Life Cycle of Fasciola Hepatica | Microorganisms | Zoology

The life-cycle of Fasciola hepatica is completed in two hosts. The primary or definite host is sheep or cattle, while the secondary or intermediate host is a small of the genus Limnaea. Its life history includes a number of larval stages which propagate by asexual multiplication (polyembryony).

Copulation, Fertilization and Capsule Formation:

Copulation occurs in the bile duct of sheep. Copulation is mutual and cross-fertilization is the general rule. However, self-fertilization may also occur. During copulation the cirrus or penis of each worm is inserted into the vaginal opening of the other worm and sperms are ejaculated. It is also reported that the cirrus of a worm is inserted into the Laurer’s canal of other individual and sperms are ejaculated. The prostatic secretion enables the sperms to survive in the uterus. Sperms travel down the uterus.

Fertilized egg gets about 30 or so yolk cells and shell globules from vitelline glands by the way of various vitelline ducts. The shell is formed with a lid or operculum on one side. According to Rowen (1956-57), there is a viscous granular cushion at the opercular end of the egg, situated immediately beneath the operculum. The zygote and a mass of yolk-cells enveloped by the shell constitute the capsule. When complete the capsule passes into the uterus.

The eggs are fertilized in the uterus or in the ootype. The eggs become surrounded by the yolk cells produced by the vitelline glands in the ootype. The yolk cells contain yolk and many shell globules (male of proteins and a phenol). The shell globules are released from the yolk cells. They form a capsule or the shell around the egg. The secretion of Mehlis gland lubricates the eggs and makes them slippery. A single fluke may produce about 2,00,000 eggs in about 11 years and 30,000 to 35,000 eggs per year.

Capsulated Eggs:

The fully formed fertilized capsulated eggs are light brown, oval structures measuring about 130 x 150µ in size its capsule or shell is marked off into an operculum by a distinct line. Such eggs are called operculate. Situated immediately beneath the operculum is a granular cushion. At a later stage of development, the eggs are deposited in the bile ducts of the host and carried to the intestine along with the bile and are finally passed out with faeces.

Segmentation:

The division or the cleavage of the eggs starts while they are in the uterus. The first division is unequal as a result of which a small granular propagatory cell and a large somatic or ectodermal cells are formed. The somatic cell divides repeatedly to form the ectoderm of the larva.

The divisions of the propagatory cell result in the formation of germ cells and somatic cells. The somatic cells form the body organs. Further development of egg does not take place in the uterus. The eggs are then released in the bile ducts of the host from where they travel to the intestine and come out of the body of the host with its faces.

The eggs develop further if they are dropped in damp places. The development remains arrested while the embryos remain in the faeces. They may survive in wet faecal matter for several months. If washed free, the development of the embryo proceeds. The optimum temperature for development ranges from 10 –  30°C.

At 30°C the encapsulated embryo differentiates into miracidium larva within 8 days. The availability of oxygen is also a factor. The fully formed miracidium is a more or less conical little animal covered with ciliated epithelium. It does not look at all alike an adult fluke but does show resemblance to some free living flat worm.

Larval Stages:

1. Miracidium Larva:

It is the first larval stage in the life cycle of Fasciola hepatica. It swims actively in water in search of secondary host, the snail of genus, Limnaea. As the miracidium is formed, the hatching enzyme is secreted in response to exposure to light. The enzyme dissolves the cementing material by which the operculum is attached, thus releasing the operculum. Expansion of the granular cushion, accompanied by exosmosis of salts and other materials from within the egg pushes off the operculum. The hatching occurs in water and free swimming miracidium penetrates the intermediate host.

External Structure:

Miracidium of Fasciola is about 0.07mm long, oval or conical. It broad anterior end is produced into an apical lobe or apical papilla or terebratorium.

It bears opening of:

(i) Pouch-like multinucleate apical gland and

(ii) A number of unicellular penetration glands.

