Pathogenesis of Urogenital Tuberculosis

Abstract

Tuberculosis (TB) is a contagious disease caused mainly by Mycobacterium tuberculosis (Mtb); M. bovis is a rather rare etiological agent of UGTB. After first contact with TB infection about 90 % of individuals remain healthy, although at least every third of them will be infected and, so, will have latent tuberculosis.

There is a genetically deterministic innate response on TB. A first meeting with Mtb provokes development of an aquired immune response on TB in an immunocompetent person; immunocompromise condition may disturb this process. Mtb survives inside macrophages by manipulating microbicidal functions such as phago-lysosome fusion, production of reactive oxygen species and nitric oxide, and by rendering macrophages non-responsive to IFN-gamma. Apoptosis prevents the release of intracellular components and the spread of mycobacterial infection by sequestering the pathogens within apoptotic bodies. Apoptosis of infected macrophages may result in self-recovery.

Thus there is an innate resistance of the human organism to Mtb – and it is a main reason why TB, a potentially lethal disease, doesn’t destroy all mankind. Mtb itself stimulates acquired response on TB that improves the resistance of the human organism. Special vaccines increase this resistance too.

Tuberculosis used to be healed by forming a scar. Such scar is a benefit outcome for pulmonary TB – but in UGTB we receive “a desirable scarring in an undesirable place”. Inappropriate therapy for TB ulcer of ureter may result in stricture and kidney death due to obstruction – even if this kidney is healed of TB. Redundant scarring of ductus deference may lead in obstructive infertility.