Borrelia spp

The determination of antibodies specific against antigens of human pathogenic strains of Borrelia is one of the tools used in the diagnosis of Lyme borreliosis (LB). The detection of this multisystem disease is based on the detection of early IgM and late IgG antibodies by ELISA and LIA. Monitoring the dynamics of specific antibodies is very important for successful treatment.

The ELISA-VIDITEST and MONO-VIDITEST anti-Borrelia kits can be achieved to calculate the intrathecal synthesis of specific antibodies in cerebrospinal fluid. Elevated antibody levels may be a major indicator of neuroborreliosis infections in the central nervous system (CNS).

ELISA-VIDITEST uses 96-well microtiter plates, still MONO-VIDITEST cassette format. All testing and evaluation takes place automatically in combination with our VIDIMAT analyzer. LIA-VIDITEST mainly uses recombinant antigens for individual strains in precisely defined positions on nitrocellulose strips. The testing process can be achieved on RoboBlot, BeeBlot and B-20 devices. We provide VidiScan2 software for automatic evaluation of results.

Borrelia is a genus of gram-negative, microaerophilic bacteria of the class Spirochaetes. The Borrelia burgdorferi sensu lato complex comprises a total of 21 strains, 4 of which are pathogenic to humans (B. burgdorferi sensu stricto, B. afzelii, B. garnii and B. bavariensis). All types of Borrelia differ in their antigenic composition and different affinity for individual organs.

In order to survive in the body of ticks and borrelia hosts, they have gained the ability to adapt to a changing environment by expressing and constantly altering external surface proteins (Osp) and utilizing tick proteins for transmission.

Borrelia have a thin, spirally wound body (4-30 μm long and 0.2-0.5 μm in diameter) with 4-15 regularly spaced threads. Their movement takes place with the help of whips (7-11). They are thus able to cross the blood-brain and epithelial barriers. They can also enter and survive in cells of the host's immune system, such as macrophages or dendritic cells. Cell wall proteins are constantly changing. They reproduce by transverse or longitudinal division every 12-18 hours.

Lyme borreliosis (LB) is a serious disease in which there is a risk of developing systemic diseases, autoimmune reactions and post-infectious disease. The causative agents are strains of the genus Borrelia. The vector of transmission is all developmental stages of the tick Ixodes. In Europe, it is a common tick (Ixodes ricicnus). The infection occurs mainly 36 hours after the tick bite. The disease is divided into several stages into early localized, disseminated and late disseminated. There are only about 10% of chronic forms in the late stage. The primary feature is a localized skin lesion, erythema migrans (50% of cases). Clinical manifestations depend in part on the type of borrelia, as each tends to migrate to other tissues. Lyme arthritis is the most common in B. burgdorferi sensu stricto (71%), neuroborreliosis in B. garinii (22%) and cutaneous manifestations in B. afzelii (5%).

IgM antibodies are formed about 3 weeks after infection, reach a maximum in 6 weeks, then their level usually decreases, followed by the formation of IgG class antibodies. In the early phase of infection, the determination of specific antibodies is important, especially in cases where typical clinical signs are not evident. Most diseases caused by Borrelia burgdorferi are asymptomatic, which is evident in the fact that up to 10% of our population can detect anti-Borrelia IgG antibodies.

Some clinical symptoms of LB may be similar to those of other diseases, so the determination of antibodies against Borrelia is also used in the differential diagnosis of neuroinfections, arthropathy, carditis and skin diseases.

LB can be treated with antibiotics at all stages. Therefore, diagnostics detecting the early stage of the disease play a crucial role. When antibiotic treatment is started early, antibodies may not be produced and the activation of the immune system may only be manifested by T cell proliferation. Upon replication, Borrelia changes its surface structure to defend against the immune system, and B-lymphocytes are stimulated to produce new IgM antibodies.