o = oesophagus
i = intestine
g = glandular ventriculum
❖Genus: Amplicaecum

Ventriculum absent, appendix absent; intestinal


caecum present.

o = oesophagus
i = intestine
g = glandular ventriculum
Life history:

• Most life cycles unknown.


• First intermediate hosts of heterocheilid nematodes are
small crustaceans like copepods or amphipods.
• Larval Contracaecum, Porrocaecum and Eustrongylides
develop into adults in piscivorous birds (herons, cormorants,
pelicans, darters & grebes).
• Definitive hosts of Amplicaecum are Nile monitors, water
snakes, crocodiles, frogs and toads.
If the nematode has a DIRECT life cycle,

then it does not need an intermediate

host and infection can spread directly

from one fish to another by ingestion of

eggs or larvae.
If the nematode has an INDIRECT life cycle:
• the eggs or larvae are excreted into the water and,
• during development, immature stages pass through at
least two different types of organisms,
➢ one of which may be a fish.

• Depending upon the role of the fish, indirect life cycles


can also be subcategorized by whether the fish is:
❖ (i) the definitive (final) host or
❖ (ii) an intermediate host.
Indirect life cycle where the fish is the final
(definitive) host:

If fish is the definitive or final host, then the


nematode will enter another organism -
usually an aquatic invertebrate such as a
copepod, side swimmer (such as Gammarus
spp.), tubifex worm, or insect larva - in which
it will further develop prior to being eaten by
a fish. After being eaten by the correct
species of fish, some species of nematode
reach sexual maturity and reproduce in these
fish. In such a case, the fish are considered
the "definitive" or "final" host for these
nematode species.
Indirect life cycle where the
fish is an intermediate host:

Nematodes that have this


type of life cycle use fish
species as intermediate
hosts only. The final host
(which contains the
reproductive adult stage of
the nematode) may be a
piscivorous (fish-eating) fish,
bird or mammal.
Pathology:
• Pathological changes caused by encapsulating larvae
include tissue changes leading to the formation of a
fibrous capsule.
• Extensive damage to host is often caused by non-
encapsulated larvae, which invade sub-dermis, somatic
muscles and muscular sheath of gut.
• Cellular degeneration and necrosis.

Control:
• No control measures.
Contracaecum
SPINY-HEADED WORMS
Acanthocephala spp.

Species affected:
• Many fish families.
Gross signs:
• None, parasites are found in the alimentary system, attached to the
intestinal mucosa.
Cause:
• Parasites belonging to genus Acanthocephala.

Diagnosis:
• Examination of interior of intestine.
• Worms are elongated with retractile proboscis armed with varying
number of spines.
Morphology:
Life history:

• All acanthocephalans develop via an intermediate host.


• Eggs end up in water through faecal droppings, are swallowed
by a suitable arthropod host will hatch and larvae will encyst
as acanthella in host’s muscles or connective tissue.
• Intermediate hosts of Acanthocephala infecting fish are
Amphipoda, Isopoda or aquatic insects.
• Larval Acanthocephala when swallowed with their arthropod
host by fish, will excyst and will develop to adult stage.

• Some Acanthocephala undergo an additional larval stage in a


fish before reaching maturity. In this larval stage the acanthor
is encysted in fish’s visceral organs. Intermediate fish host is
usually different from definitive host species (predatory fish).
Pathology:
• Insertion of spiny proboscis into intestinal lining
destroys mucosal and connective tissue.
• Necrosis and tissue changes – ulceration, formation of
granuloma or encapsulation takes place.

Control:
• Bithionol.
HIRUDINEA spp.
Species affected:
• Cichlidae, Clariidae, Synodontidae, Bagridae, and Mormyridae.

Gross signs:
• Attach to skin or fins of fish.
• Recently abandoned sites are characterized by small, well defined
rounded, bleeding wounds.
Cause:
• Leeches of the families: Glossiphonidae (Genera:
Batrachobdella & Placobdella) and Piscicolidae (Genera:
Phyllobdella & Piscicola).

Placobdella sp.
Morphology:
• Leeches (Hirudinea) are annelids in which the anterior end
of the body is suctorial while the body terminates with a
posterior rounded attachment sucker.
• Body is divided into annuli.
Life history:
• Leeches attack fish for feeding.
• Eggs are laid in a cocoon attached to a substrate.
• Hatching offspring attach themselves inside the brood
pouch on the ventral body wall of the parent and are
carried this way by the leech until they reach a state of
development, which enables independent life and
feeding.
Pathology:
• Heavy infections with leeches cause anaemia.
• Also result in secondary bacterial contamination of the
ulcers resulting at the feeding site on the skin of fish.
• Epithelial hyperplasia and inflammatory changes – cellular
infiltration, hyper-anaemia and haemorrhages in dermal
and sub-dermal layers.

Control:
• Dipterex.
The End

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