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The test kit Vitrotest® Borrelia-IgM is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgM class antibodies to Borrelia burgdorferi sensu lato in human serum or plasma.
Determination of IgM antibodies to B. burgdorferi in the test kit Vitrotest® Borrelia-IgM is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК085 - 96 tests- Solid phase: breakable microplate ELISA is coated with Borrelia burgdorferi sensu lato antigens.
- Conjugate: a monoclonal antibodies to human IgM conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Lyme disease (tick-borne borreliosis) is the most common tick-borne disease in the Northern hemisphere. The causative agent of borreliosis is spirochetes of the Borrelia burgdorferi group - were first identified in 1982 by the American microbiologist Willie Burgdorfer. Today, the most pathogenic spirochetes belong to the Borrelia burgdorferi sensu lato group, which includes Borrelia burgdorferi sensu stricto, Borrelia afzelii and Borrelia garinii.
Lyme borreliosis is a progressing disease which encompasses several clinical syndromes (erythema migrans (EM), neuroborreliosis, Lyme arthritis, and acrodermatitis chronica atrophicans). The most common clinical manifestation of early localized LD is EM, which appears in approximately 70% of patients 3-30 (average 7) days after bite. EM is a rash which appears at the site of the tick bite and gradually expands to a ring with a central clear zone. If the infection remains unnoticed and untreated in this early localized stage, B. burgdorferi can spread to other tissues and organs. The second, so-called early disseminated stage of the disease causes more severe manifestations that can involve the skin, nervous system, joints, or heart. This stage is mainly characterized by neurological signs (neuroborreliosis) or joint aches (Lyme arthritis). The third stadium is late disseminated LD. It’s typical presentations are acrodermatitis chronica atrophicans and arthritis. Manifestations of LD are similar to such immune-mediated disorders as rheumatoid arthritis, multiple sclerosis and systemic lupus.
Ticks most frequently acquire spirochetes from infected rodents during their larval feeding. Once infected, a tick can transmit infection throughout its life.
Not all ticks of competent species are carriers of an infectious agent. The prevalence of B. burgdorferi among ticks was measured to be as different as 19% and 60%. The probability to be infected is regarded as high if the tick remains attached to skin for more than 24 hours.
People living in or visiting rural areas, particularly campers and hikers, are most at risk. The infection risk appears not only in forests but more and more in parks, which attract more attention from the public. Ixodes ticks are the only natural agents through which humans have been shown to become infected. There is no evidence that LD is transmitted from person-to-person.
B.burgdorferi infection is known to induce strong humoral immune response in the host. IgM titres are typically highest between 3rd and 6th week after disease onset and then decline, however in many patients IgM remains high during later manifestations of illness, reflecting disease activity. IgG titres start increasing 1-2 weeks after onset, but reach highest titers only months later when arthritis is already present.
If the patient is cured, antibody levels in the first weeks after convalescence increase, and only then begin to decrease. If LD reaches an advanced stage, IgM and especially IgG are still detectable after cure for many years in the majority of patients. On the contrary, prompt antibiotic treatment at localized stage often aborts the development of a sustained humoral response, resulting in an absence of IgG and IgM after cure. Hence, reinfection is possible after successfully treated early, but not late LD.
B. burgdorferi genome encodes around 1500 proteins; almost half of them are plasmid encoded. Of these proteins, around 100 are immunogenic. Significant serological cross-reactivity exists between B.burdhoferi and causative agents of human spirochetal infections, particularly relapsing fever and syphilis.
Only several proteins are proven specific antigens and therefore valuable for serodiagnosis. These proteins include FlaB (BB0147), the P66 outer membrane protein (BB0603), OspA and OspB (BBA15 and BBA16), decorinbinding protein B (BBA25), OspC (BBB19), fibronectin-binding protein (BBK32), and VlsE (BBF33). FlaB is a part of flagellar apparatus; the rest are outer membrane proteins.
Currently, there is no “gold standard” in the diagnostics of LD. LD diagnosis is based upon:
a) signs and symptoms;
b) history of exposure to infectious ticks;
c) laboratory diagnosis.
The only manifestation characteristic to LD is EM, whereas clinical features of later stage presentations are not unique to B. burgdorferi infection. Unfortunately, only around 70% of patients develop EM; many patients present to the clinics at disseminated stage. Exposure to ticks may easily left unnoticed as many humans are bitten by ticks at their juvenile stage, called nymphs, which are much smaller in size. Therefore, laboratory support of LD must be sought by isolation of B. burgdorferi in culture, PCR or immunoassays.
Assays available for serology are ELISAs (or EIAs) and indirect fluorescent antibody (IFA) assays. Their performance is best at the late stages of LB. ELISAs are available as first, second or third generation tests. First generation ELISAs use whole cell lysates as antigens; second generation ELISAs use native purified antigens; and third generation ELISAs use recombinant or synthetic antigens. Immunoblots are mainly used as confirmatory tests. Apart from testing for antibody response in serum, antibody response may also be measured in cerebrospinal fluid. -
The test kit Vitrotest® Anti-Ascaris is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG class antibodies to Ascaris lumbricoides in human serum or plasma.
Determination of IgG antibodies to Ascaris lumbricoides in the test kit Vitrotest® Anti-Ascaris is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК051 - 96 tests
○ ТК110 - 192 tests- Solid phase: breakable microplate ELISA is coated Ascaris lumbricoides antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis 10 μl.
- Assay time: 1h 15 min.
Ascariasis is the most prevalent helminth infection on earth. Around one-fifth of human population is infected with Ascaris lumbricoides; the majority of infected live in rural or deprived urban settings in developing countries. In these endemic regions, disease prevalence is around 90% whereas in developed countries, the infection is rare. A. lumbricoides is the largest nematode (15-35 cm) parasitizing in the lumen of human small intestine.
Fertile eggs of ascaris become infective after an embryo moults twice within an egg (18 days to several weeks depending on the environmental conditions). After infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa, and are carried via bloodstream to the lungs. The larvae undergo two moults in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. Upon reaching the small intestine, they develop into adult worms which can live 1-2 years.
Daily ascaris egg production is around 200,000 eggs, which are shed in the feces. An infection can occur if a person swallows the microscopic eggs in contaminated food or water, or the eggs are transferred from hands to mouth after touching contaminated soil. Eggs can remain viable in the soil for up to 15 years.
The manifestations of ascariasis can be divided into acute and chronic. Patients experience acute lung inflammation, difficulty in breathing and fever as a result of larval migration through the pulmonary tissue (acute ascariasis). Abdominal distension and pain, nausea and diarrhoea are characteristic symptoms of adult worm invasion (chronic ascariasis). In small percentage of patients, entangled adult worms could lead to mechanical intestinal obstruction. The majority of invasions with A.lumbricoides are asymptomatic, and patients usually seek medical advice because they have seen a worm in their faeces. -
The test kit Vitrotest® Anti-Echinococcus is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG class antibodies to Echinococcus granulosus in human serum or plasma.
Determination of IgG antibodies to Echinococcus granulosus in the test kit Vitrotest® Anti-Echinococcus is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК066 - 96 tests- Solid phase: breakable microplate ELISA is coated Echinococcus granulosus antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Echinococcosis is a chronic disease of humans and animals caused by parasitizing the larvae of the helminth Echinococcus. The causative agent of this helminthiasis is most often the larva of Echinococcus granulosus. Echinococcosis is quite common all over the world, especially in southern countries, where livestock breeding, mainly sheep breeding, is widespread.
Echinococcus eggs enter the human body through dirty hands after contacting dogs (less often - cats). Also, infection is not excluded when eating unwashed vegetables, berries, fruits, water that are contaminated with helminth eggs.
In the digestive canal of the intermediate host, the egg of the echinococcus is freed from the membrane, and the embryo (oncosphere) deepens into the mucous membrane of the small intestine, entering the internal organs, where, in most cases, they linger and develop into echinococcal cysts. More often, echinococcus affects the liver (in 44-85 % of cases) and lungs (10 % of cases).
The pathological effect of echinococcus is due to the sensitization of the body by the metabolic products of the parasite and mechanical damage to the affected organs and tissues. The sizes of cysts are from 1-5 cm in diameter to large blisters, which can contain several liters of fluid. The mechanical effect of such a cyst leads to dysfunction of the affected organ, its hypertrophy.
To diagnose echinococcosis, cysts visualization methods are used: X-ray and ultrasound studies, computed and magnetic resonance imaging. Puncture biopsy of a cyst is considered dangerous due to the possibility of spreading parasites into adjacent tissues.
The detection of antibodies specific to the antigens of echinococcus in the blood is a reliable indicator of parasite invasion. The level of the immune response largely depends on the organ localization of the cyst and its morphology. Low antibody levels are observed at the onset of cyst formation or at a late inoperable stage of the disease.
Today, methods of indirect hemagglutination and fluorescence, enzyme immunoassay are used to detect specific antibodies to Echinococcus granulosus. These methods are characterized by a sensitivity of 60-90 %, therefore, the best information content is achieved using a combination of serological methods.
Serological methods are also quite informative for monitoring the patient’s postoperative state - a gradual decrease in the level of specific antibodies 4-6 months after surgical removal of the cyst indicates a successful result of the surgical intervention. With relapses of cyst formation, specific antibodies are kept at a high level for years. -
The test kit Vitrotest® Anti-Opisthorchis is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG class antibodies to Opisthorchis felineus in human serum or plasma.
Determination of IgG antibodies to Opisthorchis felineus in the test kit Vitrotest® Anti-Opisthorchis is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК057 - 96 tests- Solid phase: breakable microplate ELISA is coated Opisthorchis felineus antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Opisthorchiasis - helminthiasis, affecting mainly the hepatobiliary system and the pancreas of humans, cats, dogs, etc. The disease is marked by a long course (in human body the parasite exists for 10-20 years), proceeds with frequent exacerbations, contributes to the occurrence of primary cancer of the liver and pancreas.
The causative agents of opisthorchiasis are two species of trematodes of the Opisthorchidae family - Opisthorchis felineus (Siberian fluke), common in Western Siberia, Kazakhstan and some areas of the Dnieper region; and Opisthorchis viverrini (squirrel fluke), found in countries with tropical climates (mainly in Thailand).
These small trematodes have a flat body 4-13 mm long and 1-3.5 mm wide. The oral sucker is located at the anterior end of the body, and the abdominal sucker is located at the border of the first and second quarter of the body.
Infection occurs when eating raw fish (thawed, frozen), slightly salted and insufficiently calcined carp fish containing helminth larvae - metacercariae. In the stomach, the upper parts of the small intestine, metacercariae are freed from the membrane and through 3-5 h reach the gallbladder, liver, pancreatic ducts, where after 2 weeks turn into sexually mature forms, capable of further releasing eggs.
At the early stage of invasion, a pronounced allergization of the body is observed. Mature opisthorchis injure mucous membranes of the pancreatic and bile ducts, create barriers to the outflow of bile, contribute to the development of cystic enlargements and neoplasms of the liver and carry out toxic and neuro-reflex effect.
Diagnosis of opisthorchiasis according to the clinical manifestations of the disease is difficult due to the absence of symptoms and syndromes characteristic only for this disease. Therefore, it is necessary to carry out a thorough clinical, laboratory and X-ray (ultrasound inclusive) examination.
