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Fasciolosis in humans: routes of infection and development cycle
Last reviewed: 05.07.2025
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Fascioliasis (Latin: fasciolosis, English: fascioliasis) is a chronic zoonotic biohelminthiasis caused by parasitism of trematodes of the Fasciolidae family with predominant damage to the liver and biliary tract.
Human fascioliasis was first described by Malpighi (1698) and P.S. Pallas (1760).
Epidemiology
The main source of invasion for humans is sheep and cattle. Humans become infected by drinking water contaminated with adolescaria, eating vegetables and greens (usually watercress). Fascioliasis is common in almost all regions of the world, but is more widespread in Asia, Africa and South America. In Europe, the largest number of cases of fascioliasis is registered in Portugal and France. In some regions of Russia and in the CIS countries, sporadic cases are registered, and individual outbreaks sometimes occur in Central Asia and Transcaucasia.
F. hepatica parasitizes in the bile ducts of the liver of many herbivorous animals and occasionally in humans. One individual lays an average of 25,000 eggs per day. The main source of infection is infested herbivorous farm animals, mainly cattle. Humans do not play a major role in the epidemic process of fascioliasis, as they are only an accidental host of the parasite.
Fasciola eggs survive in water bodies and pastures for up to 2 years in winter. Parasite larvae in the body of mollusks can overwinter and emerge from them in early spring. Adolescaria at 100% relative humidity tolerate temperature fluctuations from -18 to +42 °C; at 25-30% relative humidity they die at 36 °C. Encysted adolescaria can survive in dry hay for several months, and remain viable in moist soil and water for up to 1 year.
A person becomes infected by eating wild plants (watercress, kok-saghyz, wild onion, sorrel) growing in stagnant or slowly flowing bodies of water, as well as in wet pastures where infested mollusks may live. One can also become infected by drinking water from bodies of water contaminated with adolescaria or by swimming in them, as well as by eating ordinary garden vegetables (lettuce, onion), which were watered with water from such sources. The peak of infection occurs in the summer months.
The development cycle of fascioliasis
Together with feces, eggs enter the external environment. Their further development occurs in water. At a temperature of 20-30 °C, miracidia develop in the eggs after two weeks. At lower temperatures, egg development slows down, at a temperature above 40 °C, miracidia die. In the dark, eggs develop faster, but miracidia do not emerge from them. The lifespan of miracidium in water is no more than 2-3 days. Having penetrated the internal organs of the gastropods Lymnea truncatula and other species of Lymnea, miracidia turn into sporocysts, in which rediae develop. In the redia, either the second generation of rediae or tailed cercariae are formed. They emerge from the mollusk 2-3 months after its infection and within the next 8 hours they encyst, attaching themselves to aquatic plants or to the surface film of water. The encysted larva of the liver fluke - adolescaria - enters the gastrointestinal tract of the definitive host when drinking water from reservoirs, eating vegetation from flood meadows, or using contaminated water for household needs (washing vegetables and fruits, watering beds, etc.). Having entered the intestines of the definitive host with food (semi-aquatic and aquatic plants) or with water, adolescaria are excysted, and the larvae penetrate the intestinal wall, migrate to the abdominal cavity, and then through the capsule and parenchyma of the liver - into the bile ducts. The second migration route is hematogenous, through the intestinal veins into the portal vein, and then into the bile ducts of the liver. From the moment adolescaria enter the body of the definitive host until the development of the mature stage, 3-4 months pass. The lifespan of fasciola in the human body is 5 years or more.
Moving through the liver tissue, fascioles damage capillaries, parenchyma, and bile ducts. Passages are formed that later turn into fibrous cords. Sometimes fascioles are carried by the bloodstream to other organs, most often to the lungs, where they encapsulate and die without reaching sexual maturity. In addition, young fascioles carry microflora from the intestines to the liver, causing the breakdown of stagnant bile, which causes intoxication of the body, the formation of microabscesses and micronecrosis.
Fascioliasis caused by Fasciola hepatica is common in most countries of the world. It is especially common in areas of Europe, the Middle East, South America, and Australia where livestock farming is developed. Sporadic cases are generally reported, but outbreaks affecting hundreds of people have been reported in France, Cuba, Iran, and Chile. Outbreaks of fascioliasis have been described in the Baltics, Uzbekistan, and Georgia. The largest known outbreak of fascioliasis occurred in Iran in 1989, when over 10,000 people fell ill, including about 4,000 children. In the last century, in Peru, the incidence of fascioliasis among schoolchildren in some villages reached 34%.
The most intense outbreaks associated with F. gigantica have been reported in Vietnam and other countries in Southeast Asia, the Hawaiian Islands, and some countries in tropical Africa.
Causes fasciolosis
Fascioliasis is caused by two types of trematodes. Fasciola hepatica (liver fluke) has a flat leaf-shaped body 20-30 mm long and 8-12 mm wide. Fasciola gigantea (giant fluke), 33-76 mm long and 5-12 mm wide, is found in Vietnam, the Hawaiian Islands and some African countries. Fasciola hepatica and Fasciola gigantea belong to the type Plathelminthes, class Trematoda, family Fasciolidae.
