Fasciola hepatica

Source: Wikipedia, the free encyclopedia.
This article is about the organism. For the infection, see Fasciolosis.

Fasciola hepatica
Adult Fasciola hepatica specimen
Scientific classification Edit this classification
Domain: Eukaryota
Kingdom: Animalia
Phylum: Platyhelminthes
Class: Trematoda
Order: Plagiorchiida
Family: Fasciolidae
Genus: Fasciola
Species:
F. hepatica
Binomial name
Fasciola hepatica

Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a

flukes are sister species; they share many morphological features and can mate with each other.[5]

Life cycle

Galba truncatula, an amphibious freshwater lymnaeid snail that serves as the main intermediate host of Fasciola hepatica in Europe
The lifecycle of Fasciola hepatica

Fasciola hepatica occurs in the liver of a

L. cubensis are most common intermediate hosts in Central and South America.[5][8][6] Several other lymnaeid snails may be naturally or experimentally infected with F. hepatica, but their role in transmission of the fluke is low.[5] The list of lymnaeid snails that may serve as natural or experimental intermediate hosts of F. hepatica include:[9]

The

metacercariae and the life cycle begins again.[10]

Morphology and anatomy

Fasciola hepatica is one of the largest

oral sucker is small but powerful and is located at the end of a cone-shape projection at the anterior end. The acetabulum is a larger sucker than the oral sucker and is located at the anterior end.[10]

A simple diagram to show the difference between the teguments of free-living and parasitic flatworms: a. shows the syncytial epithelial tegument found in parasitic flatworms, such as F. hepatica. b. shows the multicellular, nonsyncytial, epithelia, found in nonparasitic, free-living flatworms.

Tegument

The outer surface of the

Golgi bodies, and endoplasmic reticulum).[17] The tegument plays a key role in the fluke's infection of the host. Studies have shown that certain parts of the tegument (in this case, the antigen named Teg) can actually suppress the immune response of the mammalian host. This means that the fluke is able to weaken the immune response, and increase its chances of a successful infection. A successful infection is needed for the fluke to have enough time to develop into an adult and continue its lifecycle.[18]

Digestive system

Image showing the location of the mouth, labelled mo, and the anterior sucker, as labelled sckr

The alimentary canal of F. hepatica has a single mouth which leads into the

intestine of the host. The waste materials are egested through the mouth. The nonwaste matter is adsorbed back in through the tegument and the general surface of the fluke. The tegument facilitates this adsorption by containing many small folds to increase the surface area.[19]

Respiratory system

Diagram of the main organ systems of F. hepatica throughout the progressive life stages of the fluke (1938). A - egg; B - miracidium; C - sporocyst; D - rediae, E - immature cercaria, F - cercaria, G - encysted stage, H - adult fluke (nervous and reproductive systems omitted)

F. hepatica has no

fatty acids. This process provides the fluke with energy.[20]
In contrast, the free-living
aerobically, to gain the most energy from their environment.[21]

Excretory system

F. hepatica's

parenchyme cells. In F. hepatica, their role is to perform excretion, but more importantly, osmoregulatory functions. Flame cells are therefore primarily used to remove excess water.[20]

Nervous system and sensory organs

The nerve system of F. hepatica consists of a pair of

oesophagus. Around the oesophagus is a nerve ring, which connects the two nerve ganglia together. The nerves stem from this ring, reaching the posterior end of the body. At the posterior end, one pair of nerves becomes thicker than the others; these are known as the lateral nerve cords. From these lateral nerve cords, the other nerves branch. Sensory organs are absent from F. hepatica.[22][23]

Reproductive system

F. hepatica adult flukes are

muscles and spines.[22]

F. hepatica reproduces both sexually, via the

miracidia can reproduce asexually within the intermediate snail host.[24]

Genome

With its draft genome sequence published in 2015, F. hepatica is known to have the largest nuclear genome size among trematodes so far sequenced. It is about 1.3 Gb,[25] which is two times that of Opisthorchis viverrini with 634.5 Mb, the second largest genome among trematodes.[26] The genome is contained in 10 pairs of chromosomes. The protein-coding sequence covers about 21.8 Mb and repetitive DNA sequence about 32% of the total genome.[25] The number of genes predicted is 14,642.[27] The mitochondrial genome consists of 14462 bp, containing 12 protein-encoding, 2 ribosomal and 22 transfer RNA genes.[28]

Prevalence

Fasciola hepatica prevalence. The countries in red are those with high prevalence, those in orange have low-medium prevalence.[29][30][31]

