Diphyllobothriasis is an intestinal parasitosis from the group of cestodoses caused by tapeworms of the family Diphyllobothriidae, most often a broad tapeworm. Disease occurs with nausea, abdominal pain, decreased appetite, salivation, weight loss, stool disorder, anemic syndrome; in severe cases, intestinal obstruction develops. The diagnosis is confirmed by studies of feces, which make it possible to detect helminth eggs or fragments of its strobila. Specific dehilmintization is carried out with praziquantel or niclosamide.
General information
Diphyllobothriasis is an intestinal worms that occurs due to human invasion by parasitic tapeworms. Pathogens of diphyllobothriasis parasitize in the small intestine, causing dyspeptic manifestations and megaloblastic anemia. Natural foci of diphyllobothriasis are located mainly in temperate and cold climates (northern Europe, Canada, USA). The incidence of this type of helminthiasis is closely related to fishing and fish processing.
Causes
The causative agents of human diphyllobothriasis can be 12 species of parasitic tapeworms, the most frequent representative of which is Diphyllobothrium latum (broad tapeworm). D. Latum is a large parasitic worm whose length can reach 7-10 m. The strobila (body) of a broad tapeworm consists of 3-4 thousand proglottid segments; the scolex (head) is equipped with two slit–like suckers, through which it is attached to the wall of the small intestine.
The life cycle of the development of a broad sloth involves the change of three hosts; in this case, the final host is a person or animals (cats, dogs, foxes, bears), intermediate – freshwater crustaceans, additional – freshwater fish (perch, pike, ruff, burbot, salmon). From the intestines of the final host, the eggs of the idler with feces enter the environment.
Their further development takes place in the water, where after a few weeks the larvae – coracidia come out of the eggs. In water, they are swallowed by intermediate hosts – oar-footed crustaceans, in whose body they pass into the next larval stage of development – procercoids. The invaded crustaceans serve as food for freshwater fish, in whose body the procercoids turn into plerocercoid larvae that are invasive for humans. In the muscles, caviar, liver of fish, the larvae of the sloth can be viewed with the naked eye.
Infection of a person occurs when eating raw, poorly heat-treated, lightly salted fish or caviar containing plerocercoids. Once in the small intestine of the final host, the larvae attach to its mucous membrane and turn into sexually mature helminths capable of secreting eggs. In the human body, a wide tapeworm is able to parasitize for 20-25 years. A person is not contagious to others.
Pathogenesis
In the pathogenesis of diphyllobothriasis, the leading role belongs to mechanical damage to the intestinal wall, ulceration, necrosis and atrophy of the injured areas. Catarrhal inflammation (enteritis) leads to a violation of the digestive processes. Massive helminth invasion can cause intestinal obstruction. Sensitization to helminth antigens causes the development of catarrhal phenomena and eosinophilia in the early period of diphyllobothriasis. Megaloblastic anemia is based on a deficiency of vitamin B12 and folic acid, which are not absorbed due to the release of a specific releasing factor by the helminth. With prolonged parasitization of a broad tapeworm, anemia acquires malignant features and leads to damage to the nervous system.
Symptoms
The course of diphyllobothriasis can be latent or clinically pronounced (manifest). However, in both cases, a specific sign is the departure of large fragments of the helminth strobila in the form of whitish ribbons with fecal masses. From the moment of infection to the development of clinical symptoms, about 1.5 months pass. Manifestations of diphyllobothriasis develop gradually and are initially nonspecific: decreased appetite, nausea, unstable stool, subfebrility, fatigue, weight loss. Cramping abdominal pains, hypersalivation are characteristic.
The development of anemia is accompanied by dizziness, weakness, tachycardia, arterial hypotension. A pathognomonic sign of diphyllobothriasis B12-deficient anemia is Hunter’s glossitis, accompanied by the appearance of bright red spots and painful cracks on the tongue, later – shiny (“varnished”) language. Inflammatory and dystrophic changes can spread to the gums, the mucous membrane of the palate, cheeks, pharynx, esophagus, causing pain and burning when eating.
Complications
In severe diphyllobothriasis, there is an increase in the liver and spleen, a decrease in gastric secretion up to achilia. The accumulation of a large number of helminths in the small intestine can cause obstructive intestinal obstruction. Due to severe B12-deficiency anemia, patients with diphyllobothriasis may develop neurological disorders: astheno-neurotic syndrome, paresthesia, ataxia, hyperreflexia, irritability, depression, etc.
Diagnostics
Epidemiological anamnesis (eating fish, staying in endemic areas), as well as clinical data (dyspeptic syndrome, anemia) are informative for the diagnosis of diphyllobothriasis. In peripheral blood, there is eosinophilia, a decrease in the number of erythrocytes and hemoglobin, neutropenia, lymphocytosis, acceleration of ESR. A decrease in the content of vitamin B12 in the blood serum is characteristic.
The main method of diagnosing diphyllobothriasis is the examination of feces, in which helminth eggs or scraps of broad-tapeworm strobila are detected. As part of diagnostic measures, diphyllobothriasis is differentiated with hemolytic and hyperchromic anemia, as well as other helminthiasis accompanied by anemic syndrome (ankylostomidosis, trichocephalosis).
Treatment
Treatment of diphyllobothriasis is started immediately after confirmation of the diagnosis. Patients are prescribed a semi-liquid easily digestible diet, taking iron, folic acid, cyanocobalamin injections. Specific therapy of diphyllobothriasis is carried out with anthelmintic drugs praziquantel or niclosamide. It is possible to use phytopreparations – male fern or decoction of pumpkin seeds. After deworming, control studies of feces are performed twice; if helminth eggs are detected, repeated treatment is prescribed.
Prognosis and prevention
With timely recognition of diphyllobothriasis and effective anthelmintic therapy, the prognosis is favorable. However, immunity after treatment is unstable; re-infection with diphyllobothriasis is possible. Prevention involves the protection of reservoirs from fecal contamination, compliance with the technology of cutting and cooking fish, education of the population in the centers of the spread of helminth infestation. It is mandatory to conduct a parasitological examination of workers of the fishing industry and commercial fish entering the trading network.
