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Diphyllobothrioses
Last reviewed: 05.07.2025
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Diphyllobothriasis (Latin: diphyllobothriosis: English: diphyllobothriasis, fish tapeworm infection) is an intestinal helminthiasis caused by tapeworms.
They are characterized by a chronic course with predominant disruption of the gastrointestinal tract and the development of megaloblastic anemia.
Epidemiology of diphyllobothriasis
The main source of environmental contamination is humans, and domestic and wild animals that eat fish may play a certain role. The mechanism of human infection is oral. Transmission factors are infected raw, insufficiently salted or poorly heat-treated fish, as well as caviar. The incidence of diphyllobothriasis is focal. Adults are most often affected, especially those engaged in catching and processing fish. Diphyllobothriasis is widespread mainly in the northern hemisphere: in northern European countries, the USA, and Canada.
What causes diphyllobothriasis?
Diphyllobothriasis in humans is caused by the broad tapeworm (Diphyllobothrium latum) and a number of so-called small tapeworms (more than 10 species of diphyllobothria).
D. latим belongs to the type Plathelminthes, class Cestoda, family Diphyllobothriidae. The broad tapeworm reaches a length of 10 m or more, has two slit-like suckers on the scolex, with the help of which it attaches to the wall of the small intestine of a person. The body of the helminth consists of 3-4 thousand segments, the transverse size of which is greater than the longitudinal one. In mature hermaphroditic segments, oval-shaped eggs are formed, covered with a yellowish-brown membrane with a lid at one end.
The development of D. latum occurs with a change of three hosts. The final hosts are humans, less often animals that feed on fish (cats, dogs, bears, foxes, etc.). Unlike tapeworms, mature segments of the tapeworm do not break away from the strobila. The eggs are excreted with feces and remain viable for 3-30 days, but continue to develop only when they enter water. In water, after 2-3 weeks, a coracidium emerges from the egg, which is swallowed by the intermediate host. The second larval stage, the procercoid, develops in its body. The crustaceans containing invasive larvae are swallowed by an additional host - a predatory fish (pike, perch, ruff, burbot) or anadromous salmon (chum salmon, pink salmon) - in whose intestines the crustaceans are digested, and the procercoids migrate to the muscles, eggs, liver and other organs, where they turn into plerocercoids (the stage that is invasive for humans).
Pathogenesis of diphyllobothriasis
Tapeworms, attaching to the mucous membrane of the small intestine, infringe on it with bothria, ulcerating, necrotizing and atrophying the injured areas. With multiple invasions, helminths can cause intestinal obstruction. Eosinophilia and catarrhal phenomena in the mucous membrane in the early period of the disease are due to sensitization of the body to helminth antigens. Endogenous hypo- and avitaminosis of B 12 and folic acid underlies the pathogenesis of diphyllobothriasis megaloblastic anemia. The helminth secretes a specific protein component (releasing factor), disrupting the connection between vitamin B 12 and gastromucoprotein. As a result of long-term parasitism of the pathogen (up to 20 years), even one individual of the helminth, anemia acquires features of pernicious and is accompanied by damage to the peripheral nerves and spinal cord.
Symptoms of diphyllobothriasis
Symptoms of diphyllobothriasis are often absent or manifest as mild discomfort in the abdomen. However, with any clinical course, large fragments of the helminth are observed to pass with feces. With the manifest course of the invasion, symptoms of diphyllobothriasis such as abdominal pain, periodically acquiring a cramping character, nausea, hypersalivation occur. Appetite is sometimes increased, but weight loss and decreased performance are noted. With the development of anemia, increased fatigue, dizziness, and palpitations are more pronounced. An early manifestation of anemia is glossitis, accompanied by a burning sensation of the tongue. Later, pain may appear when eating due to the spread of inflammatory-dystrophic changes to the gums, mucous membrane of the cheeks, palate, pharynx and esophagus. In severe cases, an enlargement of the liver and spleen is observed. Neurological disorders in diphyllobothriasis: paresthesia, impaired sense of vibration, numbness, ataxia - occur more often than in true pernicious anemia, may not be accompanied by signs of anemia. Later, conduction along the lateral columns is impaired, spasticity and hyperreflexia appear; patients become irritable, depression may develop.
Complications of diphyllobothriasis
Diphyllobothriasis can be complicated by B12 deficiency anemia, and sometimes intestinal obstruction can develop.
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Diagnosis of diphyllobothriasis
Diagnosis of diphyllobothriasis is based on clinical and epidemiological data (fish consumption, combination of dyspeptic syndrome with signs of anemia), detection of helminth eggs during coproscopic examination or as a result of examination of fragments of helminth strobila isolated during defecation.
In peripheral blood smears, aniso- and poikilocytosis, basophilic granularity of erythrocytes (Jolly bodies are often visible in them), reticulocytopenia, thrombocytopenia, and neutropenia are determined. Diphyllobothriasis B12 - deficiency anemia develops in approximately 2% of those infected with D. latum; approximately 40% of patients have low levels of the vitamin in their blood serum. Hematological changes are more often recorded in elderly people.
Differential diagnosis of diphyllobothriasis
Differential diagnosis of diphyllobothriasis is carried out with other diseases accompanied by anemia (ancylostomiasis, trichuriasis), hyperchromic and hemolytic anemia.
Indications for consultation with other specialists
In case of severe anemia, a consultation with a hematologist is indicated.
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Treatment of diphyllobothriasis
Indications for hospitalization
Hospitalization is indicated for severe anemia.
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Drug treatment of diphyllobothriasis
Specific treatment for diphyllobothriasis is with praziquantel or niclosamide (see "Taeniasis").
In cases of severe anemia and serum cyanocobalamin levels less than 100 pg/ml, treatment with cyanocobalamin at a dose of 200-400 mcg/kg for 2-4 weeks is indicated before deworming.
Approximate periods of incapacity for work
The period of incapacity for work is determined individually.
Clinical examination
Diphyllobothriasis does not require medical examination. Control stool tests for the presence of broad tapeworm eggs are performed 1 and 3 months after antihelminthic therapy. If the passage of tapeworm fragments resumes or helminth eggs are found in the feces, a repeat course of antiparasitic treatment is performed.
How to prevent diphyllobothriasis?
To prevent diphyllobothriasis, fish should be eaten after thorough heat treatment or long salting (the latter also applies to the use of caviar). It is necessary to protect water bodies from contamination by human and animal feces, and conduct sanitary and educational work among the population of foci.