In the laboratory analysis, it is possible to detect the invasion of opisthorchis one month after the infection when helminths begin to lay eggs (ovoscopic examination of feces and duodenal juice of the patient). More significant complications arise in recognizing early phases of opisthorchiasis. However, more and more studies are being carried out to detect specific antibodies to Opisthorchis felineus by enzyme immunoassay. In the chronic stage invasion is diagnosed by detecting helminth eggs in bile and stools, as well as by ELISA. -
The test kit Vitrotest® Opisthorchis-IgM is an enzyme linked immunosorbent assay (ELISA) for the detection of IgM class antibodies to Opisthorchis felineus in human serum or plasma.
Determination of IgM antibodies to Opisthorchis felineus in the test kit Vitrotest® Opisthorchis-IgM is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК012 - 96 tests- Solid phase: breakable microplate ELISA is coated Opisthorchis felineus antigens.
- Conjugate: a monoclonal antibodies to human IgM conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Opisthorchiasis - helminthiasis, affecting mainly the hepatobiliary system and the pancreas of humans, cats, dogs, etc. The disease is marked by a long course (in human body the parasite exists for 10-20 years), proceeds with frequent exacerbations, contributes to the occurrence of primary cancer of the liver and pancreas.
The causative agents of opisthorchiasis are two species of trematodes of the Opisthorchidae family - Opisthorchis felineus (Siberian fluke), common in Western Siberia, Kazakhstan and some areas of the Dnieper region; and Opisthorchis viverrini (squirrel fluke), found in countries with tropical climates (mainly in Thailand).
These small trematodes have a flat body 4-13 mm long and 1-3.5 mm wide. The oral sucker is located at the anterior end of the body, and the abdominal sucker is located at the border of the first and second quarter of the body.
Infection occurs when eating raw fish (thawed, frozen), slightly salted and insufficiently calcined carp fish containing helminth larvae - metacercariae. In the stomach, the upper parts of the small intestine, metacercariae are freed from the membrane and through 3-5 h reach the gallbladder, liver, pancreatic ducts, where after 2 weeks turn into sexually mature forms, capable of further releasing eggs.
At the early stage of invasion, a pronounced allergization of the body is observed. Mature opisthorchis injure mucous membranes of the pancreatic and bile ducts, create barriers to the outflow of bile, contribute to the development of cystic enlargements and neoplasms of the liver and carry out toxic and neuro-reflex effect.
Diagnosis of opisthorchiasis according to the clinical manifestations of the disease is difficult due to the absence of symptoms and syndromes characteristic only for this disease. Therefore, it is necessary to carry out a thorough clinical, laboratory and X-ray (ultrasound inclusive) examination.
In the laboratory analysis, it is possible to detect the invasion of opisthorchis one month after the infection when helminths begin to lay eggs (ovoscopic examination of feces and duodenal juice of the patient). More significant complications arise in recognizing early phases of opisthorchiasis. However, more and more studies are being carried out to detect specific antibodies to Opisthorchis felineus by enzyme immunoassay. In the chronic stage invasion is diagnosed by detecting helminth eggs in bile and stools, as well as by ELISA. -
The test kit Vitrotest® Anti-Toxocara is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG class antibodies to Toxocara canis in human serum or plasma.
Determination of IgG antibodies to Toxocara canis in the test kit Vitrotest® Anti-Toxocara is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК058 - 96 tests
○ ТК112 - 192 tests- Solid phase: breakable microplate ELISA is coated Toxocara canis larvae antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Toxocariasis is an widespread parasitic disease of humans caused by infection with the second stage larvae of two main species of parasitic nematodes, Toxocara canis and Toxocara cati. The role of toxocaras in human disease was disclosed in the 1950th by Wilder and Beaver et al. who first identified toxocara larvae in ocular and visceral tissues respectively.
Adult worms of T. canis and T.cati live within the lumen of the small intestine of dogs and cats respectively which serve as definitive hosts for these helminths. Unembryonated eggs produced by adult worms are shed in the feces of the definitive hosts. Eggs embryonate in the environment, and could be ingested by definitive hosts as well as accidental, paratenic hosts. After ingestion by the definitive hosts, microscopic (300 µm long and 20 µm in diameter) larvae hatch in the intestine, penetrate the intestinal wall, reach lungs via bloodstream, penetrate alveolar walls, ascend the bronchial tree to the throat where they are swallowed, and mature into adult worms. In humans and other paratenic hosts, the larvae are unable to undergo the full development cycle described above; instead, they are carried by the circulation to a wide variety of organs and tissues (liver, heart, lungs, brain, muscle, eyes), and cause severe local reactions that are the basis of toxocariasis.
The degree of host damage, and the concomitant signs and symptoms, varies with regard to which tissue has been invaded; the liver, lungs, and CNS (including the eyes) appear to be most sensitive. In the eye, migrating larvae can damage the retina, inducing granulomatous reactions leading to impaired sight or even loss of sight. The number of migrating larvae and the age of the host are two additional factors defining the presence and severity of symptoms.
Lifespan of the larvae could be as long as several years, and clinical disease could present in any time during this period, or even later, representing pathological immune response to dying or dead larvae.
For most people, an infection with these helminths causes no symptoms. Possible symptoms symptoms are nonspecific and include fever, fatigue, anorexia, or lymphadenopathy. Pulmonary symptoms and abdominal symptoms are similar to those under many other diseases; they are present when larvae migrate to the lungs or abdominal organs, respectively. Neurologic findings are diverse and also nonspecific. -
The test kit Vitrotest® Anti-Trichinella is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG class antibodies to Trichinella spiralis in human serum or plasma.
Determination of IgG antibodies to Trichinella spiralis in the test kit Vitrotest® Anti-Trichinella is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК067 - 96 tests- Solid phase: breakable microplate ELISA is coated Trichinella spiralis larvae antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Trichinosis is a helminthiasis caused by a nematode Trichinella spiralis. Trichinellas are small, thread-like worms covered with a striped cuticle.
Transmission occurs by ingestion of meat containing encapsulated trichinella larvae. During digestion under the action of the gastric juice larvae release from capsules penetrate the submucosal layer of the small intestine, adhere to the mucosa and begin to proliferate. Soon after fertilization of females, the males die and the females start producing larvae, which enter the blood and lymphatic vessels through tissue mucosa, spread throughout the body and settle in striated muscles. Thereafter this capsule is impregnated with calcium salts leading to calcification. The larvae remain viable for many years.
The incubation period of human trichinosis lasts 10-25 days. Trichinosis is characterized by fever, myalgia, facial swelling, skin rash, blood eosinophilia, and in severe cases – by damage to internal organs and central nervous system.
The diagnosis of trichinosis is based on clinical signs, epidemiological history, serological tests (complement fixation tests, the reaction of indirect hemagglutination) and ELISA. The latter method is recommended by OIE for serological diagnosis of trichinosis.
The most specific and successful method to confirm infestation is the detection of IgG antibodies to trichinella antigens in the blood. These antibodies could be determined from 2-3 to 4-6 weeks after the eating of contaminated meat. Specific IgE class antibodies are also present in the blood during the acute stage of the disease, however, they are rarely detected due to the short period of their circulation in the bloodstream. During the early stage of invasion, specific antibodies might be still undetectable. Therefore, another sample should be taken in 1-2 weeks to confirm or reject suspected trichinosis. Seroconversion usually occurs 2-5 weeks after infection depending on the infectious dose. Assessment of antibody dynamics is a very informative marker of therapy effectiveness. In cases of ineffective or untimely therapy, specific antibodies are detected for up to 20 years if trichinosis is effectively treated in the first two weeks after infection, antibodies disappear within a year. -
The test kit Vitrotest® Anti-Strongyloides is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG class antibodies to Strongyloides stercoralis in human serum or plasma.
Determination of IgG antibodies to Strongyloides stercoralis in the test kit Vitrotest® Anti-Strongyloides is based on a solid phase, indirect ELISA in a two-step incubation procedure.
- ТК146 - 96 tests
- Solid phase: breakable microplate ELISA is coated Strongyloides stercoralis antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 40 min.
Strongyloidiasis is a chronic parasitic infection of humans caused by Strongyloides stercoralis. This helminth is predominantly found in tropical and subtropical regions but can also be present in temperate climates. It is estimated that approximately 300 to 600 million people worldwide are infected.
Primary infection occurs when S. stercoralis larvae penetrate human skin through direct contact with contaminated soil. The larvae migrate via the bloodstream and lymphatic system to the respiratory tract, where they are then coughed up and swallowed, reaching the intestines. In the intestines, the parasites develop into adult worms, lay eggs, and produce larvae that can be excreted in the feces. A unique feature of S. stercoralis is its ability to cause autoinfection, as larvae may re-enter the intestines or perianal skin without leaving the host, leading to persistent infection.
In immunocompetent individuals, uncomplicated strongyloidiasis may be asymptomatic or present with mild cutaneous and gastrointestinal symptoms. Often, the only sign of infection is unexplained peripheral eosinophilia. However, in cases of heavy infestation or in immunosuppressed patients, the disease can cause severe manifestations such as abdominal pain, watery diarrhea, constipation, weight loss, vomiting, or small bowel obstruction. Hyperinfection syndrome is the most severe manifestation of the disease, with high mortality rates.
Parasitological methods (microscopy, culture) are traditionally used for diagnosis. The sensitivity and specifi city of these tests, however, are not high. The standard stool examination has a sensitivity of only 21% (5). Serological methods, especially enzyme-linked immunosorbent assay (ELISA), are highly sensitive and convenient for detecting antibodies to S. stercoralis larvae. ELISA is widely used for screening, diagnosing strongyloidiasis, and monitoring treatment effi cacy, as antibody titers signifi cantly decline within the fi rst 6 months following successful eradication therapy.
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The test kit Vitrotest® Ureaplasma-IgG is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgG class antibodies to Ureaplasma urealyticum in human serum or plasma.
Determination of IgG antibodies to U.urealyticum in the test kit Vitrotest® Ureaplasma-IgG is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК028 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant antigens of U. urealyticum.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 20 μl.
- Assay time: 1h 15 min.
The microorganism Ureaplasma urealyticum causes inflammatory diseases of the human genitourinary system and Ureaplasma is often found in women with vaginitis and cystitis.
Penetration of the pathogen into the upper parts of the reproductive system can lead to the disruption of the reproductive functions. In men, U.urealyticum is the cause of nongonococcal urethritis and prostatitis (up to 50% of cases). The role of ureaplasmas in the development of most cases of urolithiasis has been proven. Often U.urealyticum leads to postpartum sepsis in women.
To diagnose ureaplasmosis, both direct methods for identifying ureaplasmas (polymerase chain reaction, immunofluorescence reaction, isolation of pure culture) and serological methods for detecting antibodies specific to Ureaplasma urealyticum are applied. Determination of antibodies in enzyme immunoassay is especially important in chronic ureaplasmosis, as well as in ascending ureaplasma infection. ELISA is a minimally invasive research method that allows for a comprehensive diagnosis of urogenital diseases. -
The test kit Vitrotest® Ureaplasma-IgA is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgA class antibodies to Ureaplasma urealyticum in human serum or plasma.
Determination of IgA antibodies to U.urealyticum in the test kit Vitrotest® Ureaplasma-IgA is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК029 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant antigens of U. urealyticum.
- Conjugate: a monoclonal antibodies to human IgA conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 20 μl.
- Assay time: 1h 15 min.
The microorganism Ureaplasma urealyticum causes inflammatory diseases of the human genitourinary system and Ureaplasma is often found in women with vaginitis and cystitis.
Penetration of the pathogen into the upper parts of the reproductive system can lead to the disruption of the reproductive functions. In men, U.urealyticum is the cause of nongonococcal urethritis and prostatitis (up to 50% of cases). The role of ureaplasmas in the development of most cases of urolithiasis has been proven. Often U.urealyticum leads to postpartum sepsis in women.
