Fascioliasis in humans: the pathways of infection and the cycle of development

Fascioliasis (chronic fasciolosis, English fascioliasis) is a chronic zoonotic biogelmintosis caused by parasitization of trematodes of the Fasciolidae family with a predominant lesion of the liver and bile ducts.

For the first time the fascioliasis of a person is described by Malpighi (Malpighi, 1698) and P.S. Pallas (1760).

[1], [2], [3], [4], [5],

Epidemiology

The main source of infestation for humans is sheep and cattle. A person becomes infected when drinking contaminated adolescaria water, eating vegetables and greens (usually watercress salad). Fasciolosis is widespread in almost all regions of the world, but more widely in countries of Asia, Africa and South America. In Europe, the largest number of cases of fascioliasis have been reported in Portugal and France. In some regions of Russia and in the CIS countries sporadic cases are recorded, occasional outbreaks sometimes occur in Central Asia and Transcaucasia.

F. Hepatica parasitizes the bile ducts of the liver of many herbivores and occasionally in humans. In a day, one individual lays an average of 25 thousand eggs. The main source of infection is invasive herbivorous agricultural animals, mainly cattle. Man plays a big role in the epidemic process of fascioliasis, since he is only an occasional host of the parasite.

Fasciola eggs in winter in reservoirs and pastures persist up to 2 years. The larvae of parasites in the body of the mollusks can overwinter and emerge from them in the early spring. Adolescaria at 100% relative humidity tolerate temperature fluctuations in the range from -18 to +42 ° C; in conditions of relative humidity of 25-30% they die at 36 ° C. In dry hay, the incrusted adolescaria can survive for several months, while in wet soil and water they remain viable up to 1 year.

A person becomes infected when eating wild plants (watercress watercress, kok-sagyz, wild onion, sorrel) growing in standing or slowly flowing water bodies, as well as in wet pastures where invasive mollusks can live. You can catch and when you drink water from contaminated by adolescaria water reservoirs or swimming in them, as well as when eating ordinary vegetable vegetables (salad, onions) for watering which used water from such sources. The peak of infection occurs in the summer months.

The cycle of development 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 eggs in two weeks. At lower temperatures the development of eggs slows down, at a temperature above 40 ° C miracidia perish. In the dark, eggs develop faster, but miracidia do not come out of them. Life expectancy of miracidia in water is no more than 2-3 days. Having penetrated the internal organs of gastropods Lymnea truncatula and other species of Lymnea, miracidia are transformed into sporocysts, in which redias develop. In the redias, either the second generation of redids or the caudate cercariae are formed. They leave the mollusk 2-3 months after infection and within the next 8 hours are encysted, attached to aquatic plants or to a surface water film. The injected larva of the hepatic fluke - adolescaria - enters the gastrointestinal tract of the final host by drinking water from water bodies, eating vegetation from flood meadows, or using contaminated water for domestic purposes (washing fruits and vegetables, watering beds, etc.). Once in the intestine of the final host with food (water and water plants) or with water, the adolescaria is excised, and the larvae penetrate the intestinal wall, migrate into the abdominal cavity, and then through the capsule and the parenchyma of the liver into the bile ducts. The second way of migration is hematogenous, through the intestinal veins into the portal vein, and then into the bile ducts of the liver. From the moment adolescariae enters the organism of the definitive host before the development of the sexually mature stage, 3-4 months pass. The life span of fasciolae in the human body is 5 years or more.

Moving along the hepatic tissue, fasciolae damage capillaries, parenchyma, bile ducts. Shapes are formed, which later turn into fibrous cords. Sometimes fasciolae flow by current of blood into other organs, most often into the lungs, where they are encapsulated and perish, not reaching puberty. In addition, young fasciolae bring from the intestine into the liver a microflora that causes the decay of stagnant bile, which causes an intoxication of the body, the formation of microabscesses and micro-necrosis.