The internal organs of the fasciola have a branched structure. The prepharyngeal cavity and muscular pharynx together with the oral sucker form a powerful sucking apparatus. Two intestinal canals originate from the short esophagus, reaching the rear end of the body. A number of lateral branches depart from each of them, which in turn branch out.
The complexly branched testes are located in the middle part of the body, one behind the other; the vas deferens in front of the ventral sucker flow into the bursa of the cirrus, from which the arcuately curved cirrus emerges. A small branched ovary lies asymmetrically in front of the testes. The ducts of the vitelline glands, located on the sides of the body, join along the midline and form a yolk reservoir, next to which are the ootype and the gland of Mehlis. There is no seminal receptacle. A small looped uterus lies between the ducts of the vitelline glands and the ventral sucker. The eggs are large, 120-145 by 70-85 µm in size, oval, yellowish-brown in color, with a weakly expressed operculum.
They have large oval eggs measuring 0.125-0.150 x 0.062-0.081 mm. well-defined shell and lid. The eggs are yellowish-brown in color, they are released into the environment immature. The final hosts are ruminants (small and large cattle, pigs, horses, etc.), sometimes rats, and also humans. Helminths parasitize in the biliary system for 3-5 years or more. Eggs are released into the environment with feces, their further development is possible only in fresh water. Larvae (miracidia) released from the eggs penetrate the body of the intermediate host - a mollusk (small pond snail), from which, after 30-70 days, after long and complex transformations, tailed cercariae emerge. They shed their tails, encyst and transform into spherical adolescaria, which attach to the stems of underwater plants or to the surface film of water. The larvae enter the body of the final host with water or plants.
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Pathogens
Pathogenesis
Fasciola larvae migrate from the intestines to the liver in two ways - hematogenously and by means of their active penetration through the peritoneal cavity, the fibrous membrane (Glisson's capsule) of the liver. The main pathological changes occur during the migration of the larvae through the liver parenchyma, which lasts 4-6 weeks or more. Usually, sexually mature Fasciola individuals are localized in the bile ducts. Sometimes the larvae can migrate and mature in places that are not typical for them: in the pancreas, subcutaneous tissue, and brain. In the migration phase, toxic-allergic reactions are expressed due to sensitization of the body by larval antigens, as well as tissue damage along their movement. Helminths cause destructive changes in the liver, microabscesses, and subsequently - fibrous changes. Adults living in the bile ducts and gall bladder cause proliferative cholangitis with adenomatous changes in the epithelium, periductal fibrosis and fibrosis of the gall bladder wall. Obstruction of the bile ducts is possible, which creates conditions for secondary infection.
The waste products of parasites and the decay of liver tissue and bile, being absorbed into the blood, have a general toxic effect on the entire body. The functions of the gastrointestinal tract, cardiovascular, respiratory, central nervous and reticuloendothelial systems are disrupted; a sharp deficiency of vitamin A and other vitamins occurs; allergization of the body develops.
The dysfunction of the gastrointestinal tract and other organs is also facilitated by pathological reflexes that arise as a result of irritation of nerve endings by large flukes parasitizing in the bile ducts.
With prolonged fascioliasis, the lumen of the common bile duct often widens, its walls thicken. Adenomatous dilation of the bile ducts occurs, and purulent cholangitis develops.
Symptoms fasciolosis
The acute (migration) stage is similar to that of opisthorchiasis, but with fascioliasis, patients more often develop allergic myocarditis and have more pronounced signs of liver damage (acute antigenic hepatitis). Patients are bothered by non-specific symptoms of fascioliasis: weakness, malaise, headaches, decreased appetite. The temperature is subfebrile or high (up to 40 °C), the fever is laxative or wave-like. Urticaria, cough, pain in the epigastric region, in the right hypochondrium (usually paroxysmal), nausea, vomiting appear. In some patients, the liver size increases, especially its left lobe, which leads to bloating and pain in the epigastric region. Gradually (within a few weeks), these symptoms of fascioliasis significantly decrease or even disappear completely.
When examining blood in the acute stage of the disease, pronounced eosinophilic leukocytosis is revealed (leukocyte content up to 20-60 x 10 /l, eosinophils - up to 85%).
Three to six months after infection, symptoms of fascioliasis characteristic of the chronic stage of the disease appear, which are associated with organ damage to the liver and bile ducts. The liver size increases again. When palpated, its dense and painful lower edge is felt. Sometimes patients are bothered by severe paroxysmal pain in the right hypochondrium. Periods of relative well-being are replaced by periods of exacerbation, during which jaundice appears with relatively low ALT and AST levels and a significant increase in alkaline phosphatase. As liver dysfunction progresses, hypo- and dysproteinemia develops, transaminase activity increases. With a long course of the disease, bowel disorders, macrocytic anemia, hepatitis and nutritional disorders appear.
In the chronic stage, the number of leukocytes decreases and often normalizes, eosinophilia is usually 7-10%.
