Vitrotest® Chlamydia-IgG

• 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.

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.