Fasciola hepatica

Phylum : Plalyhelminthes.
Class : Trematoda
Fasciola hepatica is commonly known as liverfluke.It is a parasitic trematode seen in
sheep,cattle and other mammals.It resides in the bile duct of sheep.
It is a digenetic parasite .The defenite host is sheep and intermediate host is a gastropod
namely Lymnae sp.
The body is soft, leaf-like, bilaterally symmetrical and dorso-ventrally flattend.
The size varies from 1.0 mm to 2.5 cm in length.
The anterior end of the body has a conical projection called the head lobe.
At the tip of the head lobe is the mouth surrounded by the oral or anterior sucker . On the
ventral surface behind the head lobe is the posterior or ventral sucker (acetabulum). It is
bigger in size than the anterior sucker. Between the two suckers and close to the posterior
sucker is the genital porehe excretory opening is situated at the posterior tip of the body.
Their body is covered by a tegument, a peculiar kind of epidermal arrangement. The
tegument consists of an outer syncytial layer and an inner layer where the main cell bodies
are found. The tegument serves the functions of protection, excretion and gaseous exchange.
Beneath the the tegument there are circular, longitudinal and oblique muscles
The digestive system consists of the mouth, a pharynx and a bifurcated intestine, which is
highly branched.
The excretory system consists of longitudinal excretory canals and the associated flame
cells.Fasciola reproduces sexually .
The adults are hermaphrodites, but cross fertilization is the rule. The fertilized eggs leave the
vertebrate host through faeces and urine. Each egg hatches out as free swimming, ciliated
larva called miracidium . This larva happens to penetrate the body wall of an aquatic snail
that comes in contact with it. Once inside the snail, the miracidium metamorphoses into a sac
like sporocyst without any gut. The sporocyst contains several embryos. Each embryo
develops into another sporocyst or into a redia (after the Italian Scientist, Redi), which has a
mouth and a gut. Within the redia are several embryos, which develop into cercaria. The
cercaria has a gut, suckers and a tail. The cercaria leaves the snail host and attach itself to
green leaves. it becomes encysted to form a metacercaria. When a sheep feeds on such
infested green leaves, metacercaria enters the gut. The metacercaria now escapes from the
cyst (excysts), migrates to the bile duct and grows into the adult.
Since the life cycle includes two hosts and at least two infective stages, Fasciola is usually
termed as a digenetic trematode (belonging to the subclass Digenea).
Polyembryony
During the transition from miracidium to sporocyst, polyembryony occurs. The embryo
repeatedly divides and gives rise to numerous sporocysts of similar kind.
Polyembryony is an adaptation of parasitic mode of life. This ensures prolific breeding and
maintenance of sufficient number of the parasite through the different stages of parasitic life.

Pathogenicity
The disease caused by the infection of Fasciola hepatica is known as fascioliasis.
lt mainly affects the liver but it also causes inflammation of the bile duct causing loss of its
epithelium.
The bile duct soon becomes calcified and gall stones are formed in it.
Heavy infections cause haemorrhage. The young flukes undertake a migration through the
liver tissue, during which the liver is extensively damaged.
The liver function is seriously affected and the sheep is said to have the disease "liver rot".
The affected sheep becomes dull and sluggish. This is followed by swelling and pain in
abdomen, weight loss, inflammation of liver and finally death ofthe sheep.
Prevention

Avoid grazing of sheep on the banks of ponds and streams, especially during drought
season when the cercariae emerge from the snails.
Sacrificing heavily infected sheep and destroying the parasites will help a lot in
preventing the transmission of the parasite.
Destruction of the intermediate host (snail) by appropriate means, is also an effective
control measure. Snails can be killed by the application of copper sulphate in ponds and
ditches.
Allowing ducks to forage on the paddy fields and ponds can help in checking the
population of snails.
Proper washing of green vegetables and appropriate cooking will eliminate the chances
of transmission of the parasite to man
Fasciola hepatica can be eliminated from the final hosts by the use of anthelmintics
such as carbon tetrachloride, emetine hydrochloride tetrachlorethane and
hexachloroethane.

ECHINOCOCCUS GRANULOSUS
Phylum : Plalyhelminthes.
Class : Cestoda

Echinococcus, popularly known as the dog tapeworm or the hydalid worm.

It is an intestinal endoparasite in feline and canine carnivores such as cats, dogs,
foxes, jackals, wolves.etc.
Its intermediate hosts include a variety of mammals such as sheep, goat, cattle, deer,
horse, camel, rabbit. etc.
Man is only an incidental host,which harbours only the larvae, and never the adults.
Echinococcus enjoys wide distribution in Africa. Australia, S. America. New Zealand.
Holland and Iceland.
Echinococcus is the smallest of all tapeworms.
lts body is usually 3 - 6 mm long and is differentiated into three regions, scolex. neck
and strobila.
Scolex is globular and hears four ovoidal suckers and a protrusible and cone-shaped
rostellum. Rostellum armed with a double crown of hooklets.
Neck is a thick and narrow region. Strobila is composed of 3 proglottides, namely an
immature proglottid, a mature proglottidcs and a ripe or gravid proglottides.

