What is Fascioliasis?
Fascioliasis is an invasion of the trematodosis group with a primary lesion of the liver and biliary system.
Causes of Fascioliasis
The causative agents of fasciolis are two pigs of the genus Fasciola (Linnaeus, 1758), of the family Fasciolidae (Railliet, 1895) – Fasciola hepatica and Fasciola gigantica.
The generic name comes from the Latin saove. fascia – “ribbon”, “bandage”, “ribbon”. And indeed, the giant fasciola looks like a ribbon.
F. hepatica is a large trematode with a leaf-shaped elongated body with a length of 20–30 mm and a width of 8–13 mm. On the front cone-shaped end there is a hemispherical oral sucker. A larger abdominal sucker is located near the mouth, behind the cone-shaped part of the body of the helminth. The pharynx and esophagus are very short, two strongly branched and blindly ending intestinal loops depart from the latter. Two branched testes occupy the middle part of the body. Above them is unpaired ovary in the form of a coral twig, deer antler. Powerfully developed zheltochnik stretch along the side edges, merging into the back quarter of the body. Looped small uterus lies between the ducts of zheltochnikov and abdominal sucker.
Eggs of F. hepatica are large, oval, covered with a smooth double-circuit shell of golden-yellow color. They have a lid on one pole, on the opposite – a tubercle. The sizes of eggs are 130 – 140 x 70 – 90 microns.
Fasciola gigantica, in contrast to F. hepatica, is large in size (up to 7–8 cm long and up to 12 mm wide) and is more elongated. The eggs are larger (150 – 190 x 75 – 90 microns).
Biology fasciol studied German scientist Leykart. In humans, fascioliasis in 1760 was described by the famous naturalist and traveler Peter Simon Pallas.
Fascioliasis – biohelmintosis, zoonosis. The final owners of the pathogen are animals – cattle and small cattle, horses, camels, rodents, rarely humans. In humans, it is recorded as sporadic cases in almost all countries of the world. By 1992, there were 15,000 cases of fascioliasis in the world of people living in 40 countries of the world, including 19 countries in Europe (A.M. Sazanov, 1994). This is not a complete reflection of the true situation. In France, Cuba, Chile registered outbreaks of fascioliasis. In some villages of Peru, 4.5 – 34% of children under 15 years old, in one of the districts of Malawi, 2.4% of the 3,900 inhabitants isolated eggs fasciola.
Sporadic cases of fascioliasis are constantly recorded in the Caucasus, Central Asia, Ukraine.
Fascioliasis is one of the most dangerous and widespread helminth infections in farm animals. It is recorded on all continents of the globe and causes great damage to livestock farms due to the massive death of animals during epizootics, significant loss of live weight, reduction of milk production, reduction of hair trimming in sheep, culling of the affected liver, etc.
With cattle fascioliasis, each animal loses from 24 to 41 kg of live weight, for a year – 223 kg of milk from a cow.
Izvazirovannost herbivores – cattle and sheep in the countries of the Caucasus, Central Asia, Moldova, Belarus, calculated 50 – 80%. In the forest-steppe zone of Ukraine, fasciolosis is recorded in 70–83% of animals.
Analysis of the literature indicates a significant distribution of fascioliasis in animals in the countries of the tropical and subtropical climate. For example, in Ethiopia, from 47 to 100% of cows, sheep and goats in some provinces are fascinated by fascioli.
Animals become infected with fascioliasis by eating grass on grazing, freshly mown hay from marshlands and by ingesting adolescarias with water from the biotopes of mollusks.
The source of infection in human fascioliasis is infested animals. Infection factors are salad grass polluted with adolescariy, watercress, kok-sagyz, sorrel, garden greens. A person becomes infected by eating lettuce in an unwashed form, by drinking pond water, using it for washing greens, fruits, vegetables, berries, swallowing adolescaria during bathing. Adolescariae in water, wet soil retain viability for up to 2 years.
Fascioliasis – oral biohelminthiasis. The final owners are predominantly herbivorous animals – both domestic (large and small cattle, horse, rabbit, camel, donkey, etc.) and wild (squirrel, beaver, chamois, deer, antelope, roe deer, tour, kangaroo, etc. ) as well as a person.
The intermediate host is a freshwater mollusk, more often a small pond snail of the genus Galba (Limnaea truncatula). These mollusks live in large numbers in well-warmed small (often temporary) bodies of water with stagnant water, on lowland swampy meadows and pastures, where herbivorous animals usually graze.
In the final host, the fasciols are localized in the bile ducts of the liver, live up to 5 years, laying up to 2 million eggs during this time. Eggs are excreted with feces, further development is carried out only if released into the water.
The optimum temperature required for the development of the larva in the egg varies from 22 to 29 ° C. When the temperature is below 10 ° C, development stops, and high temperatures (30 ° C and more) act destructively. Under optimal conditions, embryogenesis lasts 17-18 days. Formed during this time Maracid hatch from the egg into the water in the light.
Miracidia freely floating in water is introduced into the body of the intermediate host, the mollusk. After 1.5 – 2.5 months, a large number of caudate larvae, cercariae, 0.23 – 0.26 x 0.2 mm in size, develop in it by parthenogenesis. After entering the water for the next 8 hours, the cercariae, throwing off the tail, become encysted on aquatic plants, sometimes on the surface of the water, and turn into the adolescarya stage — the invasive larva. Adolescarias can persist for a long time in water and on plants, but quickly die when they dry.
