CHLAMYDIA TRACHOMATIS INFECTION IN HUMAN POPULATION: DETECTION, PATHOGENESIS, TREATMENT AND PREVENTION

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Chlamydia trachomatis is a Gram-negative or variable, fastidious, obligate intracellular bacterium found in the family Chlamydiaceae andgenus Chlamydia. The Chlamydia genus mainly contains bacterial pathogens that cause sexually transmitted infections, eye infections and respiratory disease in human population. C. trachomatis is a strict human pathogen; and the organism has no animal reservoir. This implies that humans are the only natural host or reservoir of C. trachomatis. C. trachomatis is the main causative agent of venereal diseases (e.g., lymphogranuloma venereum, non-gonococcal urethritis), trachoma (a chronic eye disease), and inclusion conjunctivitis, as well as ophthalmia neonatorum in adults, children and newborns. Ophthalmia neonatorum or neonatal ophthalmia is an eye infection that commonly affects newborns, and the disease is contracted from an infected birth canal (vagina) or cervix during childbirth. C. trachomatis occurs worldwide, and it is also responsible in causing sexually transmitted diseases (STDs) such as non-gonococcal urethritis in men and cervicitis and urethritis in women. It is noteworthy that the strains of C. trachomatis responsible for causing trachoma (an eye infection) are genetically distinct from those strains that cause STDs in humans. Several serovars or serotypes of Chlamydia species are known to exist, and each is responsible for causing a typical infection or disease in either human or animal host.

Transmission of C. trachomatis is mainly through direct body contact especially during sex with an infected person or via the vagina and during child delivery – in which the conjunctiva or eyes of newborns becomes infected with the pathogen via contact with infectious genital secretions, thus causing conjunctivitis in the newborn. Secretions from the vagina, urethra and anal regions of infected persons (symptomatic or asymptomatic) are always infectious, and can serve as route via which the disease or pathogen can spread after ‘intimate’ body contact. Contaminated hand-to-eye contacts also play a role in the spread of trachoma and inclusion conjunctivitis. Severe cases of C. trachomatis infection can result in blindness in neonates if not properly treated. Some species of Chlamydia e.g., C. psittaci– (the causative agent of psittacosis) is a potential biological agent used for bioterrorism.

PATHOGENESIS OF CHLAMYDIA TRACHOMATIS INFECTION

C. trachomatis and other Chlamydia species normally exist in two cellular forms which are: elementary bodies (EB) and reticulate bodies (RB) or initial bodies; and these morphological forms of the organism further explains the reproductive and/or developmental phases of the pathogen within infected host cells. Elementary bodies, EB (which measures about 0.3 µm) is infectious, non-growing (i.e., does not multiply or divide), easily adapted to survival outside of host cells and has a rigid cell well. On the other hand, reticulate bodies, RB (which measures 1 µm) is non-infectious, rapidly multiplying, survives only within host cells and has a delicate or flaccid cell wall. Humans are the only known reservoirs or natural host of C. trachomatis. The pathogen gains entry into the body of susceptible hosts through: (1) contaminated hand-to-eye contacts (for trachoma), (2) through sexual contacts with an infected individual (for venereal diseases), and (3) through congenital means (i.e., from mother to child). The incubation period of the disease is usually between 2-8 days. C. trachomatis infection is usually prolonged due to the ability of the organism to form a host-parasite relationship; and this characteristic makes the disease or infection to be asymptomatic in most infected persons who spread the pathogen from one host to another even without knowing about it.

C. trachomatis is an intracellular bacterium that has high affinity for epithelial cells of the body especially those of the conjunctiva and genital regions where it specifically binds to, to spark series of inflammatory reactions mediated by the host immune system molecules and the pathogen’s extracellular molecules (e.g., lipopolysaccharides, LPS). As shown in Figure 1, C. trachomatis infection follows a characteristic reproductive and developmental life cycle that usually involves two morphological and cellular forms of the pathogen (i.e., EB and RB) that directs the pathogenicity of the organism in vivo.

Figure 1. Schematic diagram of Chlamydia infection, development and reproductive cycle. Source: Adapted from Roberta B. Carey et al., (2008). Medical microbiology for the new curriculum: a case based approach. John Wiley & Sons, Inc, New Jersey, USA. Morphologically, C. trachomatis exist in two forms i.e., as elementary bodies (smaller infectious forms) and reticulate bodies (larger replicative forms). Elementary bodies (EB) attaches specifically to infected host epithelial cells; and entry into the infected host epithelial cells is facilitated by phagocytosis or endocytosis. The EB is enclosed within inclusion bodies in the host cell. Several hours after entry, the EB transforms into larger replicative forms known as initial bodies or reticulate bodies (RB) within the epithelial cells. RB multiplies rapidly within the infected cells via binary fusion before its transformation to multiple elementary bodies (which are the infectious forms of Chlamydia). Newly formed EB are released from the lyses of membrane-bound host cell, and these bodies go on to infect susceptible host cells. Note: C. trachomatis carry on as metabolically-active and dividing reticulate bodies intracellularly (i.e., inside a living host cell) and as inactive and infectious elementary bodies extracellularly (i.e., outside a living host cell). 

