Diphyllobothriasis , or dibotriocephalosis ( Latin diphyllobothriasis ) - helminthiasis from the group of cestodoses , zooanthroponous invasion caused by Diphyllobothrium latum , less often D. dendriticum and D. klebanovskii ( D. luxi ). It occurs with dyspeptic disorders and the possible development of B 12 deficiency anemia.
| Diphyllobothriasis | |
|---|---|
Diphyllobothrium latum | |
| ICD-10 | B 70.0 |
| ICD-10-KM | |
| ICD-9 | 123.4 |
| ICD-9-KM | |
| Diseasesdb | 29539 |
| Medlineplus | 001375 |
| eMedicine | med / 571 |
| Mesh | D004169 |
Content
Etiology
The causative agent is the sexually mature stages of tapeworms from the genus Diphyllobothrium : wide ribbon ( Diphyllobothrium latum ), Diphyllobothrium klebanovskii , Diphyllobothrium dendriticum .
A wide ribbon reaches 10-12 m in length. The oblong flattened head ( scolex ) has 2 suction slots ( botria ). The body consists of 300-4000 segments ( proglottids ). The life expectancy of a worm in the human body can reach 25 years.
In diffilobotriosis caused by D. erinacei europaei , plerocercoid larvae live in the subcutaneous tissue and internal organs, causing the disease of sparganosis [3] .
Epidemiology
At the stage of puberty, the worm parasitizes in the small intestine . The eggs of the parasite are excreted with feces into the environment. In the water of freshwater reservoirs at a temperature of 10–20 ° C, a larva (coracidium) comes out of the egg, swallowed by the cyclops . Coracidium develops in a second-stage larva - a procercoid . Further development occurs in the body of a swallowed crustacean fish: the larvae reach the invasive stage ( plerocercoid ). In the body of a person or an animal that has eaten infected fish, the plerocercoid develops into a sexually mature individual, and the cycle repeats again [4] .
Parasite infection occurs mainly in areas with a large number of freshwater bodies of water. The invasion of the parasite into the human body occurs when fresh, insufficiently salted eggs and raw fish are consumed. The main second intermediate (additional) hosts of the broad ribbon are pike, burbot , perch , and some salmon fish. Large predatory fish that eat small fish can contain many plerocercoids. The final owners of the broad ribbon are man, dogs, cats, bears, foxes, pigs. Intermediate hosts - freshwater crustaceans ( cyclops , diaptomus), additional - freshwater fish.
In the Russian Federation, foci of diphyllobothriasis ( D. latum ) were recorded in Karelia , the Murmansk and Leningrad regions, in the river basins: Yenisei , Lena , Ob , Indigirka , Pechora , Severnaya Dvina , Volga and Kama . The formation of foci was noted on the Gorky , Kuibyshev , Volgograd , and Krasnoyarsk reservoirs.
Foci of gull diphyllobothriasis ( D. dendriticum ) are confined to the northern regions of Siberia and the Lake Baikal region .
The nosoareal of diphyllobothriasis caused by D. klebanovskii covers the shelf zones of the island, peninsular, and mainland territories of the Far Eastern seas, as well as the basins of the Far Eastern rivers flowing into the Pacific Ocean , with the exception of the northern part of the western Okhotsk region, within the boundaries of the range of the North-Eastern salmon populations.
Sparganosis is common in Japan and China.
Pathogenesis
In the intestines of a person usually lives one, less often several lentets, but cases of parasitization of 100 or more individuals are described. The life span of a parasite is calculated in years: 10, 20 or more years. At the same time, part of the end section of the strobila is periodically rejected and excreted in the form of a tape with stool during bowel movements.
The following factors underlie the pathogenic effect of the broad ribbon: mechanical action of the helminth, neuro-reflex effects, toxic-allergic reactions, the development of vitamin B12 and folic acid.
The role of the mechanical factor increases with intensive invasion. Attaching to the intestinal mucosa, the tape restrains it, which leads to local damage, micros ulceration, atrophy. With intense invasion, the accumulation of parasites can cause intestinal obstruction.
One of the indicators of the sensitization of the body, which is a consequence of the toxico-allergic effects of the vital products of the helminth, its antigens, is blood eosinophilia , which is most pronounced in the early stage of the disease.
Neuro-reflex effects as a result of irritation of the nerve endings of the intestinal wall contribute to dysfunction of the stomach and other organs of the digestive tract.
Among the severe manifestations of invasion is the development of diphyllobothriasic megaloblastic anemia, the underlying pathogenesis of which is endogenous vitamin deficiency B12 and folic acid. The etiological role of diphyllobothriasis in the development of anemia was established in 1884 by S.P. Botkin . Vitamin B12, which comes with food, is an external antianemic factor, which is not absorbed, but is absorbed by the parasite's strobila.