Except the apical lobe, the rest of the body is ciliated. It is covered with 21 closely fitted hexagonal epidermal plates, arranged in five rows. The first row consists of six plates (2 dorsal, 2 ventral and 2 lateral), the second row of 6 cells (3 dorsal and 3 ventral), the third row or 3 cells (1 dorsal, 2 ventrolateral), the fourth row of 4 cells (2 right and 2 left) and the fifth row of 2 cells (1 right and 1 left) only.

Internal Structure:

Below the epidermal plates is a thin layer of sub-epidermal musculature consisting of:

(i) An outer layer of circular and

(ii) Inner layer of longitudinal muscles.

Underneath is present a sub-epithelial layer. The interior of larva has a pair of protonephridia and groups of germ cells. In addition, there is a pair of large pigmented eyespots, a large larval brain and a simple nervous system in the anterior part of body. There is a large apical gland and a pair of penetration glands or cephalic glands in the anterior part of body. These open on the apical lobe or cephalic cone.

Infection to Secondary Host:

Miracidium does not feed. It dies within a maximum of 24 hours if it fails to reach its secondary host, which is usually Limnaea truncatula (very common in freshwater bodies and damp places). If it finds the snail, it penetrates through the soft skin and respiratory tissues of the snail.

The penetration is helped by the apical lobe and tissue dissolving (or histolytic) action of secretion of penetration glands. The snail may even swallow the miracidium or the capsule containing the miracidium. Inside the host tissue the larva discards its ciliated epidermis and penetrates deeper and finally the lymph vessels or pulmonary chamber of the host. Here it grows to form a sac-like body, the sporocyst.

2. Sporocyst Larva:

Miracidium loses its apical gland, penetration grand, brain and eyespots and changes into a sac­like sporocyst larva. It looks like an elongated sac about 0.7 mm long. Its body wall retains all the layers of miracidium’s body wall except the ciliated epithelium. It consists of a thin cuticle, a layer of circular and longitudinal muscles.

The wide interior is occupied by the protonephridia and germ cells. Each protonephridium now consists of two flame cells. These open on the surface by a common pore. A rudimentary gut is also found. The germ cells undergo repeated divisions to produce radia larvae, but rarely may also produce daughter sporocysts. A single sporocyst may contain 5-18 radia. The radia larvae migrate to the digestive gland of snail.

3. Redia Larva:

Redia is an elongated larva with a small mouth, a suctorial pharynx and a simple closed intestine in the anterior part of the body. Many unicellular pharyngeal glands open into the pharynx. These are a muscular, ring-like ridge, the collar, around the anterior region of the body. It helps in locomotion. Just behind the collar is a birth pore through which next generation of larvae come out.

In the posterior region there is a pair of lobe-like processes, the lappets or procruscla. These are used an anchor. The larval excretory system consists of anterior and posterior flame cells which open to outside through a single nephridiopore on each side. The body spaces remain filled up with parenchyma. Redia also contains groups of germ cells.

Protonephridia divide further and form a much branched system. All the flame cells of one side open out through a common excretory duct. A birth pores in present lateral to and in proximity of the mouth. Within the brood chamber are found germ balls. Redia is very active little creature. It moves about by the contractions of the body and lappets. It nourishes itself by sucking fluid and cells of the host tissues with its muscular pharynx.

It soon migrates into the digestive glands of the snail. During summer months when the food is sufficiently available, mother radiae mature in 12-18 days. The germ balls give rise to a second generation of daughter rediae. Germ balls of daughter rediae in the winter develop into next larval stage, the cercariae.

4. Cercaria Larva:

The body of a fully developed cercaria larva is oval like that of a tadpole and has a long elastic tail extending from its posterior end. The body is covered over by a thin layer of cuticle in which many backwardly directed spines are present. A mouth, a muscular pharynx, a small oesophagus and a bifid intestine are present in the anterior region of the body.

