Strongyloidiasis - routes of infection, symptoms, treatment, prevention
Русский

Strongyloidiasis - routes of infection, symptoms, treatment, prevention

Strongyloidiasis is a chronic helminthiasis with predominant damage to the gastrointestinal tract and general allergic manifestations, the causative agent of which is the intestinal acne .

Prevalence of the disease

The disease is endemic in tropical and subtropical regions of the world, where it affects about 100 million people.
In some countries in Africa, Central and South America, Asia, and Oceania, the infection rate of the population reaches 24%. In temperate climate zones, the prevalence of the population is 0.6-2%, but in some areas it can reach 20%. In neighboring countries, the most intense foci of strongyloidiasis exist in the humid subtropics of Azerbaijan, Georgia, and Ukraine. In Russia, infection is recorded mainly in the Krasnodar Territory, Stavropol Territory and Rostov Region.

Routes of infection

The main source of infection is a sick person. Some authors believe that dogs play a certain epidemiological role.

Human infection is possible in two ways:

  • through the skin and
  • orally (through the mouth).

The infection transmission factor is contaminated soil. Infection through the skin occurs when walking barefoot, lying on the ground, or performing agricultural and garden work.

Infection through the mouth is less common when eating vegetables, berries, and fruits with damaged surfaces, contaminated with soil containing larvae.

The risk group is:

  • agricultural workers;
  • miners;
  • sewage treatment plant workers;
  • road builders;
  • greenhouse farms;
  • vegetable bases;
  • prisoners;
  • patients of psychoneurological boarding schools.

Patients at risk for generalized strongoloidiasis are

  • with impaired T-cell immunity;
  • lymphomas;
  • leukemia;
  • after organ transplantation;
  • with collagen diseases;
  • diabetes mellitus;
  • malabsorption syndrome;
  • HIV infection.

Pathogenic effects on health

When infected through the skin, the larvae are able to penetrate through intact human skin, boring through the epidermis, or through sweat glands and hair follicles. Having penetrated the tissues, the individuals migrate into the bloodstream, are carried through the bloodstream into the right atrium and ventricle, then into the lungs.

There they molt and transform into males and females, then travel up the bronchial tree into the pharynx and are swallowed. Through the esophagus and stomach they enter the duodenum. Fertilization of females occurs in the lungs, trachea, and intestines. The duration of migration is 17-27 days.

When infected through the mouth, filariform larvae (which can infect humans) penetrate the mucous membranes of the oral cavity, pharynx, enter the bloodstream and also go through all stages of migration.

Sexually mature females linger in the intestines, penetrating into the mucous membrane. Males quickly die after copulation. Adult females parasitize the liberkühn glands of the duodenum ; with intense invasion, they are localized in the mucous membranes of the pyloric part of the stomach, small , cecum and colon . Females lay up to 50 eggs per day, from which rhabditiform larvae hatch and are excreted in feces.

Further formation of larvae occurs in 3 ways:

  • direct,
  • indirect,
  • intraintestinal.

In the direct route, rhabditiform larvae enter the environment, where they transform into filariform (infective) larvae.

In the indirect path, the rhabditiform larvae, once in the soil, molt and turn into free-living females and males. Fertilized females give rise to the next generation of free-living nematodes. Under optimal conditions, the existence of non-parasitic generations continues for a long time. At the same time, rhabdoid larvae of any generation can turn into filaroid larvae that can infect humans.

The intraintestinal path of development is the transformation of rhabditiform larvae into filaroid larvae in the human intestine, without their release into the external environment, followed by self-infection. Filariform larvae mature in the lumen of the small or large intestine, penetrate their wall, through the portal vein into the liver, from there into the heart and then through the lungs they complete their development.

Self-infection is promoted

With autoinvasion, strongyloides can parasitize the body for up to 30 years.

The pathogenic effect of helminths is associated with their mechanical, toxic effects, and the tension of the immune system with antibodies.

Of key importance is the effect on the immune system of the waste products of the parasite, expressed both during the period of migration of larvae and in the intestinal stage of the disease.

On the skin, at the site of penetration of the larvae, petechial hemorrhages, swelling, and a rash with itching are observed.

During the migration of individuals, granulomas and dystrophic changes appear in the liver, lungs and other organs.

Mechanical damage to the intestinal wall is caused by parasitism of females deep in the liberkühn glands. Their long-term parasitism leads to infectious-allergic inflammation, swelling, hyperemia, endovasculitis, granulomas, and enlarged mesentral lymph nodes. Erosions, ulcers, and hemorrhages form in all layers of the intestinal wall. Traumatization of the intestinal mucosa contributes to the activation of pathogenic microflora.

Symptoms

The duration of the incubation period depends on the intensity of infection and is 15-20 days or more.

In the early phase, when the larvae migrate,

  • fever,
  • itchy skin,
  • urticaria or papular rash,
  • local swelling,
  • eosinophilic infiltrates appear in the lungs,
  • the liver and spleen enlarge.

In peripheral blood the following is detected:

  • leukocytosis,
  • hypereosinophilia,
  • increase in ESR.

In most infected people, this phase is subclinical or asymptomatic.

In the late (chronic) phase of strongyloidiasis, when helminths reach sexual maturity, both cases of asymptomatic parasite carriage and patients with pronounced and even severe clinical manifestations are observed.