Immature proglottid does not contain mature genital organs.

Mature proglottid is the sexually mature segment with functional male and female
gonads.
Gravid proglottid is the largest segment with degenerated sex organs and an egg-filled
uterus. It stores 500 - 800 eggs.
The egg of Echinococcus is ovoid and heavy and it contains an onchosphere.
Onchosphere in turn, consists of a six hooked hexacanth embryo, which is enclosed and
protected by an embryophore.

Life cycle
1. It is a digenetic parasite Its life cycle is completed in two hosts namely the definitive
host(cats, dogs, foxes, jackals, wolves.etc. ) and the intermediate host(goat,cattle,
deer, horse,camel, rabbit. etc.). Mating and fertilization takes place in the intestine of
the definitive host.
2. Fertilized eggs are stored in the uterus. Development starts even when the eggs are in
the uterus and a six-hooked hexacanth embryo is formed in each fertilized egg. This
embryo is enclosed by a protective shell and an embryophore. The embrvo and its shell
and embryophore together form the onchosphere. Then, the uterus disinte-grates and
the gravid proglottid detaches itself from the strobila. These embryonated eggs pass to
the outside along with the faeces of the host.
3. They may be ingested by the intermediate host while it is grazing in the field. Man gets
the infection while fondling infected pet dogs.
4. ln the duodenum of man or the intermediate host, shell and embryophore get dissolved
and the hexacanth embryo is set free.
5. Within eight hours, the hexacanth bores through the intestinal wall. enters the blood
stream, and gets lodged in liver or lungs, or sometimes in kidneys, spleen, heart. brain,
bone, muscles. etc.
6. In about ten days after this localization. the hexacanth embryo develops to a bladderlike and fluid-filled larva, known as hydatid cyst.
7. The wall of a fully formed cyst has three concentric layers. namely outer pericyst,
middle ectocyst and inner endocyst. Pericyst is secreted by the host, while the others
are embryonic structures. Pericyst is a fibrous layer,ectocyst is a hyaline and opaque
cuticular layer, and endocyst is a syncytial germinal layer. The cystic cavity or hydatid
is filled with a watery fluid, called hydatid fluid.
8. From the germinal epithelium of the cyst several endogenous buds grow inward. They
enlarge and form vesicular bodies, known as brood capsules . They either detach from
the parent cyst and drop to the cystic fluid or remain attached to the endocyst by a
stalk or pedicel.
9. Each capsule, in turn, may undergo budding and produce daughter capsules. Apart
from the brood capsules, blind exogenous daughter cysts may also be budded off from
the cyst wall.
10.In a fully formed hydatidcyst, the germinal layer of some of the daughter capsules buds
off several protoscolices (singular - protoscolex), provided with suckers and hooks.
11.The daughter capsules, capable of producing protoscolices, are called fertile capsules
or cephalocysts and those which do not produce protoscolices are called sterile
capsules or acephalocysts.
12.Each protoscolex is attached to the capsule wall by a stalk and it swings freely inside
the capsule. Later it develops to a typical adult scolex, which in turn can develop to an
adult Echinococcus in the definitive host. Transmission of fertile cysts from the
intermediate host to the definitive host occurs when the latter feeds on the hydatid
infested flesh of the former.
Pathogenicity in man

