Opisthorchis felineus, IgG antibodies

Why this test?
For the diagnosis of opisthorchosis - helminthiasis caused by Opisthorchis felineus;
for the differential diagnosis of diseases with similar symptoms of damage to the gastrointestinal tract: inflammatory bowel diseases, diseases accompanied by malabsorption.
In what cases is it prescribed?
Diagnosis of acute opisthorchosis (early phase);
the presence of initial symptoms of infection (increased body temperature, pain in muscles and joints, vomiting, diarrhea, soreness and enlargement of the liver, allergic rashes on the skin);
the presence of signs of damage to the liver, gall bladder or pancreas, indicating a possible infection with trematodes;
epidemiological indications - living in endemic areas (areas with a high prevalence of this disease);
when eating poorly processed carp fish;
high-risk group (fishermen, indigenous peoples of the North).
Test information
Opisthorchosis is an oral biohelminthiasis, a natural focal disease. The causative agents of this helminthosis are parasitic flatworms (trematodes) belonging to the Opisthorchidae family - Opisthorchis felineus, feline or Siberian fluke. The sources of infection are humans, cats, dogs, foxes, infected with the pathogen and secreting helminth eggs in their feces.
Human infection occurs when eating raw or thermally poorly processed fish containing live larvae of the pathogen (metacercariae). With the feces of the carriers, the eggs of the causative agents of opisthorchosis fall into the water, where they are swallowed by snails, in which the larvae of the parasite reproduce, which ends with the release of cercariae larvae into the water. Cercariae penetrate into carp fish. Infection of the final hosts (humans and mammals) occurs when eating raw, lightly salted, dried or insufficiently heat-treated fish containing invasive larvae. It is very easy to become infected with opisthorchiasis in endemic areas.
Since the larvae of the parasites are located directly in the muscles of the river fish, processing equipment and other products are contaminated during its processing. Once in the stomach, the capsule of the metacercariae is digested, and the thin hyaline membrane is torn by the larva itself in the duodenum, from where the larvae of opisthorchosis pathogens penetrate into the gall bladder, bile ducts and ducts of the pancreas. Having penetrated the hepatobiliary system and pancreas, metacercariae reach sexual maturity in 3-4 weeks and begin to lay eggs.
Thus, the complete development cycle of the causative agent of opisthorchiasis (from an egg to a sexually mature parasite) lasts 4-4.5 months, after which the production of eggs begins. In the body of the final host, the growth of the invasion occurs only when repeatedly infected with opisthorchiasis. The lifespan of opisthorchosis reaches 20-25 years. The clinical picture of opisthorchiasis is polymorphic and depends on the individual characteristics of the organism, as well as on the intensity and duration of infection. There is a distinction between acute opisthorchosis (from a few days to 4-8 weeks or more) and chronic opisthorchosis (lasting 15-25 years and for life).
Acute opisthorchosis is characterized by fever, urticaria, pain in the muscles and joints, pain in the right hypochondrium, enlargement of the liver and gallbladder, pain and a feeling of heaviness in the epigastrium, nausea, vomiting, heartburn, flatulence. Fibrogastroscopy reveals erosive gastroduodenitis, stomach ulcers, and duodenal ulcers. In some patients, symptoms of lung damage appear, which are allergic in nature and proceed according to the type of astmoid bronchitis.
Chronic opisthorchosis is manifested by symptoms of chronic cholecystitis, gastroduodenitis, pancreatitis, hepatitis. There are constant pains in the right hypochondrium, reminiscent of biliary colic, moving to the right half of the chest. There is a dyspeptic syndrome, pain during palpation at the point of the gallbladder, dyskinesia of the gallbladder. The stomach is also involved in the pathological process, manifested by signs of gastroduodenitis and intestinal dysfunction, pancreatitis. An allergic syndrome is also possible with chronic opisthorchosis, which is manifested by skin itching, urticaria, Quincke's edema, arthralgia, food allergy. The peculiarity of the chronic form of opisthorchosis is that after successful deworming, irreversible changes in the form of chronic hepatitis, cholangitis, cholecystitis, gastritis, and an imbalance in the immune system may remain in the body.
The diagnosis of opisthorchosis is made on the basis of clinical data and the results of laboratory tests of blood, urine, coprological studies, fibrogastroduodenoscopy, and epidemiological anamnesis must also be taken into account: living or staying in endemic foci, eating poorly thermally processed carp fish. The immune system, upon contact with opisthorchosis antigens, is the first to produce M-class immunoglobulins (IgM) specific to them. Their synthesis reaches its maximum value after 1.5-2 weeks, and after 6-8 weeks immunoglobulins of class G (IgG) begin to be produced. However, with long periods (more than 10 years) of opisthorchiasis, there is a significant decrease in the level of specific antibodies - below the threshold - due to the development of the patient's immunodeficiency state and the adsorption of plasma proteins on the cuticle of the parasite.
Low concentrations of antibodies can be determined only by modern methods. In the acute stage, the patient's body produces anti-opistorch antibodies, so the ELISA method (enzyme-linked immunosorbent assay) gives almost 100 percent accuracy. However, the effectiveness decreases to 70% in the case of transition of the infection into a chronic form. In addition, residents of regions where there is an increased risk of opisthorchiasis have a significant underestimation of serological test indicators. This is explained by their hereditary reduced sensitivity to these parasites.
At the same time, those who have recently arrived in such regions, on the contrary, may have false-positive results of serological reactions of the stomach with the lack of innate tolerance. IgM antibodies are detected in the blood a few days after infection. They indicate an early stage of cat fluke development. The peak production of these antibodies falls on the second week of the disease. One and a half to two months after the onset of the disease, the IgM titer rapidly decreases.