To diagnose ureaplasmosis, both direct methods for identifying ureaplasmas (polymerase chain reaction, immunofluorescence reaction, isolation of pure culture) and serological methods for detecting antibodies specific to Ureaplasma urealyticum are applied. Determination of antibodies in enzyme immunoassay is especially important in chronic ureaplasmosis, as well as in ascending ureaplasma infection. ELISA is a minimally invasive research method that allows for a comprehensive diagnosis of urogenital diseases. -
The test kit Vitrotest® Ureaplasma-IgМ is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgM class antibodies to Ureaplasma urealiticum in human serum or plasma.
Determination of IgM antibodies to Ureaplasma urealiticum in the test kit Vitrotest® Ureaplasma-IgМ is based on a solid phase, «IgM-capture» ELISA in a two-step incubation procedure.
○ ТК096 - 96 tests- Solid phase: breakable microplate ELISA is coated with monoclonal anti-IgM antibodies.
- Conjugate: recombinant U. urealiticum antigen, conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 30 min.
The microorganism Ureaplasma urealyticum causes inflammatory diseases of the human genitourinary system and Ureaplasma is often found in women with vaginitis and cystitis.
Penetration of the pathogen into the upper parts of the reproductive system can lead to the disruption of the reproductive functions. In men, U.urealyticum is the cause of nongonococcal urethritis and prostatitis (up to 50% of cases). The role of ureaplasmas in the development of most cases of urolithiasis has been proven. Often U.urealyticum leads to postpartum sepsis in women.
To diagnose ureaplasmosis, both direct methods for identifying ureaplasmas (polymerase chain reaction, immunofluorescence reaction, isolation of pure culture) and serological methods for detecting antibodies specific to Ureaplasma urealyticum are applied. Determination of antibodies in enzyme immunoassay is especially important in chronic ureaplasmosis, as well as in ascending ureaplasma infection. ELISA is a minimally invasive research method that allows for a comprehensive diagnosis of urogenital diseases. -
The test kit Vitrotest® Mycoplasma hominis-IgG is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgG class antibodies to Mycoplasma hominis in human serum or plasma.
Determination of IgG antibodies to M. hominis in the test kit Vitrotest® Mycoplasma hominis-IgG is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК024 - 96 tests- Solid phase: breakable microplate ELISA is coated with native Mycoplasma hominis antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Mycoplasmas are opportunistic pathogens, since they are often detected as part of the normal human microflora. At the same time, these microorganisms may be involved in the inflammatory process during urogenital diseases. Data on the frequency of mycoplasma spread among the population of different countries are contradictory, and infection rates vary from 10 to 80%.
Mycoplasma hominis infects primarily the organs of the genitourinary system and causes various destructive inflammatory processes. In men, M. hominis usually causes urethritis and prostatitis, and in women is provokes urethritis, cervicitis and inflammatory lesions of the pelvic organs. Urogenital mycoplasmosis in pregnant women is especially dangerous, as it can cause miscarriage, premature birth, infection of the fetus and the development of postpartum sepsis.
Clinical manifestations caused by the presence of M. hominis are often similar to symptoms of other diseases of the urogenital tract of bacterial, viral and other etiologies. Therefore, for successful diagnosis of urogenital mycoplasmosis, laboratory tests are required to differentiate them.
Serological methods for diagnosing mycoplasmosis include precipitation and immunofluorescence reactions. To detect serum antibodies to M. hominis, a passive hemagglutination reaction and an enzyme-linked immunosorbent assay are used, which makes it possible to determine the stage and nature of the disease. This is especially important in chronic disease. The presence of IgG antibodies to M. hominis reflects the overall picture of the immune response as a result of prolonged or previous infection. In the latter case, IgG may remain at low levels for many years. -
The test kit Vitrotest® Mycoplasma hominis-IgA is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgA class antibodies to Mycoplasma hominis in human serum or plasma.
Determination of IgA antibodies to M. hominis in the test kit Vitrotest® Mycoplasma hominis-IgA is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК025 - 96 tests- Solid phase: breakable microplate ELISA is coated with native Mycoplasma hominis antigens.
- Conjugate: a monoclonal antibodies to human IgA conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Mycoplasmas are opportunistic pathogens, since they are often detected as part of the normal human microflora. At the same time, these microorganisms may be involved in the inflammatory process during urogenital diseases. Data on the frequency of mycoplasma spread among the population of different countries are contradictory, and infection rates vary from 10 to 80%.
Mycoplasma hominis infects primarily the organs of the genitourinary system and causes various destructive inflammatory processes. In men, M. hominis usually causes urethritis and prostatitis, and in women is provokes urethritis, cervicitis and inflammatory lesions of the pelvic organs. Urogenital mycoplasmosis in pregnant women is especially dangerous, as it can cause miscarriage, premature birth, infection of the fetus and the development of postpartum sepsis.
Clinical manifestations caused by the presence of M. hominis are often similar to symptoms of other diseases of the urogenital tract of bacterial, viral and other etiologies. Therefore, for successful diagnosis of urogenital mycoplasmosis, laboratory tests are required to differentiate them.
Serological methods for diagnosing mycoplasmosis include precipitation and immunofluorescence reactions. To detect serum antibodies to M. hominis, a passive hemagglutination reaction and an enzyme-linked immunosorbent assay are used, which makes it possible to determine the stage and nature of the disease. This is especially important in chronic disease. The presence of IgG antibodies to M. hominis reflects the overall picture of the immune response as a result of prolonged or previous infection. In the latter case, IgG may remain at low levels for many years.
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The test kit Vitrotest® Mycoplasma hominis-IgM is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgM class antibodies to Mycoplasma hominis in human serum or plasma.
Determination of IgM antibodies to Mycoplasma hominis in the test kit Vitrotest® Mycoplasma hominis-IgM is based on a solid phase, «IgM-capture» ELISA in a two-step incubation procedure.
○ ТК097 - 96 tests- Solid phase: breakable microplate ELISA is coated with monoclonal anti-IgM antibodies.
- Conjugate: recombinant M. hominis antigen, conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 30 min.
Mycoplasmas are opportunistic pathogens, since they are often detected as part of the normal human microflora. At the same time, these microorganisms may be involved in the inflammatory process during urogenital diseases. Data on the frequency of mycoplasma spread among the population of different countries are contradictory, and infection rates vary from 10 to 80%.
Mycoplasma hominis infects primarily the organs of the genitourinary system and causes various destructive inflammatory processes. In men, M. hominis usually causes urethritis and prostatitis, and in women is provokes urethritis, cervicitis and inflammatory lesions of the pelvic organs. Urogenital mycoplasmosis in pregnant women is especially dangerous, as it can cause miscarriage, premature birth, infection of the fetus and the development of postpartum sepsis.
Clinical manifestations caused by the presence of M. hominis are often similar to symptoms of other diseases of the urogenital tract of bacterial, viral and other etiologies. Therefore, for successful diagnosis of urogenital mycoplasmosis, laboratory tests are required to differentiate them.
Serological methods for diagnosing mycoplasmosis include precipitation and immunofluorescence reactions. To detect serum antibodies to M. hominis, a passive hemagglutination reaction and an enzyme-linked immunosorbent assay are used, which makes it possible to determine the stage and nature of the disease. This is especially important in chronic disease. The presence of IgG antibodies to M. hominis reflects the overall picture of the immune response as a result of prolonged or previous infection. In the latter case, IgG may remain at low levels for many years. -
The test kit Vitrotest® Chlamydia-IgG is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgG class antibodies to Chlamydia trachomatis in human serum or plasma.
Determination of IgG antibodies to Chlamydia trachomatis in the test kit Vitrotest® Chlamydia-IgG is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК014 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant Chlamydia trachomatis antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 20 μl.
- Assay time: 1h 15 min.
Chlamydiosis is a common sexually transmitted disease (STD) caused by infection with a Gram-negative bacteria Chlamydia trachomatis. The family Chlamydiaceae contains besides C.trachomatis two important pathogenic species, C. psittaci and C.pneumoniae.
The importance of C.trachomatis as a sexually transmitted agent became apparent in the mid-1970-s, with reports of pelvic inflammatory disease (PID), endometritis and salpingitis, resulting in ectopic pregnancy and infertility, as well as conjunctivitis (paratrachoma) and pneumonia of the newborns. In men, untreated chlamydial infections can lead to urethritis and epididymoorchitis, and primarily in men, chlamydiosis is known to cause autoimmune disease, reactive arthritis. Besides these conditions, in poor developing countries C.trachomatis could cause trachoma, a specific ocular disease, which is one of the leading causes of blindness, as well as systemic sexually transmitted disease called lymphogranuloma venereum (LGV).
C.trachomatis develops in biphasic cycle. The bacterium is normally found in two highly specialized morphologic forms — the extracellular, metabolically inactive, infectious elementary body (EB) and the metabolically active, dividing, non-infective intracellular form known as reticulate body (RB). The infectious EB enters the mucosal host cells via endocytosis. Inside endosome EBs reorganize into RBs. RBs divide by binary fission, filling the endosome with hundreds of RBs. Multiplication ceases after 48 – 72 h, and RBs transform into metabolically inactive infectious EBs. The EBs are released from the cell by cell rupture or exocytosis, and target new host cells. In women, C.trachomatis infection may involve not only cervix, but also endometrium and fallopian tubes in around 10% of individuals. The disease sequelae caused by this process include PID and its complications. After PID has occurred, even with treatment, it could cause significant reproductive and gynaecological morbidity, including infertility, ectopic pregnancy, and chronic pelvic pain. In one study, 18% of women developed infertility after clinically diagnosed single episode of PID; the risk of infertility increases considerably after every new episode of PID.
Infertility or subfertility are the result of damage to the cilia lining the fallopian tubes, fallopian tube blockage or closure, or adhesion formation among pelvic organs. The issue of whether chlamydial PID is a consequence of persistent infection, immunopathology, or autoimmune reaction remains unresolved. C.trachomatis can also spread perinatally from an untreated mother to her baby during childbirth, resulting in paratrachoma, urethritis, proctitis, nasopharyngeal infection or pneumonia in many exposed infants. The risk of neonatal chlamydiosis in children born through an infected birth canal is around 15%. Conjunctival infections are detected within the first 22 days of life, eventually followed by nasopharyngeal infections and pneumonia, rectal and vaginal infections during the first several month of life.
Chlamydiosis is known as a ‘silent’ infection because most infected people, especially women, are asymptomatic and lack abnormal physical examination findings. Unfortunately, there might not be a relationship between the severity of symptoms and the severity of the disease. The symptoms of cervicitis may appear 1-3 weeks after infection, and may include mucopurulent endocervical discharge and easily induced endocervical bleeding; if cervicitis develops into PID, abdominal and/or pelvic pain could arise.
C.trachomatis is transmitted if infected secretions from urethra, cervix, rectum, conjunctivae and throat come into contact with mucous membranes of the above-mentioned organs. Chlamydiosis is usually transmitted by sex. Therefore, young people (up to 25 years) are at highest risk of acquiring chlamydiosis. In addition, an infected mother can infect her baby during vaginal delivery. C.trachomatis is grouped into 18 separate serovars, which are distinguished by the antigenic and molecular polymorphism within major outer membrane protein, OmpA. Serovars A-C infect the conjunctive epithelium and lead to ocular infections that can progress to trachoma; serovars L1-L3 are able to infect not only the genital epithelium, but also monocytes and lead to LGV; classical sexually transmitted non-LGV infections are caused by serovars D-K. Protective immunity to chlamydiosis is not absolute, being much stronger to the same serovar; therefore, reinfections are usually by the heterologous serovar. -
The test kit Vitrotest® Chlamydia-IgА is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgА class antibodies to Chlamydia trachomatis in human serum or plasma.