Human infection occurs by ingestion of adolescarias when drinking water, while bathing or by eating salad herbs (watercress, wild-growing kok-sagyz, sorrel), and animals grazing.
The fasciolae that have got into the gastrointestinal tract of the larvae are released from the membranes and penetrate into the liver and gallbladder, and sometimes into other organs. There are two ways of penetration of the larvae: tissue and hematogenous.
In the first case, they penetrate through the intestinal wall into the abdominal cavity, advance to the liver and through the glisson capsule into its parenchyma, and then into the bile ducts, where in 3–4 months they reach sexual maturity. In the second case, the larvae invade the blood vessels of the intestine and enter the liver through the portal vein system. In this case, the larva can be introduced into any organ, giving an unusual localization of the matured individual – in the mammary gland, skin, lungs, etc.
Pathogenesis during Fascioliasis
The pathogenesis of fascioliasis has a lot in common with other trematodosis. Migration of fasciol larvae, the period of their maturation determine the early stage of invasion. The leading role in the pathogenesis of this stage is played by allergic reactions of the patient’s body to the parasite’s metabolic products and, to a lesser extent, the mechanical factor, tissue damage by young fascioli.
In the chronic stage, adults of helminths with their suction cups and cuticle spines cause mechanical damage to the walls of the bile ducts. The helminths themselves and the accumulation of their eggs violate the outflow of bile, create conditions for the attachment of secondary microbial flora and the development of purulent angiocholitis. With a long course of the disease may develop liver fibrosis with symptoms of portal hypertension.
Symptoms of Fascioliasis
In the clinic of fascioliasis, as with other hepatic trematodoses, the early acute and chronic phases of invasion are clearly distinguished.
The incubation period is 1-8 weeks. In the early phase, fasciolosis occurs as an acute allergic disease. Invasion begins acutely with common symptoms: fever, weakness, headache, malaise. Allergic symptoms appear on this background: high fever, jaundice, itching, skin rash, urticaria, abdominal pain, nausea, vomiting, which is accompanied by high eosinophilia (up to 80-85%) and leukocytosis. On palpation, the liver is enlarged, dense, painful. Sometimes in the acute phase, signs of allergic myocarditis are expressed – chest pains, tachycardia, muffled heart sounds, transient arterial hypertension. In some cases, there are changes in the respiratory system.
With uncomplicated course of invasion, acute manifestations of sensitization gradually subside, eosinophilia is reduced to 5 – 15%.
The chronic phase proceeds in two main variants: in the form of relatively compensated chronic gastroduodenitis with signs of cholepathy, sometimes pancreatopathy. When joining a secondary infection, a picture of bacterial cholecystocholangitis or cholangiohepatitis occurs with pain and dyspeptic syndromes, dysfunction of the liver.
Possible development of purulent cholangitis, liver abscesses, obstructive jaundice. With intensive and prolonged invasion, cirrhotic changes in the liver are possible. Of the complications should also be noted cases of perverse fasciola localization in the lungs, brain, breast, subcutaneous abscesses, etc.
The prognosis for joining a secondary infection is severe.
Diagnosis of Fascioliasis
Diagnosis of the acute phase of fascioliasis is difficult, the diagnosis can only be assumed in evaluating anamnestic, epidemiological and clinical data: eating unwashed salad herbs, koky-sagyz, sorrel, drinking pond water, washing dishes, fruits, berries with this water and the acute onset of the disease with symptoms acute allergies. The possibility of a group disease of tourists, geologists, etc. is not excluded.
Currently, for the diagnosis using immunological methods – serological test systems, REMA, RIF, RAC.
At a later date (after 2.5 – 3 months after infection) the diagnosis is confirmed by the detection of fasciol eggs in the duodenal contents and in the feces.
It should be remembered that with the occasional use of a fasciolous liver (this happens with a violation of the veterinary and sanitary examination) in the feces appear so-called transit eggs. This is not the result of infection and disease, but the result of the destruction of fasciola in the human intestine and the release of eggs from the worm’s uterus.
Therefore, to establish the truth, it is necessary to reexamine the feces after 7–10 days, excluding the liver, pates, liver sausages, etc., from the food ration of the patient being examined, and also probing again.
Treatment of Fascioliasis
In the acute stage of fascioliasis with vivid allergic manifestations, desensitization therapy is carried out (antihistamines, calcium chloride), with the development of hepatitis and myocarditis, prednisone is prescribed in a dose of 30-40 mg per day for 5-7 days with a rapid decrease and elimination of the drug. When relieving acute events, chloxyl is prescribed at a dose of 60 mg per 1 kg of body weight per day in 3 doses after meals for 5 days. In the chronic stage, fascioliasis is treated with chloxyl, drugs that eliminate cholestasis, fortifying agents. When a bacterial infection of the biliary tract is attached, antibiotics are pre-prescribed.
Prevention of Fascioliasis
The fight against fasciolosis is an important problem of healthy health and veterinary medicine. In the line of the veterinary service, molluscicidal preparations are used in the improvement of pastures to combat intermediate hosts, anthelmintics, for the treatment of animals and chemoprophylaxis – valbazen, iveomecol plus, fazinex, vermitan, atsamidofen, etc. Change pastures, forage feeding and other measures are the basis of prevention in animals.
The identification and treatment of patients with fascioliasis – the main task of medicine – depends on the level of expertise of physicians, gastroenterologists, infectious disease specialists, etc.
The basis of personal prevention of fascioliasis: drink from ponds (under special conditions of people’s stay) only filtered water (if boiling cannot be boiled) water; herbs, salad herbs thoroughly wash or pour boiling water.