An oral sucker is present surrounding the mouth and a ventral sucker is found between the arms of the intestine. Many germ cells, flame cells and excretory ducts are found in the internal cavity. All the excretory ducts open into the excretory bladders which open to the outside through a small excretory duct.

From the digestive glands of the snail, the cercaria passes into the pulmonary sac and then escape into the surrounding water. Cercaris swims about five minutes to an hour in summer. Afterwards, it settles down on some green leaves of water plants.

The excretory pore is situated at the base of tail. Many unicellular cystogenous glands are present below the body wall. The substance secreted by these glands form a cyst around the larva after which the cercaria changes into a metacercaria larva. The cercariae, coming out with the current of water, swim for some time and then attack themselves to the leaves of some aquatic plant. Their tails disintegrate and cysts are formed around them by the secretions of the cystogenous glands. Now the larva is known as metacercaria.

5. Metacercaria:

The metacercaria is somewhat rounded with thick outer covering of cuticle in the form of cyst. The cystogenous cells of the cercaria disappear and the flame cells increase in number.

Infection to the Final Host:

The metacercaria enters the final or definitive host, the sheep, when it grazes on the aquatic weeds and reaches the intestine. In the intestine the cyst is dissolved by the action of digestive enzymes and young fluke comes out. It reaches the liver through the hepatic portal system and starts its existence inside the bile passage.

Nature of Life History:

Due to the presence of several larval stages, the life history of Fasciola hepatica is very much complicated. Previously it was assumed that the radiae and cercariae develop by parthenogenesis from the propagatory or germ cells, which were believed to be the eggs such type of asexual parthenogenetic reproduction by larval forms is known as heterogamy.

This view was widely accepted for some time and under its way, three terms were coined. These are parthenitae for sparocyst and radiae larvae, adolescariae for cercaria larvae, and maritae for adult flukes. This view, however, is now considered erroneous and has been given up. Later on it was suggested that the germ cells present in the larval forms are not eggs. Instead they are diploid cells derived by the mitotic divisions of propagatory cell which is separated from the zygote at its first cleavage.

Thus it may be stated that they are parts of zygote. It thus follows that one zygote produces several larval. Thus this process of reproduction in sporocysts and radiae has been looked upon as polyembryony by Ishii (1934), Chen (1937), Rees (1940) and Cart (1944). Since all the larvae resulting from a zygote are not formed simultaneously but at intervals, the phenomenon should be called delayed polyembryony.

Pathogenesis or Effect on the Host:

Fasciola hepatica chiefly affects the liver but it also causes other diseases during sojourn from intestine of host. They cause hepatitis and inflammation in the bile ducts, with the result that bile ducts become thickened and their epithelium destroyed. Eventually the bile ducts are calcified, resulting in the formation of gall stones.

In heavy infections they cause haemorrhage when wandering in the substance of liver and in other tissues. The bye products produced by the worms are very toxic and cause anaemia, diarrhea, eosinophilia, etc. Worms also contain proteolytic, glycolytic and fat-splitting enzymes and the degenerating dead worm is very harmful.

F. hepatic causes liver rot or fascioliasis due to irritation inflicted by its cuticular spines and by upsetting the normal functions of the liver. The acute liver rot is a common disease in sheep. Its symptoms, more acute in lambs than in sheep, appear about a month after infection. Sheep becomes dull, sluggish, accompanied by swelling and pain in abdomen, weight is lost, eye-sockets become pale, liver is enlarged and finally the animal dies.

The other type of liver rot is chronic liver rot. It is caused by slow and successive entry of cercariae in sheep or cattle. The host becomes weak. Loss of blood and toxins secreted by the worms causes anaemia. Milk production and breeding are substantially reduced. At times there is fever and increase in respiratory activity. Dry and brittle wool falls off. Watery swellings occur in the jaws (bottle jaw), appetite declines, rumination become irregular and animal dies in a few months.