Determination of IgА antibodies to Chlamydia trachomatis in the test kit Vitrotest® Chlamydia-IgА is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК015 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant Chlamydia trachomatis antigens.
- Conjugate: a monoclonal antibodies to human IgА conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 20 μl.
- Assay time: 1h 15 min.
Chlamydiosis is a common sexually transmitted disease (STD) caused by infection with a Gram-negative bacteria Chlamydia trachomatis. The family Chlamydiaceae contains besides C.trachomatis two important pathogenic species, C. psittaci and C.pneumoniae.
The importance of C.trachomatis as a sexually transmitted agent became apparent in the mid-1970-s, with reports of pelvic inflammatory disease (PID), endometritis and salpingitis, resulting in ectopic pregnancy and infertility, as well as conjunctivitis (paratrachoma) and pneumonia of the newborns. In men, untreated chlamydial infections can lead to urethritis and epididymoorchitis, and primarily in men, chlamydiosis is known to cause autoimmune disease, reactive arthritis. Besides these conditions, in poor developing countries C.trachomatis could cause trachoma, a specific ocular disease, which is one of the leading causes of blindness, as well as systemic sexually transmitted disease called lymphogranuloma venereum (LGV).
C.trachomatis develops in biphasic cycle. The bacterium is normally found in two highly specialized morphologic forms — the extracellular, metabolically inactive, infectious elementary body (EB) and the metabolically active, dividing, non-infective intracellular form known as reticulate body (RB). The infectious EB enters the mucosal host cells via endocytosis. Inside endosome EBs reorganize into RBs. RBs divide by binary fission, filling the endosome with hundreds of RBs. Multiplication ceases after 48 – 72 h, and RBs transform into metabolically inactive infectious EBs. The EBs are released from the cell by cell rupture or exocytosis, and target new host cells. In women, C.trachomatis infection may involve not only cervix, but also endometrium and fallopian tubes in around 10% of individuals. The disease sequelae caused by this process include PID and its complications. After PID has occurred, even with treatment, it could cause significant reproductive and gynaecological morbidity, including infertility, ectopic pregnancy, and chronic pelvic pain. In one study, 18% of women developed infertility after clinically diagnosed single episode of PID; the risk of infertility increases considerably after every new episode of PID.
Infertility or subfertility are the result of damage to the cilia lining the fallopian tubes, fallopian tube blockage or closure, or adhesion formation among pelvic organs. The issue of whether chlamydial PID is a consequence of persistent infection, immunopathology, or autoimmune reaction remains unresolved. C.trachomatis can also spread perinatally from an untreated mother to her baby during childbirth, resulting in paratrachoma, urethritis, proctitis, nasopharyngeal infection or pneumonia in many exposed infants. The risk of neonatal chlamydiosis in children born through an infected birth canal is around 15%. Conjunctival infections are detected within the first 22 days of life, eventually followed by nasopharyngeal infections and pneumonia, rectal and vaginal infections during the first several month of life.
Chlamydiosis is known as a ‘silent’ infection because most infected people, especially women, are asymptomatic and lack abnormal physical examination findings. Unfortunately, there might not be a relationship between the severity of symptoms and the severity of the disease. The symptoms of cervicitis may appear 1-3 weeks after infection, and may include mucopurulent endocervical discharge and easily induced endocervical bleeding; if cervicitis develops into PID, abdominal and/or pelvic pain could arise.
C.trachomatis is transmitted if infected secretions from urethra, cervix, rectum, conjunctivae and throat come into contact with mucous membranes of the above-mentioned organs. Chlamydiosis is usually transmitted by sex. Therefore, young people (up to 25 years) are at highest risk of acquiring chlamydiosis. In addition, an infected mother can infect her baby during vaginal delivery. C.trachomatis is grouped into 18 separate serovars, which are distinguished by the antigenic and molecular polymorphism within major outer membrane protein, OmpA. Serovars A-C infect the conjunctive epithelium and lead to ocular infections that can progress to trachoma; serovars L1-L3 are able to infect not only the genital epithelium, but also monocytes and lead to LGV; classical sexually transmitted non-LGV infections are caused by serovars D-K. Protective immunity to chlamydiosis is not absolute, being much stronger to the same serovar; therefore, reinfections are usually by the heterologous serovar. -
The test kit Vitrotest® Chlamydia-IgМ is an enzyme linked immunosorbent assay (ELISA) for the qualitative determination of IgM class antibodies to Chlamydia trachomatis in human serum or plasma.
Determination of IgM antibodies to Chlamydia trachomatis in the test kit Vitrotest® Chlamydia-IgМ is based on a solid phase «IgM-capture» ELISA in a two-step incubation procedure.
○ ТК036 - 96 tests- Solid phase: breakable microplate ELISA is coated with monoclonal anti-IgM antibodies.
- Conjugate: recombinant antigen MOMP of Chlamydia trachomatis, conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 30 min.
Chlamydiosis is a common sexually transmitted disease (STD) caused by infection with a Gram-negative bacteria Chlamydia trachomatis. The family Chlamydiaceae contains besides C.trachomatis two important pathogenic species, C. psittaci and C.pneumoniae.
The importance of C.trachomatis as a sexually transmitted agent became apparent in the mid-1970-s, with reports of pelvic inflammatory disease (PID), endometritis and salpingitis, resulting in ectopic pregnancy and infertility, as well as conjunctivitis (paratrachoma) and pneumonia of the newborns. In men, untreated chlamydial infections can lead to urethritis and epididymoorchitis, and primarily in men, chlamydiosis is known to cause autoimmune disease, reactive arthritis. Besides these conditions, in poor developing countries C.trachomatis could cause trachoma, a specific ocular disease, which is one of the leading causes of blindness, as well as systemic sexually transmitted disease called lymphogranuloma venereum (LGV).
C.trachomatis develops in biphasic cycle. The bacterium is normally found in two highly specialized morphologic forms — the extracellular, metabolically inactive, infectious elementary body (EB) and the metabolically active, dividing, non-infective intracellular form known as reticulate body (RB). The infectious EB enters the mucosal host cells via endocytosis. Inside endosome EBs reorganize into RBs. RBs divide by binary fission, filling the endosome with hundreds of RBs. Multiplication ceases after 48 – 72 h, and RBs transform into metabolically inactive infectious EBs. The EBs are released from the cell by cell rupture or exocytosis, and target new host cells. In women, C.trachomatis infection may involve not only cervix, but also endometrium and fallopian tubes in around 10% of individuals. The disease sequelae caused by this process include PID and its complications. After PID has occurred, even with treatment, it could cause significant reproductive and gynaecological morbidity, including infertility, ectopic pregnancy, and chronic pelvic pain. In one study, 18% of women developed infertility after clinically diagnosed single episode of PID; the risk of infertility increases considerably after every new episode of PID.
Infertility or subfertility are the result of damage to the cilia lining the fallopian tubes, fallopian tube blockage or closure, or adhesion formation among pelvic organs. The issue of whether chlamydial PID is a consequence of persistent infection, immunopathology, or autoimmune reaction remains unresolved. C.trachomatis can also spread perinatally from an untreated mother to her baby during childbirth, resulting in paratrachoma, urethritis, proctitis, nasopharyngeal infection or pneumonia in many exposed infants. The risk of neonatal chlamydiosis in children born through an infected birth canal is around 15%. Conjunctival infections are detected within the first 22 days of life, eventually followed by nasopharyngeal infections and pneumonia, rectal and vaginal infections during the first several month of life.
Chlamydiosis is known as a ‘silent’ infection because most infected people, especially women, are asymptomatic and lack abnormal physical examination findings. Unfortunately, there might not be a relationship between the severity of symptoms and the severity of the disease. The symptoms of cervicitis may appear 1-3 weeks after infection, and may include mucopurulent endocervical discharge and easily induced endocervical bleeding; if cervicitis develops into PID, abdominal and/or pelvic pain could arise.
C.trachomatis is transmitted if infected secretions from urethra, cervix, rectum, conjunctivae and throat come into contact with mucous membranes of the above-mentioned organs. Chlamydiosis is usually transmitted by sex. Therefore, young people (up to 25 years) are at highest risk of acquiring chlamydiosis. In addition, an infected mother can infect her baby during vaginal delivery. C.trachomatis is grouped into 18 separate serovars, which are distinguished by the antigenic and molecular polymorphism within major outer membrane protein, OmpA. Serovars A-C infect the conjunctive epithelium and lead to ocular infections that can progress to trachoma; serovars L1-L3 are able to infect not only the genital epithelium, but also monocytes and lead to LGV; classical sexually transmitted non-LGV infections are caused by serovars D-K. Protective immunity to chlamydiosis is not absolute, being much stronger to the same serovar; therefore, reinfections are usually by the heterologous serovar. -
The test kit Vitrotest® Chlamydia-IgG/IgA is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgG and/or IgА class antibodies to Chlamydia trachomatis in human serum or plasma.
Determination of IgG and/or IgА antibodies to Chlamydia trachomatis in the test kit Vitrotest® Chlamydia-IgG/IgA is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК013 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant Chlamydia trachomatis antigens.
- Conjugate anti-IgG: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Conjugate anti-IgA: a monoclonal antibodies to human IgA conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 20 μl.
- Assay time: 1h 15 min.
Chlamydiosis is a common sexually transmitted disease (STD) caused by infection with a Gram-negative bacteria Chlamydia trachomatis. The family Chlamydiaceae contains besides C.trachomatis two important pathogenic species, C. psittaci and C.pneumoniae.
The importance of C.trachomatis as a sexually transmitted agent became apparent in the mid-1970-s, with reports of pelvic inflammatory disease (PID), endometritis and salpingitis, resulting in ectopic pregnancy and infertility, as well as conjunctivitis (paratrachoma) and pneumonia of the newborns. In men, untreated chlamydial infections can lead to urethritis and epididymoorchitis, and primarily in men, chlamydiosis is known to cause autoimmune disease, reactive arthritis. Besides these conditions, in poor developing countries C.trachomatis could cause trachoma, a specific ocular disease, which is one of the leading causes of blindness, as well as systemic sexually transmitted disease called lymphogranuloma venereum (LGV).
C.trachomatis develops in biphasic cycle. The bacterium is normally found in two highly specialized morphologic forms — the extracellular, metabolically inactive, infectious elementary body (EB) and the metabolically active, dividing, non-infective intracellular form known as reticulate body (RB). The infectious EB enters the mucosal host cells via endocytosis. Inside endosome EBs reorganize into RBs. RBs divide by binary fission, filling the endosome with hundreds of RBs. Multiplication ceases after 48 – 72 h, and RBs transform into metabolically inactive infectious EBs. The EBs are released from the cell by cell rupture or exocytosis, and target new host cells. In women, C.trachomatis infection may involve not only cervix, but also endometrium and fallopian tubes in around 10% of individuals. The disease sequelae caused by this process include PID and its complications. After PID has occurred, even with treatment, it could cause significant reproductive and gynaecological morbidity, including infertility, ectopic pregnancy, and chronic pelvic pain. In one study, 18% of women developed infertility after clinically diagnosed single episode of PID; the risk of infertility increases considerably after every new episode of PID.