In mild forms, patients note

  • nausea and
  • dull pain in the epigastric region,
  • normal or mushy stool 2 times a day,
  • urticaria with itchy skin.

The nature of the rash can be different (erythematous, papular), but the most commonly observed is “linear” urticaria - a papulovesicular, rapidly progressive skin lesion that usually appears in a place where clothing fits closely to the skin and spreads at a speed of 10 cm/h. This rash looks like a red cord 2-3 mm wide, 30 mm long, lasts 12-48 hours and disappears without pigmentation or peeling.

In severe forms:

  • nausea is often accompanied by vomiting, acute pain occurs in the epigastrium, usually on an empty stomach or 2-2.5 hours after eating, sometimes at night;
  • severe attacks of pain in the right hypochondrium, accompanied by fever and urticaria;
  • loose stools with mucus (less often with blood) appear periodically 5-6 times a day;
  • headache;
  • dizziness;
  • increased fatigue;
  • neurastic and psychasthenic symptoms.

In the blood test:

  • eosinophilia (70-80%),
  • secondary anemia (with a long course of the disease).

In the duodenal contents, the amount of mucus, leukocytes, and epithelial cells is increased.

Instrumental studies reveal signs of duodenal dyskinesia.

In severe cases of the disease, observe

  • debilitating diarrhea
  • dehydration of the body,
  • malabsorption,
  • anemia,
  • cachexia.

Possible complications such as

  • ulcerative intestinal lesions,
  • perforated peritonitis,
  • intestinal obstruction,
  • pancreatitis.

Depending on the predominance of one or another clinical symptomatology, various forms of the disease are distinguished:

  1. duodeno-gallbladder - characterized by a slow, monotonous course with pain in the right hypochondrium, bitterness in the mouth, bitter belching, loss of appetite, periodic nausea, vomiting; cholecystography reveals deformation of the shadow of the gallbladder, a violation of its displacement and mobility;
  2. gastrointestinal - manifested by nausea and stool upset, as a rule, constipation alternates with diarrhea; watery stool mixed with mucus and blood, 3-4 times a day or more; upon examination, a coated tongue is detected, pain on palpation of various parts of the abdomen; Symptoms of gastritis, enteritis, gastric and duodenal ulcers are common;
  3. allergic - the skin rash has the form of oval pink-red blisters that rise above the surface of the skin, are accompanied by severe itching and “crawl” when scratched - as a result, linear stripes are formed on the stomach, buttocks, back, lower back, chest, hips; the rash does not rise to the scalp; by the movement of the stripes, you can trace the movement of the larvae in the skin (speed 5-15 cm/h); the rash lasts from several hours to 2-3 days and disappears without leaving any traces; rashes recur from several times a month to several times a year;
  4. nervous - patients complain of general weakness, headaches, dizziness, sleep disturbance, increased irritability, tearfulness, they are depressed, and fainting occurs;
  5. pulmonary - usually develops in people with weakened immune systems.

The invasion lasts for years (20-30 years), with periods of remissions and exacerbations.

Complications - pneumonia, meningitis, meningoencephalitis, hepatitis, nephritis are observed in patients with reduced immunity due to cancer, malnutrition, congenital immunodeficiency, and in HIV-infected patients.

Diagnostics

Clinical diagnosis of strongyloidiasis is difficult. At an early stage, the disease often remains unrecognized. It can be suspected on the basis of short-term, suddenly appearing allergic skin lesions on the legs and fingers in combination with disturbances in the functions of the gastrointestinal tract.

Suspicion of strongoloidiasis is supported by data on being in an endemic area.

The final diagnosis is made when strongyloides larvae are detected during stool examination using the Berman method or when examining bile.

The production of larvae by females may periodically cease, so repeated studies are necessary.

Treatment

Treatment must be carried out under the supervision of a doctor.

During the migration stage, antihistamines and calcium supplements are prescribed.

To relieve skin allergic syndrome and other manifestations of allergies, antihistamines are used:

  • diphenhydramine (diphenhydramine) orally;
  • chloropyrami (suprastin);
  • loratadine (Claritin, Lomilan, Erolin);
  • ketotifen.

Treatment with antiparasitic drugs is usually carried out at the intestinal stage of the disease:

Ivermectin and thiabendazole are widely used abroad.

In severe cases of infestation, courses of anthelmintic treatment are repeated with changes in medications.

For those with a weakened immune system, long-term preventive treatment with the same drugs in half the dose is recommended monthly for 2 days.

3 weeks after deworming, 3 scatological examinations are carried out using the Berman method with an interval of 1-2 days, then once a month and duodenal intubation, examination, general blood test must be done after 2 weeks, 2, 6 months, then once every six months.

Prognosis and prevention

With timely treatment in the early stages, the prognosis is good. If complications develop, the prognosis is poor. When the invasion generalizes and affects many organs and systems, death is possible.

For personal prevention in areas of strongoloidiasis, it is not recommended to walk barefoot or lie on the ground; to exclude foodborne infection, it is necessary to thoroughly wash vegetables, herbs, and berries.

data-matched-content-rows-num="4,2" data-matched-content-columns-num="1,2" data-matched-content-ui-type="image_stacked" data-ad-format=" autorelaxed">
Strongyloidiasis - routes of infection, symptoms, treatment, prevention Link to main publication
The scientific information provided is general and cannot be used to make treatment decisions. There are contraindications, consult your doctor.