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Trichocephalosis: causes, symptoms, diagnosis, treatment
Last reviewed: 23.04.2024
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Trichocephalosis (trichyouriosis, trichurosis, Latin trichocephalosis, trichocephaliasis, trichuriasis) is anthroponous geogelmintosis, characterized by a chronic course with a predominant gastrointestinal disorder.
ICD-10 code
Q79. Trichurosis.
Epidemiology of trichocephalus
Trichocephalosis is classified as a group of geogelmintoses. The source of environmental pollution is a sick person. Egg maturation in the soil lasts 20-25 days. A person becomes infected as a result of ingesting mature eggs with contaminated vegetables, fruits, berries, water. Vlasoglav is an ubiquitous parasite. Trichocephalosis is prevalent mainly in tropical and subtropical countries, humid areas of temperate climate. In Russia, helminthiasis is common in the Northern Caucasus and in the central chernozem regions. Mostly children aged 5 to 15 years are ill. In prevention, the central place is taken by measures to protect the soil from fecal contamination. And also observance of rules of personal hygiene.
What causes trichocephalus?
Trichocephalus is caused by a vagal head, Trichocephalus trichiurus, type Nemathelminthes, class Nematoda, order Enoplida, family Trichocephalidae. The front part of the helminth body is thin, hairy, the tail section thickened: the ratio of the threadlike part to the thickened part of the female is 2: 1, in the male it is 3: 2. The body length of the female is 30-35 mm, the body of the male is 30-45 mm. In females the posterior end is curved, in males it looks like a spiral. Eggs of the vagal head have the shape of a barrel measuring 0.02x0.05 mm, a brown thick shell, colorless cork located on the poles. Adult individuals of helminth parasitize in thick, more often in the caecum. Here females lay up to 3,500 eggs a day. Eggs with feces get into the environment. They must undergo incubation in the soil for 3 weeks or more, after which the larva acquires invasive properties. In the life cycle of Trichocephalus trichiurus there is no phase of migration, the parasite has low immunogenicity. When the egg is swallowed, the larva is released in the small intestine, it is introduced into the villi, after a few days it moves to the large intestine, where it reaches maturity after 3 months. Among the adults, females predominate. The life span of the whipworm is about 5 years.
The pathogenesis of trichocephalus
In the pathogenesis of trichocephalosis, the main role is assigned to the traumatic action of the pathogen. Vlasoglavy thin head ends damage the mucous membrane, penetrating to the submucosa, and sometimes the muscle layer. With intensive invasion observe hemorrhages, the formation of erosions and ulcers in the intestine. Vlasoglavy are facultative haematophages. It is believed that invasive people lose 0.005 ml of blood per parasite per day, so the presence of more than 800 helminths in the intestines in children causes hypochromic anemia. The sensitizing effect on the body of metabolites of the parasite also has a certain value, but it is limited more often to the tissues of the intestine, which contributes to the development of diarrhea. Clinical manifestations of helminthiosis are obvious when parasitizing a large number of vlagoslovov. Symptoms of trichocephalosis are observed in people who produce more than 5000 eggs of the pathogen in 1 g of feces.
Symptoms of trichocephalosis
In most patients with low invasion rates, the symptoms of trichocephalosis are poor or absent. With moderate invasion, patients complain of worsening appetite, nausea, salivation, diarrhea, flatulence. Possible spastic pain in the abdomen with localization in the right iliac region. Patients may note such symptoms of trichocephalosis as weakness, irritability, dizziness, headache. When massive invasion develops hemoccolitis, manifested by pain syndrome, tenesmus, bloody liquid stool. Children suffering from trichocephalosis, lag behind their peers in physical and mental development. In tropical countries, trichocephalus is attributed to the role of a factor contributing to the development of intestinal amebiasis and its severe course.
Complications of trichocephalosis - prolapse of the rectum, hypochromic anemia, intestinal dysbiosis, cachexia. Trichocephalosis is a risk factor for appendicitis.
Diagnosis of trichocephalus
Laboratory diagnosis of trichocephalosis is based on the detection of helminth eggs in faeces by enrichment methods. Adult helminths in the intestine are found during endoscopy (colonoscopy).
Differential diagnosis of trichocephalus
Differential diagnosis of trichocephalosis is carried out with other intestinal diseases, shigellosis, amebiasis, ulcerative colitis. If a surgical complication is suspected, the surgeon's consultation is indicated, if there is a suspicion of ulcerative colitis, consultation of the proctologist.
What do need to examine?
Treatment of trichocephalus
Antiparasitic treatment of trichocephalosis is performed on an outpatient basis. Patients with severe and complicated course of infection need hospitalization.
The following medicines are used:
- Albendazole - inside after eating 400 mg once a day for 3 consecutive days.
- Mebendazole - inside 100 mg twice a day after 20-30 minutes after eating for 3 days.
- Karbendatsim - inside after eating 10 mg / kg per day for 3-5 days.
Antiparasitic treatment of trichocephalosis does not require the appointment of a special diet and laxatives. With persistent violations from the digestive tract after etiotropic therapy, enzyme preparations and probiotics are prescribed.
Work capacity is disrupted with massive invasion. The terms of incapacity for work are determined individually.
In cases of persistent invasion, a second course of treatment is performed after 3-4 weeks.
A control study of feces is necessary 3-4 weeks after the completion of the course of treatment with an anthelmintic preparation.
Clinical examination
Disease of trichocephalosis does not require medical examination.
Prognosis for trichocephalosis
Trichocephalosis usually has a favorable prognosis, it can be burdened by the development of hypochromic anemia and intestinal complications with intensive invasion.