Infertility or subfertility are the result of damage to the cilia lining the fallopian tubes, fallopian tube blockage or closure, or adhesion formation among pelvic organs. The issue of whether chlamydial PID is a consequence of persistent infection, immunopathology, or autoimmune reaction remains unresolved. C.trachomatis can also spread perinatally from an untreated mother to her baby during childbirth, resulting in paratrachoma, urethritis, proctitis, nasopharyngeal infection or pneumonia in many exposed infants. The risk of neonatal chlamydiosis in children born through an infected birth canal is around 15%. Conjunctival infections are detected within the first 22 days of life, eventually followed by nasopharyngeal infections and pneumonia, rectal and vaginal infections during the first several month of life.
Chlamydiosis is known as a ‘silent’ infection because most infected people, especially women, are asymptomatic and lack abnormal physical examination findings. Unfortunately, there might not be a relationship between the severity of symptoms and the severity of the disease. The symptoms of cervicitis may appear 1-3 weeks after infection, and may include mucopurulent endocervical discharge and easily induced endocervical bleeding; if cervicitis develops into PID, abdominal and/or pelvic pain could arise.
C.trachomatis is transmitted if infected secretions from urethra, cervix, rectum, conjunctivae and throat come into contact with mucous membranes of the above-mentioned organs. Chlamydiosis is usually transmitted by sex. Therefore, young people (up to 25 years) are at highest risk of acquiring chlamydiosis. In addition, an infected mother can infect her baby during vaginal delivery. C.trachomatis is grouped into 18 separate serovars, which are distinguished by the antigenic and molecular polymorphism within major outer membrane protein, OmpA. Serovars A-C infect the conjunctive epithelium and lead to ocular infections that can progress to trachoma; serovars L1-L3 are able to infect not only the genital epithelium, but also monocytes and lead to LGV; classical sexually transmitted non-LGV infections are caused by serovars D-K. Protective immunity to chlamydiosis is not absolute, being much stronger to the same serovar; therefore, reinfections are usually by the heterologous serovar. -
The test kit Vitrotest® Chlamydia pneumoniae-IgG is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgG class antibodies to Chlamydia pneumoniae in human serum or plasma.
Determination of IgG antibodies to Chlamydia pneumoniae in the test kit Vitrotest® Chlamydia pneumoniae-IgG is based on a solid phase indirect ELISA in a two-step incubation procedure.
○ ТК081 - 96 tests- Solid phase: breakable microplate ELISA is coated with Chlamydia pneumoniae antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Chlamydiosis is a common sexually transmitted disease (STD) caused by infection with a Gram-negative bacteria Chlamydia trachomatis. The family Chlamydiaceae contains besides C.trachomatis two important pathogenic species, C. psittaci and C.pneumoniae.
The importance of C.trachomatis as a sexually transmitted agent became apparent in the mid-1970-s, with reports of pelvic inflammatory disease (PID), endometritis and salpingitis, resulting in ectopic pregnancy and infertility, as well as conjunctivitis (paratrachoma) and pneumonia of the newborns. In men, untreated chlamydial infections can lead to urethritis and epididymoorchitis, and primarily in men, chlamydiosis is known to cause autoimmune disease, reactive arthritis. Besides these conditions, in poor developing countries C.trachomatis could cause trachoma, a specific ocular disease, which is one of the leading causes of blindness, as well as systemic sexually transmitted disease called lymphogranuloma venereum (LGV).
C.trachomatis develops in biphasic cycle. The bacterium is normally found in two highly specialized morphologic forms — the extracellular, metabolically inactive, infectious elementary body (EB) and the metabolically active, dividing, non-infective intracellular form known as reticulate body (RB). The infectious EB enters the mucosal host cells via endocytosis. Inside endosome EBs reorganize into RBs. RBs divide by binary fission, filling the endosome with hundreds of RBs. Multiplication ceases after 48 – 72 h, and RBs transform into metabolically inactive infectious EBs. The EBs are released from the cell by cell rupture or exocytosis, and target new host cells. In women, C.trachomatis infection may involve not only cervix, but also endometrium and fallopian tubes in around 10% of individuals. The disease sequelae caused by this process include PID and its complications. After PID has occurred, even with treatment, it could cause significant reproductive and gynaecological morbidity, including infertility, ectopic pregnancy, and chronic pelvic pain. In one study, 18% of women developed infertility after clinically diagnosed single episode of PID; the risk of infertility increases considerably after every new episode of PID.
Infertility or subfertility are the result of damage to the cilia lining the fallopian tubes, fallopian tube blockage or closure, or adhesion formation among pelvic organs. The issue of whether chlamydial PID is a consequence of persistent infection, immunopathology, or autoimmune reaction remains unresolved. C.trachomatis can also spread perinatally from an untreated mother to her baby during childbirth, resulting in paratrachoma, urethritis, proctitis, nasopharyngeal infection or pneumonia in many exposed infants. The risk of neonatal chlamydiosis in children born through an infected birth canal is around 15%. Conjunctival infections are detected within the first 22 days of life, eventually followed by nasopharyngeal infections and pneumonia, rectal and vaginal infections during the first several month of life.
Chlamydiosis is known as a ‘silent’ infection because most infected people, especially women, are asymptomatic and lack abnormal physical examination findings. Unfortunately, there might not be a relationship between the severity of symptoms and the severity of the disease. The symptoms of cervicitis may appear 1-3 weeks after infection, and may include mucopurulent endocervical discharge and easily induced endocervical bleeding; if cervicitis develops into PID, abdominal and/or pelvic pain could arise.
C.trachomatis is transmitted if infected secretions from urethra, cervix, rectum, conjunctivae and throat come into contact with mucous membranes of the above-mentioned organs. Chlamydiosis is usually transmitted by sex. Therefore, young people (up to 25 years) are at highest risk of acquiring chlamydiosis. In addition, an infected mother can infect her baby during vaginal delivery. C.trachomatis is grouped into 18 separate serovars, which are distinguished by the antigenic and molecular polymorphism within major outer membrane protein, OmpA. Serovars A-C infect the conjunctive epithelium and lead to ocular infections that can progress to trachoma; serovars L1-L3 are able to infect not only the genital epithelium, but also monocytes and lead to LGV; classical sexually transmitted non-LGV infections are caused by serovars D-K. Protective immunity to chlamydiosis is not absolute, being much stronger to the same serovar; therefore, reinfections are usually by the heterologous serovar. -
The test kit Vitrotest® Trichomonas-IgG is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgG class antibodies to Trichomonas vaginalis in human serum or plasma.
Determination of IgG antibodies to Trichomonas vaginalis in the test kit Vitrotest® Trichomonas-IgG is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК061 - 96 tests- Solid phase: breakable microplate ELISA is coated with Trichomonas vaginalis antigens.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
The flagellated protozoan Trichomonas vaginalis is the etiologic agent of one of the most common sexually transmitted diseases in the world. On average, 25% of sexually active individuals are infected with T. vaginalis. According to the latest data, more than 170 million cases of trichomoniasis are reported worldwide each year.
In women, trichomonads cause acute and subacute vaginitis, with symptoms including frothy discharge, itching, and lower abdominal pain. The disease is cyclical – these symptoms subside during menstruation and pregnancy. During pregnancy, trichomoniasis can lead to premature birth and low birth weight in infants. In men, T. vaginalis typically causes urethritis, prostatitis, epididymitis, and dysuria. In most cases, the disease is asymptomatic. The mild symptoms in men are attributed to the flushing out of a significant portion of trichomonads from the urogenital tract during urination. The latent nature of the disease often leads to an underestimation of its spread. Chronic infection almost always results in chronic prostatitis. Trichomoniasis has also been associated with the development of prostate cancer in men.
Currently, the following laboratory methods are used to diagnose trichomoniasis:- microscopy of vaginal or cervical secretions in women and urinary tract secretions in men;
- culture of trichomonads;
- detection of pathogen DNA by polymerase chain reaction (PCR);
- detection of antibodies specific to T. vaginalis by enzyme-linked immunosorbent assay (ELISA).
According to several studies, the sensitivity of direct parasite detection methods ranges from 38% to 82%. It is also known that infected individuals develop a humoral, secretory, and cellular immune response to the parasite, which allows for the use of serological studies for diagnostic purposes. Antibodies to the trichomonad surface antigen p270 and α-actinin are produced in almost all infected individuals, and serum antibody levels correlate with active infection. Serological diagnostic methods are particularly valuable in individuals who do not exhibit clinical manifestations of trichomoniasis and in men who may be asymptomatic carriers of the parasite. -
The test-kit Vitrotest® Helicobacter screen is an enzyme linked immunosorbent assay (ELISA) for the detection of IgG, IgA and IgM specific antibodies to Helicobacter pylori in human serum or plasma.
Detection of antibodies to H. pylori in the test-kit Vitrotest® Helicobacter screen is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК045 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant antigens of H. pylori.
- Conjugate: a monoclonal antibodies to human IgA, IgG and IgM conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.
Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.
Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.
The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.
Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.
H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries. -
The test kit Vitrotest® Helicobacter-IgG is an enzyme linked immunosorbent assay (ELISA) for the quantitative and semiquantitative determination of IgG class antibodies to CagA protein of Helicobacter pylori in human serum or plasma.
Determination of IgG antibodies to CagA protein of H. pylori in the test kit Vitrotest® Helicobacter-IgG is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК046 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant CagA protein of H. pylori.
- Conjugate: a monoclonal antibodies to human IgG conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.
Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.
Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.
The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.
Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.
H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries. -
The test kit Vitrotest® Helicobacter-IgА is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgА class antibodies to CagA protein of Helicobacter pylori in human serum or plasma.
Determination of IgА antibodies to CagA protein of H. pylori in the test kit Vitrotest® Helicobacter-IgА is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК047 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant CagA protein of H. pylori.
- Conjugate: a monoclonal antibodies to human IgА conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.
Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.
Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.
The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.
Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.
H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries. -
The test kit Vitrotest® Helicobacter-IgМ is an enzyme linked immunosorbent assay (ELISA) for the qualitative and semiquantitative determination of IgМ class antibodies to CagA protein of Helicobacter pylori in human serum or plasma.
Determination of IgМ antibodies to CagA protein of H. pylori in the test kit Vitrotest® Helicobacter-IgМ is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК048 - 96 tests- Solid phase: breakable microplate ELISA is coated with recombinant CagA protein of H. pylori.
- Conjugate: a monoclonal antibodies to human IgМ conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Helicobacter pylori is a widespread microorganism with which the half of the world’s population has been infected. Its prevalence is very high in developing countries and is quite low in the developed world. According to the World Gastroenterology Organization, the rate of infected adults in Eastern Europe and Asia is about 70-80 %.
Studies during recent decades have shown the key role of bacterium Helicobacter pylori in the pathogenesis of stomach and duodenal lesions. H. pylori is detected almost in 100% of adult patients with duodenal ulcer, approximately in 80 % of patients with peptic ulcer, in 92% of patients with gastric cancer and in 92 % of patients with active chronic gastritis. Research has demonstrated that elimination of helicobacter leads to the disappearance of gastritis and significant reduction in the incidence of duodenal ulcer recurrence.
Helicobacteriosis is a chronic infection with long, often asymptomatic course. Its symptoms do not differ from clinical manifestations of gastro-duodenitis since usual constant pain in the epigastrium occurs. H. pylori is often present in patients with no clinical manifestations of disease.