The pathogenic effect associated with the infection by Echinococcus, is known as hydatid
disease (echinococcosis ). Man gets the infection by the ingestion of the embryonated eggs
present in the faeces of infected dogs or on contaminated vegetables. Since the embryonic
and larval growth of Echinococcus is very slow, clinical manifestations of the infection occur
much later. In the human intestine, the hexacanth embryo is set free. It bores through the
intestinal wall, enters the blood stream gets localised in certain parts and develops to a
hydatid cyst. The major sites of such localisation are liver (70%). lungs (10-20%), brain (nearly
5%), kidneys (2%), bone (1%), etc. Localisation in vital organs, such as liver. lungs. heart.
brain and kidneys, shows early clinical manifestations and lead to death. Localizations in other
regions remains quiescent or latent (symptomless) for several years until they attain huge
dimensions and produce pressure effects with the result that the cyst ruptures or suppurates.
Rupturing of the cyst causes the leakage of the cystic fluid and the initiation of localized or
generalized secondary ehinococcosis. Slow leakage may evoke mild and quickly disappearing
toxic and anaphylatic reactions (. On the other hand heavy leakage may cause severely
harmful reactions. Localization of cysts in bone (osseous hydatosis) often leads to the
pathological fracture of bones.
Prophylaxis
There is no specific drug for the treatment of echinococcosis. Preventive measures measures
include
(i) Avoidance of contact and caressing of dogs
(ii) Cleaning of hands before eating
(iii) Sufficient boiling of vegetables during cooking
(iv) Avoidance of feeding dogs with raw or improperly cooked flesh
(v) Administration of anti-helminthic drugs in dogs.
PARASITIC ADAPTATION OF FLATWORMS
Adaptation
Adaptation is the fitness of an organism to its environment. It is the characteristic which
results in suitable and convenient morphological and functional correlation between an
organism and its environment.
Parasitic adaptations
The parasitic flatworms, the trematodes and cestodes, have undergone profound adaptations
to suit their parasitic mode of life. These adaptations, termed parasitic adaptations in such
cases, arc of morphological as well as physiological nature.
A. Morphological adaptations
1. Body covering: The thick tegument, frequently provided with scales, affords suitable
protection to the parasite. It is probable that this thick protoplasmic layer is continually
renewed by the cells forming it.
2. Organs of adhesion: For a firm grip on or in the hosts body, some special organs of
adhesion are necessary. The flatworm, for this purpose, are variously armed with suckers,
hooks and spines. The suckers themselves may be with or without hooks and spines.

3. Organs of locomotion: Locomotion is actually an effort for procuring food. But parasites
habitually inhabit such places in the hosts body, where sufficient food is available without
effort. Thus, the organs of locomotion, such as the cilia of free-living turbellarians, are absent
in the parasitic forms. It is interesting to note that the locomotory organs are duly present in
free-living larvae of parasitic forms; the miracidium possesses cilia and the cercaria possesses
a tail for locomotion.
4. Organs of nutrition: Food of the parasite comprises the readily available digested and
semi-digested food of the host. Elaborate organs for nutrition are thus not needed.
Trematodes have an incomplete gut and, in most cases, a suctorial pharynx for sucking food.
An eversible pharynx present in free-living turbellarians is absent in this case, asthe parasite
has not to capture a large prey. In cestodes, the parasite freely bathes in the digested food of
the host which is absorbed directly. There is thus total absence of alimentation in tapeworms.
5. Neurosensory system: Need for quick and efficient response to stimuli is associated
with free active life and not with a quiet parasitic life in a safe environment. In parasites,
therefore, there is profound reduction of nervous system and total absence of sense organs.
Accordingly, the free-living miracidium possesses eye spots.
6. Reproductive system: It is the best developed system in helminth parasites, designed
and perfected to meet the need for tremendous egg production. The parasitic flatworms, with
a few exceptions like Schistosoma, are monoecious (hermaphrodite). Hermaphroditism is of
distinct advantage to the parasite, because (i) it ensures copulation even when a few
individuals are present (ii) after copulation both the individuals lay eggs, thus doubling the
rate of reproduction, and (iii) in the absence of a companion, the parasite can reproduce
offspring. In cestodes, the reproductive system is much more elaborate; each mature
proglottid possesses or two complete sets of male and female genitalia. In a gravid proglottid
all other organs of the system degenerate to make room for the uterus which becomes highly
enlarged and branched to accommodate a large number of eggs.
B. Physiological adaptations
1. Protective mechanism: The alimentary canal parasites have to protect themselves from
the action of digestive juices of the host. The tapeworms accomplish this (a) by stimulating
the walls of the gut to secrete mucus, which then forms a protective clothing around the
parasite, (b) by secreting anti- enzymes to neutralize the digestive enzymes of the host, and
(c) by probably continually renewing their protective body covering i.e., the tegument.
2. Anaerobic respiration: Environment in the gut and bile ducts is devoid of free oxygen.
The flatworms inhabiting these places, therefore, respire anaerobically by breaking down
glycogen.
3. Osmoregulation: The osmotic pressure of the endoparasites body fluids, especially in
case of trematodes, is almost the same as that of the host. This renders osmoregulation
unnecessary. But in the intestinal tapeworm the osmotic pressure is a little higher. This
permits ready absorption of hosts digested food by the parasite.
4. High fertility: Eggs produced by a parasitic flatworm face a very uncertain future. While
passing through the complex life cycle, these potential off springs face several hazards as a
result of which a very small percentage of the total eggs produced reaches adulthood. This
threat to the very existence of the species is suitably met by the parasite which in its life time
may produce eggs in millions. The reproductive organs of the flatworms, as already noted, are
accordingly developed. Additional multiplicative phases in the life-cycle of some flatworms
further increase the output of potential offspring. Several cercariae develop from a single

miracidium of liver fluke and a single hexacanth of Echinococcus produces several scolices,
each of which is a potential tapeworm.