Failure of the host immune system to fight and contain the invading organism coupled with lack of effective treatment after diagnosis leads to a progression of the disease. Recurrent or persistent C. trachomatis infection leads to chronic inflammation of the eyes and other genital and extra-genital infections in the affected host. Mucopurulent discharge from the eyes, scarring of the cornea and inflammatory changes in the cornea and conjunctiva are some of the signs and symptoms of trachoma and inclusion conjunctivitis. Trachoma is a serious public health problem and the leading cause of blindness in some developing countries. For non-gonococcal urethritis and cervicitis caused by C. trachomatis, infected males and females can remain asymptomatic for a long period of time and may occasional serve as means of spreading the pathogen to susceptible host during sexual intercourse. Frequency of urination, dysuria, non-purulent discharges from the urethra and vagina and formation of buboes at the groin region are some of the clinical signs and symptoms of non-gonococcal C. trachomatis infection. Pelvic inflammatory disease (PID) and infertility or ectopic pregnancy can ensue in untreated non-gonococcal infections in females. And in males, there could be inflammation of the prostate and unusual enlargement of the testes or epididymitis due to C. trachomatis infection.

LABORATORY DIAGNOSIS OF CHLAMYDIA TRACHOMATIS INFECTION 

Aseptically collected swabs of the vagina, cervix, urethra and conjunctiva, as well as urine samples are usually required for laboratory experimentation in suspected cases of C. trachomatis infection. C. trachomatis cannot be cultivated easily in routinely used bacteriological media because the organism is an obligate intracellular parasite and it is deficient in the synthesis of adenosine triphosphate (ATP). Thus, C. trachomatis is only cultivated using specialized cell or tissue culture techniques in experimental/laboratory animals or in embryonated eggs. Gram staining technique is not efficient in the laboratory identification of C. trachomatis from urogenital swabs or other suspected clinical samples because the organism is usually a Gram variable and obligate intracellular bacterium and is not seen on Gram stained smear. However, C. trachomatis can be identified in Giemsa-stained smears or fluorescent-antibody-stained-smears of conjunctiva specimens by direct immunofluorescence microscopy technique. ELISA, PCR and serological techniques can also be employed in the identification of C. trachomatis from clinically important specimens.    

IMMUNITY TO CHLAMYDIA TRACHOMATIS INFECTION 

Infection with C. trachomatis does not confer a long-lasting protection in the infected host. Thus, a re-infection can occur at a later time following exposure to the pathogen.

TREATMENT OF CHLAMYDIA TRACHOMATIS INFECTION 

C. trachomatis infection is usually associated with secondary bacterial infections. Macrolides (e.g., azithromycin and erythromycin), sulphamethoxazole-trimethoprim and tetracycline are usually the antibiotic of choice used for treating infections caused by C. trachomatis. Early treatment is vital to reduce the likelihood of blindness in affected individuals. Topical antibiotic applications should be used in line with oral antimicrobial agents in treating eye infections due to C. trachomatis.      

PREVENTION AND CONTROL

Trachoma is a vaccine preventable bacterial infection. The prevention and control of the disease lies in proper public awareness and health education. Good personal hygiene such as hand washing is also critical in preventing trachoma. Poor or lack of access to clean water and poor personal and environmental hygiene are some of the risk factors that predispose individuals to some C. trachomatis infection. Thus, improvement in sanitary practices and provision of clean water supply to people especially those in developing countries is critical to contain and abate the occurrence or spread of C. trachomatis infection across the world.

Further reading

Brooks G.F., Butel J.S and Morse S.A (2004). Medical Microbiology, 23rd edition. McGraw Hill Publishers. USA.

Gilligan P.H, Shapiro D.S and Miller M.B (2014). Cases in Medical Microbiology and Infectious Diseases. Third edition. American Society of Microbiology Press, USA.

Madigan M.T., Martinko J.M., Dunlap P.V and Clark D.P (2009). Brock Biology of Microorganisms, 12th edition. Pearson Benjamin Cummings Inc, USA.

Mahon C. R, Lehman D.C and Manuselis G (2011). Textbook of Diagnostic Microbiology. Fourth edition. Saunders Publishers, USA.

Patrick R. Murray, Ellen Jo Baron, James H. Jorgensen, Marie Louise Landry, Michael A. Pfaller (2007). Manual of Clinical Microbiology, 9th ed.: American Society for Microbiology.

Wilson B. A, Salyers A.A, Whitt D.D and Winkler M.E (2011). Bacterial Pathogenesis: A molecular Approach. Third edition. American Society of Microbiology Press, USA.

Woods GL and Washington JA (1995). The Clinician and the Microbiology Laboratory. Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of Infectious Diseases. 4th ed. Churchill Livingstone, New York.

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