The infection usually starts from non–acid-secreting antral region of the stomach and stimulates the increased release of gastrin. The increased gastrin levels in turn stimulate excess acid secretion from the more proximal acid-secreting fundic mucosa which is relatively free of inflammation. The increased duodenal acid load damages the duodenal mucosa, causing ulceration. If infection progresses, stomach body is damaged, which could finally cause the development of gastric adenocarcinoma. This tumour is preceded by sequential pathological changes of gastric mucosa, from normal mucosa to superficial gastritis, atrophic gastritis, gastric ulcers and intestinal metaplasia.
Main oncogenic factors are both nitrosating bacteria present in the lumen of hypochloric stomach, capable of generating potentially carcinogenic N-nitrosamines and reactive oxygen species, and H. pylori itself. Duodenal or gastric ulcers are reported to develop in 1 to 10% of infected patients, gastric cancer- in 0.1 to 3%; at the same time, the great majority of patients with H. pylori remain asymptomatic carriers.
H. pylori is usually acquired in childhood. The bacteria are most likely spread through fecal-oral or oral-oral routes from person to person; additional transmission routes, such as water, may be important in developing countries. -
The test kit Vitrotest® Anti-Lamblia is an enzyme linked immunosorbent assay (ELISA) for the detection of total antibodies to Giardia lamblia (intestinalis) in human serum or plasma.
Determination of total antibodies to Giardia lamblia in the test kit Vitrotest® Anti-Lamblia is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК030 - 96 tests
○ ТК108 - 192 tests- Solid phase: breakable microplate ELISA is coated Giardia lamblia purified antigens.
- Conjugate: a monoclonal antibodies to human IgG, IgA and IgM conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis 10 μl.
- Assay time: 1h 15 min.
Giardia lamblia (intestinalis) causes giardiasis, a parasitic infestation that can manifest as latent parasitic carriage or in more pronounced forms, such as intestinal dysfunction. Giardiasis has been recorded on all five continents and in most countries worldwide. Infection rates vary from less than 1% to 50%. In many developing countries, where basic sanitary conditions are lacking, infection with Giardia in children by the age of 2 is almost universal. In contrast, in developed countries, the infection rate of G.lamblia is only 3–7%. The disease affects all age groups, but preschool-aged children are the most affected demographic.
The primary route of transmission for G.lamblia is fecal-oral. The parasite has a simple two-stage life cycle. After the host ingests cysts, they release trophozoites in the duodenum, which then attach to the mucosal lining of the small intestine.
Trophozoites exist only on the surface of the mucosa in the upper part of the small intestine. Therefore, Giardia mechanically blocks the mucosa and disrupts membrane digestion and the motor activity of the small intestine. Giardia impairs the absorption of fats, carbohydrates, vitamins C and B12, and leads to secondary bacterial infections. Symptoms of giardiasis can include diarrhea, fatigue, bloating, apathy, weight loss, decreased appetite, pallor, and muscle twitching. From the gastrointestinal tract perspective, giardiasis mainly manifests as enterocolitis with catarrhal symptoms.
Numerous findings indicate the role of the humoral immune response in the elimination of G.lamblia. As shown in an experimental human infection model, IgM antibody levels significantly increased on days 14-21 post-infection and gradually declined following therapy. In contrast, IgG antibody levels remained elevated after successful treatment. The dynamics of IgA levels were similar to those of IgM.
The diagnosis of giardiasis is based on clinical history, symptoms, and the presence of cysts in fecal samples or trophozoites in material obtained from the small intestine during duodenal aspiration or duodenal biopsy. Alternative methods include the detection of G.lamblia antigen in feces and the determination of specific antibodies against Giardia in the patient’s serum. Serological testing is considered a valuable adjunct in the diagnosis of giardiasis. In addition to aiding in diagnosis, it can be useful for assessing the patient’s immune response and for epidemiological studies. -
The test kit Vitrotest® Lamblia-IgM is an enzyme linked immunosorbent assay (ELISA) for the detection of IgM class antibodies to Giardia lamblia (intestinalis) in human serum or plasma.
Determination of IgM antibodies to Giardia lamblia in the test kit Vitrotest® Lamblia-IgM is based on a solid phase, indirect ELISA in a two-step incubation procedure.
○ ТК031 - 96 tests- Solid phase: breakable microplate ELISA is coated Giardia lamblia purified antigens.
- Conjugate: a monoclonal antibodies to human IgM conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis 10 μl.
- Assay time: 1h 15 min.
Giardia lamblia (intestinalis) causes giardiasis, a parasitic infestation that can manifest as latent parasitic carriage or in more pronounced forms, such as intestinal dysfunction. Giardiasis has been recorded on all five continents and in most countries worldwide. Infection rates vary from less than 1% to 50%. In many developing countries, where basic sanitary conditions are lacking, infection with Giardia in children by the age of 2 is almost universal. In contrast, in developed countries, the infection rate of G.lamblia is only 3–7%. The disease affects all age groups, but preschool-aged children are the most affected demographic.
The primary route of transmission for G.lamblia is fecal-oral. The parasite has a simple two-stage life cycle. After the host ingests cysts, they release trophozoites in the duodenum, which then attach to the mucosal lining of the small intestine.
Trophozoites exist only on the surface of the mucosa in the upper part of the small intestine. Therefore, Giardia mechanically blocks the mucosa and disrupts membrane digestion and the motor activity of the small intestine. Giardia impairs the absorption of fats, carbohydrates, vitamins C and B12, and leads to secondary bacterial infections. Symptoms of giardiasis can include diarrhea, fatigue, bloating, apathy, weight loss, decreased appetite, pallor, and muscle twitching. From the gastrointestinal tract perspective, giardiasis mainly manifests as enterocolitis with catarrhal symptoms.
Numerous findings indicate the role of the humoral immune response in the elimination of G.lamblia. As shown in an experimental human infection model, IgM antibody levels significantly increased on days 14-21 post-infection and gradually declined following therapy. In contrast, IgG antibody levels remained elevated after successful treatment. The dynamics of IgA levels were similar to those of IgM.
The diagnosis of giardiasis is based on clinical history, symptoms, and the presence of cysts in fecal samples or trophozoites in material obtained from the small intestine during duodenal aspiration or duodenal biopsy. Alternative methods include the detection of G.lamblia antigen in feces and the determination of specific antibodies against Giardia in the patient’s serum. Serological testing is considered a valuable adjunct in the diagnosis of giardiasis. In addition to aiding in diagnosis, it can be useful for assessing the patient’s immune response and for epidemiological studies. -
The test kit Vitrotest® PSA Total is an enzyme linked immunosorbent assay (ELISA) for the quantitative determination of total prostate-specific antigen (PSA) in human serum or plasma.
Determination of concentration total PSA in the test kit Vitrotest® PSA Total is based on on a solid-phase "sandwich" ELISA.
○ ТК104 - 96 tests- Solid phase: breakable microplate ELISA is coated with monoclonal antibodies specific to human PSA.
- Conjugate: a monoclonal antibodies to human PSA conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
In developed countries, prostate cancer ranks second in mortality from malignant diseases among men. According to WHO data, in 2020, prostate cancer mortality in Ukraine reached 4,219 cases.
A valuable biomarker for prostate cancer, which is now widely used for population screening, diagnosis, and monitoring of patients with prostate cancer, is the prostate-specific antigen (PSA). Screening for this tumor marker was introduced in the 1990s in the USA, Canada, Japan, and the UK, where a subsequent trend of decreased prostate cancer mortality has been observed.
Prostate-specific antigen is a glycoprotein produced by the epithelial cells of the prostate gland, the urethral mucosa, and the Cowper’s glands. PSA is secreted into the seminal fluid, ensuring semen liquefaction, but is typically found in very low concentrations in the blood. In blood serum, PSA is present in various forms: complexed with α1-antichymotrypsin (70-90%), free PSA not bound to serum proteins (10-30%), and bound to alpha-2-macroglobulin.
In men’s blood serum, the normal concentration of total PSA does not exceed 4 ng/ml. Elevated levels of this tumor marker may indicate a risk of prostate cancer. According to the American Cancer Society, the likelihood of prostate cancer with serum total PSA levels of 4-10 ng/ml is 25%, while with concentrations above 10 ng/ml, this figure approaches 50%. An increase in PSA levels can also be observed with prostate hypertrophy and prostatitis. Therefore, when elevated serum PSA levels are detected, a digital rectal examination (DRE) of the prostate is recommended to differentiate pathological conditions.
For laboratory identification of prostate cancer, the measurement of total and free prostate-specific antigen in blood serum is used. When PSA concentration is in the range of 4 to 10 ng/ml, determining the percentage of free PSA can be helpful in deciding whether a prostate biopsy is necessary. Typically, a biopsy is recommended when the percentage of free PSA is below 10%, although some doctors consider a threshold level of 25%.
The serum PSA level is an informative marker not only for screening patients for prostate cancer but also for monitoring treatment effectiveness and prognosis after surgical intervention. -
The test kit Vitrotest® PSA Free is an enzyme linked immunosorbent assay (ELISA) for the quantitative determination of free prostate-specific antigen (PSA) in human serum or plasma.
Determination of concentration free PSA in the test kit Vitrotest® PSA Free is based on on a solid-phase "sandwich" ELISA followed by the use of biotin-streptavidin interaction.
○ ТК105 - 96 tests- Solid phase: breakable microplate ELISA is coated with monoclonal antibodies specific to human PSA.
- Biotinylated anti-PSA antibody solution: biotinylated monoclonal antibodies to human PSA.
- Streptavidin-HRP conjugate: streptavidin solution conjugated with horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 25 μl.
- Assay time: 1 hour.
In developed countries, prostate cancer ranks second in mortality from malignant diseases among men. According to WHO data, in 2020, prostate cancer mortality in Ukraine reached 4,219 cases.
A valuable biomarker for prostate cancer, which is now widely used for population screening, diagnosis, and monitoring of patients with prostate cancer, is the prostate-specific antigen (PSA). Screening for this tumor marker was introduced in the 1990s in the USA, Canada, Japan, and the UK, where a subsequent trend of decreased prostate cancer mortality has been observed.
Prostate-specific antigen is a glycoprotein produced by the epithelial cells of the prostate gland, the urethral mucosa, and the Cowper’s glands. PSA is secreted into the seminal fluid, ensuring semen liquefaction, but is typically found in very low concentrations in the blood. In blood serum, PSA is present in various forms: complexed with α1-antichymotrypsin (70-90%), free PSA not bound to serum proteins (10-30%), and bound to alpha-2-macroglobulin.
In men’s blood serum, the normal concentration of total PSA does not exceed 4 ng/ml. Elevated levels of this tumor marker may indicate a risk of prostate cancer. According to the American Cancer Society, the likelihood of prostate cancer with serum total PSA levels of 4-10 ng/ml is 25%, while with concentrations above 10 ng/ml, this figure approaches 50%. An increase in PSA levels can also be observed with prostate hypertrophy and prostatitis. Therefore, when elevated serum PSA levels are detected, a digital rectal examination (DRE) of the prostate is recommended to differentiate pathological conditions.
For laboratory identification of prostate cancer, the measurement of total and free prostate-specific antigen in blood serum is used. When PSA concentration is in the range of 4 to 10 ng/ml, determining the percentage of free PSA can be helpful in deciding whether a prostate biopsy is necessary. Typically, a biopsy is recommended when the percentage of free PSA is below 10%, although some doctors consider a threshold level of 25%.
The serum PSA level is an informative marker not only for screening patients for prostate cancer but also for monitoring treatment effectiveness and prognosis after surgical intervention. -
The test kit Vitrotest® HE4 is an enzyme linked immunosorbent assay (ELISA) for the quantitative determination of antigen HE4 in human serum or plasma.