Fasciola, caused by Fasciola hepatica, is common in most countries of the world. Especially often it occurs in those regions of Europe, Middle East, South America and Australia, where livestock is developed. Most sporadic cases are recorded, but outbreaks in hundreds of people have been reported in France, Cuba, Iran and Chile. Outbreaks of fascioliasis in the Baltic States, Uzbekistan and Georgia are described. The largest known outbreak of fascioliasis occurred in Iran in 1989, when more than 10,000 people became ill, including about 4,000 children. In the last century in Peru, the schoolchildren's incidence in some villages reached 34%.

The most intensive foci associated with F. Gigantica are noted in Vietnam and in other countries of Southeast Asia, the Hawaiian Islands and in some countries of tropical Africa.

[6], [7], [8], [9], [10], [11],

Causes of the fasciola

Fasciolosis is caused by two kinds of trematodes. Fasciola hepatica (liver fluke) has a flat leaf-shaped body 20-30 mm long, 8-12 mm wide. Fasciola gigantea (giant fluke), 33-76 mm long, 5-12 mm wide, occurs in Vietnam, the Hawaiian Islands and in some African countries. Fasciola hepatica and Fasciola gigantea are of the Plathelminthes type, the Trematoda class, the Fasciolidae family.

The internal organs of the fasciolae are branched. The pre-vestibular cavity and muscular pharynx together with the oral sucker form a powerful sucking apparatus. From the short esophagus originate two intestinal canals, reaching the posterior end of the body. Each of them leaves a series of lateral branches, which in turn branch.

Complexly branched testicles are located in the middle part of the body, one behind the other; the vas deferens in front of the abdominal sucker flow into the cirrus bursa, from which the curved cirrus arises. A small branchy ovary lies asymmetrically in front of the testes. The protrusions of the vitellaria, located along the sides of the body, are connected along the middle line and form a yolk reservoir, next to which are the ootype and Melis gland. The spermatheca is not present. A small looped uterus lies between the ducts of the vitellaria and the abdominal sucker. Eggs are large, 120-145 by 70-85 microns in size, oval, yellowish-brown in color, with a weakly expressed lid.

They have large oval eggs measuring 0.125-0.150 x 0.062-0.081 mm. Well-defined shell and cap. The color of the eggs is yellowish-brown, they are unripe to the external environment. The final owners are ruminants (small and large cattle, pigs, horses, etc.), sometimes rats, and also humans. Helminths parasitize in the bile excretory system for 3-5 years or more. In the environment eggs are excreted with feces, their further development is possible only in fresh water. The larvae (miracidia) that have emerged from the eggs penetrate into the body of the intermediate host, the mollusk (small pond snake), from which, after 30-70 days after long and complex transformations, the tailed cercariae exit. They dump the tail, are encysted and turn into a globular adolescaria that attach to the stems of underwater plants or to the surface water film. The larvae enter the organism of the final host with water or plants.

[12], [13], [14], [15], [16], [17], [18], [19],

Pathogenesis

Migration of fasciola larvae from the intestine to the liver takes place in two ways - hematogenically and through their active insertion through the peritoneal cavity, fibrous membrane (glisson capsule) of the liver. The main pathological changes occur during the migration of larvae through the parenchyma of the liver, lasting 4-6 weeks or more. Usually, sexually mature individuals of fasciolae are localized in the bile ducts. Sometimes larvae can migrate and ripen in places that are not peculiar to them: in the pancreas, subcutaneous tissue, brain. In the migratory phase, toxic-allergic reactions are expressed due to the sensitization of the organism by the antigens of the larvae, as well as damage to tissues during their progress. Helminths cause destructive changes in the liver, microabscesses, followed by fibrotic changes. Adult individuals that live in the bile duct and gall bladder cause proliferative cholangitis with adenomatous epithelial changes, periductal fibrosis and gallbladder wall fibrosis. Possible obstruction of the bile ducts, which creates conditions for secondary infection.

