Pathogenesis of Genital Tract Disease Due to Chlamydia Trachomatis

Introduction

Sexually transmitted infections cause a significant health concern globally. Bacteria cause a majority of STIs. This essay discusses the N. gonorrhoeae and C. trachomatis as major causes of STIs. The paper’s key focus is on the bacteria adherence to cells, fighting/adapting mechanisms, and major infections.

N. gonorrhoeae adherence to human cells

N. gonorrhoeae bacteria have the capability to stick to hosts’ cells. The bacteria possess multiple gonococcal surface molecules, which work autonomously or concertedly to facilitate adherence to human cells. It is worth noting that the gender-related anatomical differences contribute to the diverse adaptation and adherence of N. gonorrhoeae to human cells. In addition, studies have revealed adaptation and adherence are cell-specific and site-specific.2

Some of the most studied agents that facilitate N. gonorrhoeae adherence to host cells include porin (the core outer membrane protein), opacity-associated (Opa), lipooligosaccharide (LOS), and type IV-A pili. The adherence mechanisms facilitate the establishing and spread of bacterial infections.2

N. gonorrhoeae entry to the genital tract

The Neisseria gonorrhoeae infection and the entry to genital tract have gender specificity, probably due to the differences between male and female genital anatomies. It is worth noting, however, that Neisseria gonorrhoeae do not survive in any natural host other than the human body.2 As such, no studies have linked the entry of Neisseria gonorrhoeae to genital tract through toilet seats and/or similar objects.2

Oftentimes, Neisseria gonorrhoeae spread through direct contact with mucosal surfaces of an infected person during coital activity. Pili, Opa, and other surface proteins aid the initial infection and entry of Neisseria gonorrhoeae to the genital tract. The bacteria starts by attacking noncornified epithelium of the genital tract and gradually spreads to other parts of the tract and other organs such as the rectum, oropharynx, and conjunctivae.2

Compare the range of infections caused by N. gonorrhoeae and C. trachomatis

N. gonorrhoeae and C. trachomatis are both sexually transmitted. Both bacteria are responsible for a range of infections. C. trachomatis causes infections such as acute proctitis among male gays, pharyngeal infection, and the infection of the urethra among other genital infections. On the other hand, N. gonorrhoeae causes genital infections, including urethritis, cervicitis, salpingitis, bacteremia, and arthritis among others.6

The range of diseases related to both N. gonorrhoeae and C. trachomatis are comparable, especially due to their similarities in clinical manifestations.6 Both pathogens are linked to most ailments related to the urethral epithelium, infections of the epididymis, cervix, and rectum among others. Further, infections related to the two bacteria are characterized by extensive subepithelial inflammation, ulceration of epithelium, and widespread tissue scarring.6

It is imperative to note that patients with C. trachomatis are highly susceptible to Neisseria gonorrhea infections. Nonetheless, C. trachomatis has a relatively longer incubation period and, therefore, infections from the bacteria may be evident even after treatment of Neisseria gonorrhea infections, more so if the agents adopted lack the capacity to eradicate chlamydia.6

Chlamydia trachomatis structure

C. trachomatis structure entails a spherical N- and C- terminal assemblies linked by a tripartite-helical convoluted-coil. The C- end domain has folds comparable to TNT group of cytokines and other non-antibody proteins.3 The most similar Pgp3 C- terminal domain physical homologs are from the Burkholderia cenocepacia.3 On the other hand, the N- terminal domain comprises a series and links of structural motifs that are commonly present in viral proteins with three monomers. The centrally located triple-helical coil possesses a rare alternating pattern. The unusually alternating pattern comprises non-polar and polar residue sets of twos, which are responsible for the production of an uncommon right-handed superhelical spiral structure.3

The developmental cycle of C. trachomatis

The C. trachomatis develops within the host’s epithelial cells. The developmental cycle is comprised of two phases that consist the infectious and noninfectious stages. In the infectious phase, C. trachomatis is characterized by indolent metabolism commonly referred to as elementary bodies (EBs). An EB is characterized by relatively minute rigid cell walls of about 0.3 µm.1

The second phase, which is noninfectious is characterized by highly metabolically active reticulate body (RB). Apparently, RBs result from converting EBs to larger elements with 1–2 µm lengths. RBs undergo further developmental divisions that eventually converts RBs back to EBs and finally exiting the host cell. The cycle may be complete within the first two days, or more, depending on the species.1