Currently, F. hepatica has one of the widest geographical spread of any parasitic and vector-borne disease. Originating in Europe, it has expanded to colonize over 50 countries, covering all continents except Antarctica.[31] In contrast, F. gigantica is generally considered more geographically restricted to the tropical regions of Africa, Asia, and the Middle East, with some overlap between the two species.[29]

intermediate host, the snail. For example, the development of F. hepatica miracidia and larvae, and the reproduction of Galba truncatula, require a temperature range of 10 to 25 °C. In addition, they both require high levels of moisture in the air, as both are at risk of desiccation. Due to this, the prevalence, along with the intensity of infection, of F. hepatica is primarily dependent on rainfall levels and temperature.[31]

Parasitic adaptations

The left image shows the free-swimming cercariae, the swimming "tail" is clearly visible. The right side of the diagram shows the cysts attached to grass.

F. hepatica's

cercariae have a muscular tail to help them swim through the aquatic environment and also allow them to reach the plants on which they form a cyst.[30] To attach within the host, F. hepatica has oral suckers and body spines. Their pharynges also help them to suck onto the tissues within the body, particularly within the bile ducts.[32] The adult fluke's respiration is anaerobic; this is ideal, as no oxygen is available in the liver.[20] F. hepatica is adapted to produce a large number of eggs, which increases its chances of survival, as many eggs are destroyed on release into the environment. Also, F. hepatica is hermaphrodite, thus all flukes can produce eggs, increasing the number of offspring produced by the population.[22]

The genome for F. hepatica was published in 2015.[33] At 1.3 Gb, its genome is one of the largest known pathogen genomes. The genome contains many polymorphisms, and this represents the potential for the fluke to evolve and rapidly adapt to changes in the environment, such as host availability and drug or vaccine interventions.[25]

Epidemiology

For more information on the epidemiology – see the disease page, fasciolosis

Infection begins when cyst-covered aquatic vegetation is eaten or when water containing metacercariae is drunk. In the

ruminants, most commonly between March and December.[34]

Humans become infected by eating watercress or by drinking 'Emoliente', a Peruvian drink that uses drops of watercress juice. Cattle and sheep are infected when they consume the infectious stage of the parasite from low-lying, marshy pasture.[34]

Human infections have been reported from more than 75 countries around the world. In Asia and Africa, people are infected both by F. hepatica and F. gigantica whereas human fasciolosis is caused only by F. hepatica in South and Central America and Europe.[35]

The presence of F. hepatica can interfere with the detection of

bovine tuberculosis; this is, of course, a major problem in the farming industry.[37]

Fasciolosis

Main article: Fasciolosis
Slide showing Fasciola hepatica's internal organs

Both F. hepatica and F. gigantica can cause fasciolosis. Human symptoms vary depending on whether the disease is chronic or acute. During the acute phase, the immature worms begin penetrating the gut, causing symptoms of fever, nausea, swollen liver (caused by Fh8), skin rashes, and extreme abdominal pain.[38] The chronic phase occurs when the worms mature in the bile duct, and can cause symptoms of intermittent pain, jaundice, and anemia.[38] In cattle and sheep, classic signs of fasciolosis include persistent diarrhea, chronic weight loss, anemia, and reduced milk production.[39] Some remain asymptomatic. F. hepatica can cause sudden death in both sheep and cattle, due to internal hemorrhaging and liver damage.[4]

vegetables farmed from such land should be thoroughly washed and cooked before being eaten.[10]

The best way to prevent fasciolosis is by reducing the lymnaeid snail population or separating livestock from areas with these snails.[39] These two methods are not always the most practical, so control by treating the herd before they are potentially infected is commonly practiced.

Diagnosis

F. hepatica egg in stool sample.
Main article: Fasciolosis

A diagnosis may be made by finding yellow-brown eggs in the stool. They are indistinguishable from the eggs of Fascioloides magna, although the eggs of F. magna are very rarely passed in sheep, goats, or cattle. If a patient has eaten infected liver, and the eggs pass through the body and out via the faeces, a false positive result to the test can occur. Daily examination during a liver-free diet will unmask this false diagnosis.[45]

An enzyme-linked immunosorbent assay (ELISA) test is the diagnostic test of choice. ELISA is available commercially and can detect antihepatica antibodies in serum and milk; new tests intended for use on faecal samples are being developed.[46] Using ELISA is more specific than using a Western blot or Arc2 immunodiffusion.[34] Proteases secreted by F. hepatica have been used experimentally in immunizing antigens.[47]

See also

References

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External links

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