Determination of concentration antigen HE4 in the test kit Vitrotest® HE4 is based on a solid-phase “sandwich” ELISA.
○ ТК107 - 96 tests
- Solid phase: breakable microplate ELISA is coated with monoclonal antibodies specific to antigen HE4.
- Conjugate: a monoclonal antibodies to antigen HE4 conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
Ovarian cancer ranks as the second leading cause of cancer-related deaths among women worldwide. Only about 20% of ovarian cancer cases are detected at an early stage. When ovarian cancer is diagnosed at an early stage, approximately 94% of patients survive longer than five years after diagnosis. However, more than 70% of cases are diagnosed at an advanced stage, which significantly worsens the prognosis.
For the detection of ovarian cancer in patients without symptoms, two screening tests are most commonly used: transvaginal ultrasound and a blood test for the CA125 tumor marker. However, elevated CA125 levels can be found in 1-2% of healthy women and in patients with other conditions and diseases, including the first trimester of pregnancy, menstruation, endometriosis, uterine fibroids, acute salpingitis, liver disease, and peritonitis. To improve the sensitivity and specificity of laboratory diagnostic tools in patients with benign tumors, the combined determination of serum levels of two tumor markers, CA125 and HE4, is currently used.
HE4 (Human Epididymis Protein 4) is a secretory low-molecular-weight glycoprotein predominantly expressed in the epithelial cells of the fallopian tube, as well as normally in the epithelium of the mammary glands, reproductive system organs, intestines, and lungs. Although the physiological functions of this protein have not been fully studied, overexpression of HE4 is observed in serous and endometrioid ovarian carcinomas. Elevated levels of this tumor marker are found both in the early stages of ovarian cancer and in endometrial cancer. Unlike CA125, HE4 levels do not increase in endometriosis, benign gynecological diseases, or ovarian cysts.
The serum level of HE4 is an informative marker not only for screening patients for ovarian cancer but also as an important prognostic marker. High concentrations of HE4 in plasma are an independent preoperative marker of poor prognosis for ovarian cancer patients.
To improve the assessment of laboratory tests, the Risk of Ovarian Malignancy Algorithm (ROMA) was developed, which is a mathematical model that analyzes HE4 in combination with CA125, taking into account the patient’s menopausal status. The ROMA algorithm allows for a high probability of distinguishing malignant tumors from benign neoplasms in postmenopausal women. -
The test kit Vitrotest® 25-OH Vitamin Dis an enzyme linked immunosorbent assay (ELISA) for the quantitative determination of total 25-OH vitamin D (25-OH vitamin D2 and 25-OH vitamin D3) in human serum or plasma.
Determination of total 25-OH vitamin D concentration in the test kit Vitrotest® 25-OH Vitamin D is based on a competitive ELISA with a two-step incubation.
○ TK122 - 96 tests
○ TK124 - 192 tests- Solid phase: a stripped ELISA plate with wells pre-coated with monoclonal antibodies specific to 25-OH vitamin D.
- Biotinylated 25-OH vitamin D solution: biotinylated 25-OH vitamin D.
- Streptavidin-HRP conjugate: streptavidin conjugated with horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 µl.
- Assay time: 1 h 30 min.
Vitamin D is a fat-soluble steroid prohormone, whose active form is involved in the metabolism of phosphorus and calcium in the human body. Vitamin D, which is produced in the skin (D3, cholecalciferol) or obtained from food (D2, ergocalciferol), is biologically inert and requires two successive hydroxylations. First, 25-OH vitamin D (D2 and D3) is formed in the liver, which, in complex with a binding protein (vitamin D binding protein, VDBP), enters the bloodstream and is transported to the kidneys, where it is converted into the biologically active form 1,25-(OH)2 vitamin D and other metabolites whose roles are still being studied.
25-OH vitamin D is the main storage form of vitamin D in the human body and is present in the blood at much higher concentrations than its active form, 1,25-(OH)2 vitamin D. Its half-life is 2–3 weeks compared to 4-6 hours for 1,25-(OH)2 vitamin D. Additionally, the level of 1,25-(OH)2 vitamin D in serum does not provide information about the vitamin D status and is often normal or even elevated due to secondary hyperparathyroidism associated with vitamin D deficiency. For this reason, 25-OH vitamin D is the analyte of choice for determining the body’s vitamin D status.
According to the literature, the concentration of 25-OH vitamin D in human serum (plasma) within the range of 30-100 ng/ml is sufficient to support all necessary processes in the body that require vitamin D. Most experts consider a level of 25-OH vitamin D < 20 ng/ml to indicate vitamin D deficiency, while 20-30 ng/ml is considered an insufficient level. In Ukraine, only 3.3% of the population have a normal level of vitamin D, 14.9% have an insufficient level, and 81.8% live with its deficiency.
Hypovitaminosis D is widespread in the human population due to minimal exposure to sunlight and low dietary intake of vitamin D. As a result, vitamin D deficiency leads to secondary hyperparathyroidism, followed by loss of bone mass and osteoporosis. There is also evidence that vitamin D deficiency may have other adverse health effects, including an increased risk of malignant neoplasms, cardiovascular diseases, multiple sclerosis, diabetes, and more.
Currently, the reference method for determining the concentration of 25-OH vitamin D is tandem liquid chromatography with mass spectrometry (LC-MS/MS). However, in routine laboratory practice, this method is impractical due to its complexity and the need for specialized personnel. Therefore, immunoassay and immunochemiluminescent methods for determining 25-OH vitamin D have gained widespread use in diagnostic laboratories. -
The test kit Vitrotest® Total-IgE is an enzyme linked immunosorbent assay (ELISA) for the quantitative determination of total immunoglobulin E (IgE) in human serum or plasma.
Determination of total IgE content in the test kit Vitrotest® Total-IgE is based on a solid-phase “sandwich” ELISA.
○ ТК070 - 96 tests- Solid phase: breakable microplate ELISA is coated with monoclonal antibodies specific to human IgE.
- Conjugate: a monoclonal antibodies to human IgЕ conjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 10 μl.
- Assay time: 1h 15 min.
According to the World Health Organization, 10-20 % of the world’s population suffers from allergic bronchial asthma, allergic rhinitis, atopic dermatitis and other allergic reactions, moreover, the number of such patients increases every year. According to statistics, from 5 to 15% of children have food allergies, which further leads to the development of various allergic diseases.
Allergy or hypersensitivity is a state of altered reactivity of the body in the form of its increased sensitivity to repeated exposure of substances called allergens. As a result of repeated contact with the allergen, an excessively strong immune reaction of the body occurs, accompanied by tissue damage. One of the mechanisms underlying this process is mast cell degranulation mediated by immunoglobulin class E (IgE). According to the literature data, in an adult, the normal concentration of IgE can reach 100 IU/ml and decreases in the elderly. During allergy the IgE level can rise to 2000 IU/ml and above.
Among often diseases that accompanied by an increase in total IgE in the blood, as well as the presence of specific IgE are allergic rhinitis, atopic bronchial asthma, atopic dermatitis, urticaria, aspergillosis and helminthiases, etc. Less common diseases with hyper-IgE syndrome include congenital immunodeficiencies (Job syndrome, DiGeorge syndrome), selective IgA deficiency, WiskottAldridge syndrome and IgEmyeloma. Also, in clinical practice, there are often cases of elevated IgE levels associated with the action of several medications.
Nowadays, the methods of in vitro allergy diagnostics are becoming increasingly popular, one of which is ELISA for the determination of the total IgE content. This method is characterized by several advantages: it has no contraindications to the test, it does not cause additional sensitization and there is no risk of anaphylactic reactions. Most test systems are based on the «sandwich» ELISA, in which the use of monoclonal antibodies to human immunoglobulins E provides high sensitivity and specificity of the analysis. Standardization of the quantitative determination of IgE in human serum or plasma is ensured by using for the manufacture of internal calibrators ELISA kits of the WHO International Standard with an established concentration of human IgE in international units IU/ml.
Since the ELISA method is a highly sensitive and specific analysis and has no contraindications for its application, it can be widely used for the diagnosis of allergic diseases. -
The test kit Vitrotest® Specific-IgE is an enzyme linked immunosorbent assay (ELISA) for the quantitative determination of specific IgE class antibodies in human serum or plasma. The test kit is used together with biotinylated allergens Vitrotest® XX-Biotin, where XX is a code of relevant allergen or mixture.
Quantitative determination of specific IgE antibodies in the Vitrotest® Specific-IgE test kit is based on the principle of capturing IgE antibodies followed by the use of biotin-streptavidin interaction.
○ ТК071 - 192 tests- Solid phase: breakable microplate ELISA is coated with monoclonal antibodies specific to human IgE.
- Biotinylated anti-IgE: biotinylated anti-IgE antibodies.
- Conjugate streptavidin-HRP: streptavidin сonjugated to horseradish peroxidase.
- Chromogen: ready to use TMB solution.
- Volume of sample for analysis: 50 μl.
- Assay time: 1h 30 min.
Allergic diseases are among the most common diseases in the world and the severity of these conditions continues to increase. Allergy, or hypersensitivity, is a state of altered reactivity of the body in the form of increased sensitivity to repeated exposure to substances called allergens. As a result of repeated contact with the allergen, an excessively strong immune reaction of the body occurs, accompanied by tissue damage. One mechanism underlying this process is immunoglobulin E (IgE)-mediated mast cell degranulation.
The most common allergic conditions that require proper diagnosis are: anaphylaxis, allergic rhinitis, allergic conjunctivitis, bronchial asthma, etc. Accurate diagnosis coupled with optimal therapy requires the use of appropriate tests to confirm sensitization to a specific allergen and detailed information about the effect of the suspected allergen.
To diagnose in vivo allergies, several types of skin tests are used (skin prick test, intradermal test, patch test). However, the use of these samples has a number of significant limitations, namely, the need for a highly qualified doctor conducting the test and the lack of laboratories conducting these studies. In addition, in vivo diagnosis is rarely performed in children due to possible adverse reactions.
However, in vitro diagnostics of IgE-mediated allergic diseases are useful for identifying the causative allergen and usually include the following laboratory approaches:
1) determination of the level of total IgE;
2) study of the concentration of specific IgE to various allergens - is the most commonly used in vitro
diagnostic approach, performed using a single or multiplex strategy;
3) basophil activation test (BAT), which is quite specific, but difficult to perform, and therefore limited to selected situations.
Today, to detect specific antibodies of the IgE class, the enzyme-linked immunosorbent assay method, which provides high sensitivity and specificity, has become widely used. A separate supply of a wide range of biotinylated allergens, depending on the needs of the diagnostic laboratory, ensures maximum convenience and cost-effectiveness of the study. -
The Vitrotest® Total-IgG immunodiffusion kit is designed for the quantitative determination of total immunoglobulin G (IgG) in human serum or plasma by radial immunodiffusion in a Mancini technique.
The determination of IgG antibodies in the Vitrotest® Total-IgG immunodiffusion kit is based on an immunoprecipitation reaction. Immunoglobulins of the test sample diffuse in a semi-solid agarose gel containing immune polyclonal serum and form a precipitation ring when equivalent concentrations are reached. The diameter of the ring depends on the concentration of IgG. Comparison with the control allows to determine the concentration of immunoglobulins in the tested serum.
○ TK100 - 70 tests- Immunodiffusion medium - ready-to-use agar gel with wells containing highly specific to human IgG immune serum.
- Control - is a mixture of purified human immunoglobulins of classes G, A, and M with known concentrations.
- The volume of sample for analysis - 3 μL.