The products of the vital activity of parasites and the decay of the hepatic tissue and bile, absorbed into the blood, have a general toxic effect on the whole organism. Violated the functions of the gastrointestinal tract, cardiovascular, respiratory, central nervous and reticulo-endothelial systems; there is a sharp deficit of vitamin A and other vitamins; allergic organism develops.

Violation of the functions of the gastrointestinal tract and other organs is also facilitated by pathological reflexes that arise as a result of irritation of the nerve endings by large parasitic bile ducts in the bile ducts.

With a prolonged course of fascioliasis, the lumen of the common bile duct often widens, its walls thicken. There is an adenomatous dilatation of the bile ducts, purulent cholangitis develops.

[20], [21], [22]

Symptoms of the fasciola

The acute (migratory) stage is similar to that in opisthorchiasis, but in patients with fascioliasis, allergic myocarditis develops more often and signs of liver damage (acute antigenic hepatitis) are more pronounced. Patients are concerned about the nonspecific symptoms of fascioliasis: weakness, malaise, headaches appear, and appetite decreases. The temperature is low-grade or high (up to 40 ° C), the fever is laxative or undulating. Appear hives, cough, pain in the epigastric region, in the right upper quadrant (often paroxysmal), nausea, vomiting. In some patients, the size of the liver increases, especially its left share, which leads to the appearance of swelling and pain in the epigastric region. Gradually (within a few weeks) these symptoms of fascioliasis are significantly reduced or even completely disappear.

In the study of blood in the acute stage of the development of the disease, pronounced eosinophilic leukocytosis (leukocyte count to 20-60 x 10 / L, eosinophils - up to 85%) is revealed.

In 3-6 months after infection, there are symptoms of fascioliasis, characteristic of the chronic stage of the disease, which are associated with organ damage to the liver and bile ducts. The dimensions of the liver increase again. When palpation, a dense and painful lower edge is probed. Sometimes patients are concerned about severe paroxysmal pain in the right hypochondrium. Periods of relative well-being are followed by periods of exacerbation, during which jaundice occurs with relatively low rates of AlAT and ASAT and a significant increase in alkaline phosphatase. As liver function disorders progress, hypo- and disproteinemia develop, transaminase activity increases. In the long course of the disease, there are disorders of stool, macrocytic anemia, hepatitis and malnutrition.

In the chronic stage, the number of leukocytes decreases and is often normalized, eosinophilia is usually 7-10%.

In the case of secondary infection of the biliary system with bacterial flora, the number of leukocytes increases sharply, the ESR increases. Indicators of the degree of destructive necrotic and inflammatory changes in the liver are an increase in alkaline phosphatase, transaminase, as well as hypoproteinemia and hypoalbuminemia.

When parasitizing single fasciolia, the symptoms of acute-stage fascioliasis may be absent. In these cases, the disease can occur in an inpatient form.

As casuistry, there were cases of penetration of hepatic fluke into other organs, accompanied by a violation of their function. With the localization of parasites in the brain, severe headache, epileptiform seizures are possible; when getting into the lungs - coughing, hemoptysis; when in the larynx - a sore throat, suffocation; in Eustachian tubes - pain in the ears, hearing loss.

[23], [24]

Complications and consequences

Fasciolosis can have the following complications: purulent angiocholangitis, liver abscesses, sclerosing cholangitis, obstructive jaundice. The forecast is favorable. Very rarely (up to 0.06% of cases) cirrhosis develops.

[25], [26], [27], [28], [29], [30]

Diagnostics of the fasciola

The diagnosis of fascioliasis is based on the analysis of the totality of the epidemiological history and clinical symptoms:

• the presence of fascioliasis in this area;
• the consumption of unwashed greens, growing on unprotected fecal contaminations of waterlogged banks of water bodies or on wetlands;
• acute onset of the disease, fever in combination with allergic reactions (Quincke's edema, urticaria), pain in the right hypochondrium or epigastric region, enlargement of the liver, leukocytosis, eosinophilia.