Clinic
The clinical course of diphyllobothriasis depends on the intensity of the invasion and the individual characteristics of the patient's body.
In some cases, the invasion is asymptomatic or subclinical. Sometimes the presence of an invasion is established in connection with the release of a helminth during defecation, after which some complaints of the patient are clarified, for example: abdominal pain, nausea, belching, etc.
With severe forms of invasion, pathological phenomena from the digestive organs, nervous and hematopoietic systems come to the fore. Such patients complain of decreased appetite, nausea and vomiting, abdominal pain, unstable stools, decreased ability to work, weakness, drowsiness, paresthesias , discomfort in the tongue when taking acidic, salty foods, drugs. Urticaria sometimes appears on the skin; epileptiform convulsions are rarely described.
Some patients with diphyllobothriasis, about 2% of invaded D. latum, develop pernicious, B12-deficient anemia. With the development of anemia, weakness, fatigue, drowsiness increases, patients complain of dizziness, palpitations, tinnitus, darkening in the eyes when turning the head. Pallor of the skin, puffiness of the face, and sometimes swelling on the legs are noteworthy.
As with Addison-Birmer anemia , Gunther glossitis may develop when inflammatory changes occur in the tongue, bright red extremely painful spots appear, and cracks appear as a “scalded” tongue. Later, acute events subside, atrophy of the papillae occurs, the tongue becomes smooth shiny - “varnished”. The abdomen is often swollen, the stool is often liquid, the liver, spleen are sometimes enlarged. In 80-90% of patients - achilia .
Lesions of the nervous system are manifested in the form of feelings of numbness, burning, tickling and paresthesia , impaired sensitivity of skin areas, instability of gait, as manifestations of myelosis.
Very characteristic changes occur in the blood system. Their main feature is the megaloblastic, embryonic type of hematopoiesis, as a result of which immature, young forms of red blood cells enter the peripheral blood: megaloblasts, normoblasts, erythrocytes with nuclear residues, Kebot rings, Jolly bodies, polychromatophiles, poikilocytes.
Leukopenia , thrombocytopenia is characteristic. The hemogram changes: the number of red blood cells decreases, their hemoglobin saturation is increased, the color index is usually high - hyperchromic anemia; ESR accelerated.
The severity of anemia depends on the intensity of the invasion, the presence of concomitant diseases in the invaded, and the quality of nutrition.
Research, Treatment, and Prevention Methods
Research methods: detection of helminth eggs in bowel movements, eosinophilia .
The treatment is usually outpatient, according to the patient’s indications, they are hospitalized, for example, with anemia. Prescribe pathogenetic and specific agents. In severe anemia, pathogenetic therapy should be started before deworming. Folic acid is prescribed, intramuscularly cyanocobalamin (vitamin B 12 ). Specific therapy is the use of phenasal, praziquantel .
The prognosis is favorable subject to the timely recognition of the disease and the implementation of effective therapy.
When salting fish from foci of infection with D. latum , the following technology should be observed:
| Ambassador | Brine density | Duration of salting to ensure decontamination |
|---|---|---|
| Strong | 1.20 | 14 days |
| Average | 1.18 | 14 days |
| Weak | 1.16 | 16 days |
Ambassador should be held at a temperature of + 2-4 ° C. The disinfection of whitefish, salmon and grayling fish from gull lentic larvae is ensured by a mixed weak salting (brine density 1.18-1.19) for 10 days. When salting chilled omul, it is recommended to salt the gutted fish, because diphyllobotriid larvae located on internal organs are removed together with them [5]
Notes
- ↑ Disease Ontology release 2019-05-13 - 2019-05-13 - 2019.
- ↑ Monarch Disease Ontology release 2018-06-29sonu - 2018-06-29 - 2018.
- ↑ V.V. Podyapolskaya, V.F. Kapustin Human helminthic diseases. 1958. - M.: Medgiz. - 663s.
- ↑ Ichthyopathology / N.A. Golovina, Yu.A. Strelkov, P.P. Golovin et al. - M.: Mir, 2007 .-- 448 p.
- ↑ 1 2 SanPin 3.2.569-96 “Prevention of parasitic diseases in the territory of the Russian Federation” (approved by the Decree of the State Committee for Sanitary and Epidemiological Surveillance of Russia No. 43 dated October 31, 1996)
Literature
- Serdyukov A.M. Difillobotriids of Western Siberia / Otv. ed. S. L. Delamure . - Novosibirsk: Science . Sib. Otdel, 1979.- 120 s. [one]