- Assay time - 24 hours.
Immunoglobulins (antibodies) are a group of glycoproteins found in mammalian plasma and tissue fluid. Five classes of immunoglobulins are found in humans - IgG, IgA, IgM, IgD, and IgE - which differ in function, molecular size, charge, and carbohydrate content.
IgG is the main isotype of immunoglobulins in normal human serum, comprising for 70-75% of the total amount of serum immunoglobulins. Its concentration normally ranges from 6.0 to 16.0 g/L. Class G immunoglobulins are major class of antibodies of the secondary immune response, they are synthesized for a longer time after an antigenic stimulus and have the unique property of initiating anti- and pro-inflammatory reactions. Antibodies of this class bind also soluble antigens, so they are the main part of antitoxins. In humans, IgG is transported from mother to fetus across the placenta, creating passive immunity for the neonatal period. Excessive production of immunoglobulins G may be associated with an active infectious process, certain types of immunoproliferative diseases, or other conditions that lead to hyperstimulation of B-cell clones that produce IgG. IgG deficiency can be primary (congenital), which is rare, or secondary (acquired), caused by factors that suppress humoral immunity.
To determine the content of total human IgG in diagnostic laboratories, the radial immunodiffusion (RID) method is widely used, which is considered the standard for measuring of different classes immunoglobulins in human serum and plasma. -
The Vitrotest® Total-IgA immunodiffusion kit is designed for the quantitative determination of total immunoglobulin A (IgA) in human serum or plasma by radial immunodiffusion in a Mancini technique.
The determination of IgA antibodies in the Vitrotest® Total-IgA immunodiffusion kit is based on the immunoprecipitation reaction. Immunoglobulins of the test serum diffuse in a semi-solid agar gel containing immune polyclonal serum and form a precipitation ring when equivalent concentrations are reached. The diameter of the ring depends on the concentration of IgA. Comparison with the control allows to determine the concentration of immunoglobulins in the tested serum.
○ TK101 - 70 tests- Immunodiffusion medium - ready-to-use agar gel with wells containing highly specific immune serum to human IgA.
- Control - a mixture of purified polyclonal antibodies of classes G, A, and M of human with known concentrations.
- Sample volume for analysis - 3 µL.
- Analysis time - 24 hours.
Immunoglobulins (antibodies) are a group of glycoproteins found in the blood plasma and tissue fluid of mammals. Five classes of immunoglobulins are found in humans - IgG, IgA, IgM, IgD, and IgE - which differ in molecular size, charge, and carbohydrate content.
IgA presents in two forms - serum and secretory, in serum comprise up 15% of all immunoglobulins, and can be both in monomeric form and as a dimer. Its concentration in normal ranges from 0,8 to 3,0 g/L. Serum immunoglobulin A can activate complement in an alternative pathway and neutralize microbes and toxins circulating in the blood, but its action is weaker than secretory IgA.
Secretory IgA neutralizes bacterial toxins, localizes viruses, and stimulates phagocytosis, providing local resistance to infection. An increased IgA concentration is observed in many inflammatory diseases: acute and chronic bacterial, fungal, parasite infection, chronic liver disease, and cirrhosis. A reduced IgA level is observed at physiologic hypogammaglobulinemia in children (at the age of 3-5 months), congenital hypogammaglobulinemia or agammaglobulinemia, neoplasms of the immune system, treatment with cytostatics and immunosuppressants.
To determine the content of total human IgA in diagnostic laboratories, the radial immunodiffusion (RID) method is widely used, which is considered the standard for measuring of different classes immunoglobulins in human serum and plasma.
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The Vitrotest® Total-IgM immunodiffusion kit is designed for the quantitative determination of total immunoglobulin M (IgM) in human serum or plasma by radial immunodiffusion in a Mancini technique.
The determination of IgA antibodies in the Vitrotest® Total-IgA immunodiffusion kit is based on an immunoprecipitation reaction. Immunoglobulins of the test serum diffuse in a semi-solid agarose gel containing immune polyclonal serum and form a precipitation ring when equivalent concentrations are reached. The diameter of the ring depends on the concentration of IgM. Comparison with the control allows the concentration of immunoglobulins in the test serum to be determined.
○ TK102 - 70 tests- Immunodiffusion medium - ready-to-use agar gel with wells containing highly specific human IgM immune serum.
- Control - a mixture of purified polyclonal antibodies of classes G, A, and M with known concentrations.
- Sample volume for analysis - 3 μL.
- Analysis time - 48 hours.
Immunoglobulins (antibodies) are a group of glycoproteins found in mammalian plasma and tissue fluid. In humans, as well as in most higher mammals, five classes of immunoglobulins are found - IgG, IgA, IgM, IgD, and IgE - which differ in molecular size, charge, and carbohydrate content.
IgM is the first immunoglobulin to be synthesized in response to primary antigenic stimulation and is a marker of the primary immune response. The high avidity of IgM antibodies makes them particularly effective at binding antigens present at low levels and non-protein antigens, such as carbohydrates or lipids, present on microbial surfaces. A very important property of IgM is the activation of phagocytosis. Polyreactive “natural” IgM, which is detected in human serum starting from the 20th week of pregnancy, plays an important role in the innate defense against infectious pathogens. The content of IgM is 5-10% of all serum immunoglobulins. Normally, the concentration of M-class immunoglobulins in the blood ranges from 0.4 to 2.5 g/L. Elevated IgM level is observed in acute and chronic infections, rheumatoid arthritis, acute and chronic lymphocytosis, myeloma, Waldenström's macroglobulinemia, endothelioma, osteosarcoma, candidiasis, and cystic fibrosis. Also, a significant increase in the amount of IgM occurs in hyperimmunoglobulinemia M.
Decreased IgM concentration is observed at physiological hypogammaglobulinemia in children (aged 3-5 months), congenital hypogammaglobulinemia or agammaglobulinemia, neoplasms of the immune system, treatment with cytostatics and immunosuppressants, and ionizing radiation exposure. To determine the content of total human IgM in diagnostic laboratories, the radial immunodiffusion (RID) method is widely used, which is considered the standard for measuring of different classes immunoglobulins in human serum and plasma. -
Biotinylated allergens Vitrotest® XX-Biotin for the quantitative determination of specific IgE class antibodies in human serum or plasma. It is used exclusively with the
Vitrotest® Specific-IgE test kit.
○ 1 vial - 30 testsBiotinylated allergens Vitrotest® XX-Biotin, where XX is the code of the relevant allergen or mixture - each microtube contains 1.55 ml of a solution of biotinylated allergens, ready to use. The content of one bottle is enough to conduct 30 studies.
№ Allergen name BA-D1 Dermatophagoides pteronyssinus BA-D2 Dermatophagoides farina BA-Н1 House Dust Mixture № Allergen name BA-E1 Cat (epithelial) BA-E2 Dog (epithelial) BA-E3 Horse (epithelial) BA-E6 Guinea Pig (epithelial) BA-E70 Goose (feathers) BA-E78 Budgerigar (feathers) BA-E82 Rabbit (еpithelia) BA-E84 Hamster (epithelia) BA-E85 Chicken (feathers) BA-E86 Duck (feathers) № Allergen name BA-F1 Egg white BA-F2 Cow milk BA-F3 Сod BA-F4 Wheat flour BA-F5 Rye flour BA-F6 Barley flour BA-F7 Oats flour BA-F8 Corn flour BA-F9 Rice BA-F10 Sesamе BA-F11 Buckwheat flour BA-F13 Peanut BA-F14 Soybean BA-F17 Hazelnut BA-F20 Almond BA-F23 Crab meat BA-F24 Shrimp BA-F25 Tomato BA-F26 Pork BA-F27 Beef BA-F31 Carrot BA-F33 Orange BA-F34 Mandarin BA-F35 Potato BA-F37 Mussel BA-F41 Salmon BA-F44 Strawberry BA-F45 Baker’s yeast BA-F49 Apple BA-F75 Egg yolk BA-F76 Alpha-lactalbumin BA-F77 Beta-lactoglobulin BA-F78 Caseine BA-F79 Gluten BA-F83 Chicken meat BA-F84 Kiwi BA-F92 Banana BA-F93 Cocoa BA-F94 Pear BA-F205 Herring BA-F206 Mackerel BA-F208 Lemon BA-F213 Rabbit meat BA-F221 Coffee BA-F245 Whole Egg BA-F247 Honey BA-F256 Walnut BA-F259 Grape BA-F328 Fig BA-F343 Raspberry № Allergen name BA-T2 European Alder / Alnus glutinosa BA-T3 Silver Birch/Betula verrucosa BA-T4 Common Hazel / Corylus avellana BA-T7 Common Oak/ Quercus robur BA-Т12 Goat Willow/ Salix caprea BA-T14 Eastern Cottonwood /Populus deltoides № Allergen name BA-W1 Common Ragweed/ Ambrosia elatior BA-W6 Common Mugwort/ Artemisia vulgaris BA-W8 Common Dandelion/ Taraxacum vulgare BA-W9 Ribwort Plantain/ Plantago lanceolata BA-W10 White Goosefoot/ Chenopodium album BA-W12 European Goldenrod/ Solidago virgaurea № Allergen name BA-G2 Bermuda Grass/ Cynodon dactylon BA-G3 Cock’s-foot/ Dactylis glomerata BA-G4 Red Fescue/ Festuca elatior BA-G5 Perennial Ryegrass/ Lolium perenne BA-G6 Timothy Grass/ Phleum pratense BA-G8 Kentucky Bluegrass/ Poa pratensis BA-G12 Rye/ Secale cereale № Allergen name BA-M1 Penicillium notatum BA-M2 Cladosporium herbarum BA-M3 Aspergillus fumigatus BA-M4 Mucor racemosus BA-M5 Candida albicans BA-M6 Alternaria alternata (tenius) № Allergen name BA-I1 Bee Venom/ Apis mellifera BA-I3 Wasp Venom/ Vespula spp. BA-I6 Cockroach/ Blatella germanica № Allergen name BA-DEM1 Indoor allergens mixture:
D. pteronyssinus (D1), D. farinae (D2), Cat (epithelial) (E1), Dog (epithelial) (E2)BA-EМ1 Feathers mixture:
Goose (E70), Chicken (E85), Duck (E86)BA-FM1 Food mixture (seafood):
Crab meat (F23), Shrimp (F24), Mussel (F37)BA-FM2 Food mixture (cereals):
Wheat flour (F4), Rye flour (F5), Barley flour (F6), Oats flour (F7), Corn flour (F8), Sesame (F10), Buckwheat flour (F11)BA-FM3 Food mixture (fish):
Cod (F3), Salmon (F41), Herring (F205), Mackerel (F206)BA-TM1 Tree pollens mixture:
Alnus glutinosa (T2), Corylus avellana (T4), Betula verrucosa (T3), Quercus robur (T7), Salix caprea (T12), Populus deltoides (T14)BA-TM2 Tree pollens mixture (early flowering):
Alnus glutinosa (T2), Betula verrucosa (T3), Corylus avellana (T4)BA-TM3 Tree pollens mixture (late flowering):
Quercus robur (T7), Salix caprea (T12), Populus deltoides (T14)BA-WМ1 Weed pollen mixture:
Ambrosia elatior (W1), Artemisia vulgaris (W6), Taraxacum officinale (W8), Plantago lanceolata (W9), Solidago virgaurea (W12)BA-GМ1 Meadow grass pollens mixture:
Cynodon dactylon (G2), Dactylis glomerata (G3), Festuca elatior (G4), Phleum pratense (G6), Secale cereale (G12)