[31], [32], [33], [34], [35]

Laboratory diagnostics of fascioliasis

Already in the acute stage of the disease, informative serological diagnosis of fascioliasis (RIGA, RIF, ELISA) is informative, however, due to lack of sensitivity and specificity, they can not be used to establish a definitive diagnosis.

3-4 months after infection, the diagnosis can be confirmed by the detection of helminth eggs in duodenal contents or in feces. Parasitological diagnosis of fascioliasis presents certain difficulties due to the fact that parasites do not lay eggs for a long time (3-4 months), and also because of the relatively small number of eggs that are allocated. Therefore, in the study of faeces, it is advisable to use methods of enrichment.

After consuming liver of cattle infected with fasciolae, transient eggs can be found in faeces. In these cases, it is necessary to conduct repeated parasitological studies 3-5 days after exclusion of liver and offal from the patient's diet.

In some cases, fasciolae can be detected by ultrasound examination of the liver, while helminths are found in the gallbladder and large bile ducts.

Differential diagnosis of fascioliasis

Differential diagnosis of fascioliasis is carried out with opisthorchiasis, clonorchiasis, viral hepatitis, leukemia and diseases of biliary tract of other etiology.

Differential diagnosis in the acute stage is carried out with trichinellosis, opisthorchiasis, clonorchosis, viral hepatitis, eosinophilic leukemia; in chronic - with cholecystitis, cholangitis, pancreatitis.

Indications for a surgeon's consultation are a suspicion of the development of bacterial complications from the hepato-biliary system.

[36], [37], [38], [39], [40],

Treatment of the fasciola

In acute stage, diet is prescribed (table number 5), antihistamines. After the symptoms subsided, anthelmintic treatment of fascioliasis. The choice agent on the recommendation of WHO - triklabendazole, which is used in a daily dose of 10 mg / kg in a single dose, in severe cases, the drug is used at a dose of 20 mg / (kg x day) in two divided doses with an interval of 12 hours. Less effective praziquantel in the daily a dose of 75 mg / kg in three meals after a meal for one day.

To free the bile duct from the dead parasites, cholagogue drugs are used.

Antihelminthic treatment of fascioliasis is assessed by the disappearance of eggs of fasciolae in duodenal contents in studies at 3 and 6 months.

Also use prazikvantel in the same doses as in opisthorchiasis. However, the effectiveness of praziquantel against F. Hepatica does not exceed 30-40%, and in relation to F. Gigantica it is comparable with the efficacy in the treatment of opisthorchiasis.

Control of the effectiveness of treatment is carried out 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 prolonged course of the invasion, development of purulent cholangitis and cirrhosis of the liver is possible.

Terms of incapacity for work

Determine individually.

Clinical examination

Not regulated.

[41], [42], [43], [44]

Prevention

In the endemic region of the Fasciola area, it is recommended that water from non-current water bodies be used for drinking only boiled or filtered. Plants growing in wet places, or vegetable greens, for watering which was used water from faecally contaminated livestock ponds, before eating should be boiled or scalded with boiling water.

It should be remembered that the cuisine of south-eastern and southern countries with a large volume of fresh herbs, especially aquatic plants, presents the danger of infection with fascioliasis if hygienic cooking rules are violated.

Fascioliasis can be prevented if veterinary measures aimed at eradicating fascioliasis in farms are carried out: prophylactic deworming of livestock, changing pastures, feeding hay from disadvantaged meadows on fasciola of meadows not earlier than 6 months after harvesting, when adolescaria are already dead. The struggle against mollusks (intermediate hosts of fasciolae) is carried out by melioration of wetlands. They also use chemical means of fighting mollusks (molluscicides). An obligatory component of the complex of preventive measures should be the sanitary and educational work among the population living in the endemic area on the fasciola.

[45], [46], [47], [48], [49], [50], [51], [52],

Forecast

Fascioloz has a favorable prognosis for life. Rare deaths are caused by complications.

[53], [54], [55], [56], [57]