How C. trachomatis avoid elimination by the immune system

Upon infection, the human body tries to eliminate the C. trachomatis by using defense mechanisms that involve both the innate and the adaptive immunity systems.1 However, the bacteria fights back to avoid elimination by the host’s antimicrobial factors.1 The bacteria adopts varied mechanisms, including the modification of host proteins, counteracting host cell apoptosis, proteolysis, and evading immune recognition.1

The significance of the transcriptional regulator FarR in N. gonorrhoeae

The human body has mechanisms of fighting bacterial infections, including the infections resulting from Neisseria gonorrhoeae bacteria.5 Therefore, many bacteria species possess survival mechanisms that enable them to endure antibacterial fatty acids emitted by the human body in fighting infections.5

FarR, for instance, is a crucial survival mechanism for Neisseria gonorrhoeae. Once infected by Neisseria gonorrhoeae, the human body produces antibacterial fatty acids. The antibacterial fatty acids produced by the human body make the survival of bacteria in the human body difficult. Neisseria gonorrhoeae, therefore, possesses FarAB operon, which facilitates the encryption of an efflux pump that helps in the fight against defense mechanisms from the host.5 The FarAB productions in Neisseria gonorrhoeae have to be regulated in manners that are pertinent to the production of antibacterial fatty acids by the human body. The FarR, therefore, plays a significant role in the regulation of FarAB. As such, Neisseria gonorrhoeae resistance to antibacterial fatty acids and the subsequent survival in the host depend on the regulation of FarB by FarR.5

Non-gonococcal urethritis and the causative bacteria species

The inflammation of the urethra can result from other bacteria apart from the Neisseria gonorrhoeae. Therefore, non-gonococcal urethritis (commonly referred to as NGU) is the inflammation of the urethra that is caused by bacteria other than Neisseria gonorrhoeae.6 Patients with non-gonococcal urethritis have many symptoms, including discharge, dysuria, and urethra discomforts. However, some cases of non-gonococcal urethritis have no symptoms.6

For accurate diagnoses of NGU, therefore, patients should possess excess polymorpho-nuclear leucocytes (PMNLs). However, in a case where the excess leucocytes have single nuclei, chances of a viral etiology are high. To rule out the possibilities of gonorrhoea infections, NGU symptomatic patients should be screened using microscopy of stained smears.6

Various pathogens have been linked to the cause of NGU. Different species of pathogens including Chlamydia trachomatis, Mycoplasma genitalium, Ureaplasma urealyticum, Trichomonas vaginalis, cause inflammation of the urethra.4

It is worth noting that Chlamydia trachomatis is the most common cause of NGU contributing 20-50% of all reported cases.4 The second among the most common species is Mycoplasma genitalium, which is linked to 10-30% of all NGU infections.4

Conclusion

STIs are considered as major health risks. Many people suffer from STIs globally. C. trachomatis and N. gonorrhoeae are some of the most common causative agents for STIs. This essay has discussed some of the key issues pertinent to the two bacteria. It is apparent that Neisseria gonorrhoeae and C. trachomatis cause a range of infections in human beings. A proper understanding of the two bacteria is paramount in efforts to treat and avoid related STIs.

References

Darville, T., & Hiltke, T. J. Pathogenesis of Genital Tract Disease due to Chlamydia trachomatis. The Journal of Infectious Diseases. 2011; 201(Suppl 2): S114–S125.

Edwards, J. L., & Butler, E. K. The Pathobiology of Neisseria gonorrhoeae Lower Female Genital Tract Infection. Frontiers in Microbiology. 2011; 2:102.

Galaleldeen, A., Taylor, A., Chen, D., Schuermann, J., Holloway, S., Hou, S.,… & Hart, P. Structure of the Chlamydia trachomatis Immunodominant Antigen Pgp3. The Journal of Biological Chemistry. 2013; 288(30): 22068-79.

Moi, H., Blee, K., & Horner, P. J.Management of Non-gonococcal Urethritis. BMC Infectious Diseases. 2015; 15: 294.

Schielke, S., Frosch, M., & Kurzai, O. Virulence Determinants Involved in Differential Host Niche Adaptation of Neisseria meningitidis and Neisseria gonorrhoeae. Medical Microbiology and Immunology. 2010; 199(3): 185–196.

Shim, B. S. Current Concepts in Bacterial Sexually Transmitted Diseases. Korean Journal of Urology. 2011; 52(9):589-597.

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