Fascioliasis is a parasitic invasion caused by hepatic or giant fluke and characterized by a predominant lesion of the hepatobiliary system. The course of fascioliasis is accompanied by malaise, fever, urticaria, nausea, pain in the right hypochondrium, an increase in the size of the liver, jaundice. In the diagnosis of fascioliasis, serological methods (ELISA, RPH), examination of duodenal contents and faeces for helminth eggs, ultrasound of the liver and biliary tract are informative. The complex therapy of fascioliasis includes a diet, taking anthelmintic drugs (triclabendazole, praziquantel), choleretic, antihistamines.
B66 Other trematodes
Fascioliasis is an extra-intestinal helminthiasis caused by parasitism in the liver parenchyma and bile ducts of the hepatic or giant fasciole (sucker). Along with opisthorchiasis, clonorhosis, paragonimosis, schistosomiasis, fascioliasis is one of the most common human trematodoses. Fascioliasis caused by hepatic fluke is common in Australia, Europe and South America. Fascioliasis associated with the giant sucker is found in Africa, East Asia and Central Asia. Both sporadic and massive outbreaks of the disease, covering hundreds of people, are described. According to available data, fascioliasis affects from 2.5 to 17 million of the world’s population.
Characteristics of the pathogen
The causative agents of fascioliasis are two types of flukes (flukes): liver fluke (Fasciola hepatica) and giant fluke (Fasciola gigantea). The hepatic fasciole has a flat leaf-shaped body, at the head end of which there are 2 suckers. The length of the adult parasite is 20-30 mm, the width is 8-12 mm. Giant fasciola has larger dimensions: length 33-76 mm, width 5-12 mm.
The final hosts of suckers are herbivorous farm animals, less often – humans. Parasitizing in the biliary system, helminths lay eggs, which enter the environment with feces and their further development takes place in fresh water. There, larval stages (miracidia) released from eggs are introduced into the body of gastropods, which are intermediate hosts of the pathogen fascioliasis.
In the internal organs of mollusks, the miracidia turn first into sporocysts, and then into caudate cercariae. After 1-2 months, the cercariae go back into the water, encyst, turning into an adolescarium, and attach to the surface of aquatic plants or an aqueous film. At this stage, the larvae become invasive, i.e. capable of causing fasciolosis in animals and humans.
Infection of animals with fascioliasis occurs when eating grass in pasture contaminated with fluke larvae; human infection is possible when eating wild or garden plants, watering of which was carried out with water from fresh reservoirs; drinking unboiled water; while bathing, etc. In the gastrointestinal tract, the fasciole larvae are released from the shells, through the intestinal wall they enter the abdominal cavity, where they are introduced into the liver parenchyma through the capsule and thus enter the bile ducts. A hematogenic migration path is possible – through the intestinal and portal veins into the hepatic ducts.
After 3-4 months of parasitizing in the body of the final host, the fascioles reach the sexually mature stage and begin to lay eggs. In the human hepatobiliary system, fascioliasis pathogens can parasitize for 5-10 or more years.
Toxic-allergic reactions developing in the migration phase of invasion are associated with sensitization of the organism by larval antigens, as well as mechanical injury of tissues on the way of their advancement. In the chronic stage of fascioliasis, pathological effects are caused by parasitization of helminths in the bile ducts. Sexually mature helminths cause damage to the hepatic parenchyma with the development of microabsesses and fibrous changes in the liver.
Accumulating in the bile ducts, fascioles can contribute to their obstruction and disruption of bile outflow, the development of proliferative (and in the case of secondary infection – purulent) cholangitis. The general toxic effect on the body in fascioliasis is due to the entry into the blood of the waste products of helminths and the decay of liver tissue. In the outcome of a long course of fascioliasis, cirrhosis of the liver and portal hypertension may develop.
In the development of fascioliasis, the incubation period, acute (migration) and chronic (associated with parasitization of adult helminths) stages are distinguished. Depending on the invasive dose, the incubation period can last from 1 to 8 weeks.
In the migration phase, general toxic and allergic symptoms are mainly expressed. Patients with fascioliasis complain of fever, weakness, malaise, headache. Fever can be subfebrile or high (up to 39-40 ° C), have a remitting or undulating character. Against this background, urticaria and itching of the skin appear, Quincke’s edema, high (up to 80-85%) eosinophilia in the blood. Dyspeptic disorders develop: nausea, vomiting, pain in the epigastrium and right hypochondrium; there is an increase in the size of the liver, accompanied by jaundice. In the early period, allergic myocarditis often develops, characterized by chest pains, arterial hypertension, tachycardia. After a few weeks, the clinical manifestations of acute fascioliasis subside significantly or completely.
After 3-6 months, the disease enters a chronic stage, the symptoms of which are caused by direct damage to the liver and biliary tract. The course of chronic fascioliasis is accompanied by hepatomegaly, paroxysmal pain in the right side; during periods of exacerbation – jaundice. Prolonged invasion leads to the development of dyspeptic syndrome, anemia, hepatitis, cirrhosis of the liver.
Secondary infection is fraught with the appearance of purulent cholecystitis and cholangitis, liver abscesses, strictures of the biliary tract. The literature describes casuistic cases of fascioliasis with atypical localization of flukes in the brain, lungs, mammary glands, Eustachian tubes, larynx, subcutaneous abscesses.
Most often, fascioliasis is diagnosed already in the chronic stage, when patients turn to a therapist or gastroenterologist with disturbing complaints. The presumed diagnosis is based on a combination of epidemiological data and clinical data. In favor of fascioliasis, the presence of previously recorded cases of invasion in this area, group morbidity, eating salad plants, drinking water from open sources or using it for washing dishes, fruits, vegetables, etc. testifies.
- Methods for detecting the pathogen. In the early period of fascioliasis, the diagnosis is confirmed by serological methods (ELISA, RPH, IFT). In the chronic stage, the detection of fasciole eggs in faeces or duodenal contents is informative. Parasites can be detected by ultrasound of the liver and gallbladder, CT of the liver.
- Blood biochemistry. In biochemical liver samples, there is an increase in the activity of transaminases and alkaline phosphatase, hypoproteinemia, hypoalbuminemia.
Fascioliasis must be distinguished from opisthorchiasis, clonorhosis, viral hepatitis, pancreatitis, cholangitis, cholecystitis of other etiology.
Treatment of fascioliasis is carried out inpatient. In the acute phase, a sparing diet, desensitizing drugs are prescribed; with the development of myocarditis and hepatitis, glucocorticosteroids are indicated. Antiparasitic therapy is switched to only after the acute phenomena subside. Triclabendazole, hexachlorparaxylene, praziquantel are used as etiotropic drugs for fascioliasis. In order to expel the dead fascioles from the bile ducts, choleretic agents are prescribed.
A control parasitological examination (analysis of feces for helminth eggs, duodenal probing with examination of bile portions) is carried out after 3 and 6 months. In case of purulent complications, antibiotics are prescribed and surgical intervention is required (drainage of liver abscess, drainage of bile ducts, etc.).
Prognosis and prevention
Early diagnosis of fascioliasis allows for timely therapy and recovery. With high-intensity invasion or secondary bacterial infection, the prognosis can be serious, up to a fatal outcome. Individual prevention of fascioliasis consists in preventing the use of raw water from reservoirs, poorly washed garden greens. Public control measures include the cleaning of reservoirs, their protection from fecal contamination, the elimination of intermediate hosts of fascioliasis – mollusks, veterinary examination and deworming of livestock, sanitary and educational work.