In case of secondary infection of the biliary system with bacterial flora, the number of leukocytes increases sharply, ESR increases. Indicators of the degree of destructive-necrotic and inflammatory changes in the liver are an increase in alkaline phosphatase, transaminases, as well as hypoproteinemia and hypoalbuminemia.
When parasitizing single fasciolae, symptoms of acute stage fascioliasis may be absent. In these cases, the disease may proceed in an inapparent form.
As a casuistry, there have been cases of liver flukes penetrating other organs, accompanied by dysfunction. When parasites are localized in the brain, severe headaches and epileptiform attacks are possible; when they enter the lungs, coughing and hemoptysis are possible; when they are in the larynx, sore throat and suffocation are possible; in the Eustachian tubes, ear pain and hearing loss are possible.
Complications and consequences
Diagnostics fasciolosis
Diagnosis of fascioliasis is based on the analysis of a combination of epidemiological history data and clinical symptoms:
- the presence of cases of fascioliasis in the given area;
- eating unwashed greens growing on waterlogged banks of bodies of water or in marshy areas that are not protected from faecal contamination;
- acute onset of the disease, fever combined with allergic reactions (Quincke's edema, urticaria), pain in the right hypochondrium or epigastric region, enlarged liver, leukocytosis, eosinophilia.
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Laboratory diagnostics of fascioliasis
Even in the acute stage of the disease, serological diagnostics of fascioliasis (RIGA, RIF, IFA) is informative; however, due to insufficient sensitivity and specificity, they cannot be used to establish a final diagnosis.
Three to four months after infection, the diagnosis can be confirmed by detecting helminth eggs in the duodenal contents or feces. Parasitological diagnosis of fascioliasis presents certain difficulties due to the fact that parasites do not lay eggs for a long time (3 to 4 months), and also due to the relatively small number of eggs excreted. Therefore, when examining feces, it is advisable to use enrichment methods.
After eating cattle liver infected with fasciola, transit eggs may be found in the feces. In these cases, it is necessary to conduct repeated parasitological studies 3-5 days after excluding liver and offal from the patient's diet.
In some cases, fasciola can be detected during an ultrasound examination of the liver, when helminths are found in the gallbladder and large bile ducts.
Differential diagnosis of fascioliasis
Differential diagnostics of fascioliasis is carried out with opisthorchiasis, clonorchiasis, viral hepatitis, leukemia and biliary tract diseases of other etiologies.
Differential diagnostics in the acute stage are carried out with trichinellosis, opisthorchiasis, clonorchiasis, viral hepatitis, eosinophilic leukemia; in the chronic stage - with cholecystitis, cholangitis, pancreatitis.
Indications for consultation with a surgeon are suspicion of the development of bacterial complications in the hepatobiliary system.
How to examine?
Who to contact?
Treatment fasciolosis
In the acute stage, a diet (table No. 5) and antihistamines are prescribed. After the symptoms subside, anthelmintic treatment of fascioliasis is used. The drug of choice according to WHO recommendations is triclabendazole, which is used in a daily dose of 10 mg / kg in one dose, in severe cases the drug is used in a dose of 20 mg / (kg x day) in two doses with an interval of 12 hours. Less effective is praziquantel in a daily dose of 75 mg / kg in three doses after meals during one day.
To free the bile ducts from dead parasites, choleretic drugs are used.
Anthelmintic treatment of fascioliasis is assessed by the disappearance of fasciola eggs in the duodenal contents in studies after 3 and 6 months.
Praziquantel is also used in the same doses as for opisthorchiasis. However, the effectiveness of praziquantel against F. hepatica does not exceed 30-40%, and against F. gigantica it is comparable to the effectiveness in the treatment of opisthorchiasis.
The effectiveness of treatment is monitored 3 and 6 months after the course of therapy by examining feces or duodenal contents.
The prognosis for timely detection and treatment of fascioliasis is favorable. With a long-term course of invasion, the development of purulent cholangitis and liver cirrhosis is possible.
Periods of incapacity for work
Determined individually.
Clinical examination
Not regulated.
Prevention
In areas where fascioliasis is endemic, it is recommended to drink only boiled or filtered water from stagnant bodies of water. Plants growing in damp places or garden greens that were watered with water from bodies of water contaminated with cattle feces should be boiled or scalded with boiling water before consumption.
It should be remembered that the cuisine of southeastern and southern countries with a large amount of fresh greenery, especially aquatic plants, poses a risk of infection with fascioliasis if hygiene rules for preparation are violated.
Fascioliasis can be prevented by following veterinary measures aimed at eliminating fascioliasis in farms: preventive deworming of livestock, changing pastures, feeding hay from meadows unfavorable for fascioliasis should be carried out no earlier than 6 months after harvesting, when the adolescaria have already died. The fight against mollusks (intermediate hosts of fascioliasis) is carried out by melioration of swampy areas of land. Chemical means of fighting mollusks (molluscicides) are also used. A mandatory component of the complex of preventive measures should be sanitary and educational work among the population living in areas endemic for fascioliasis.