Recognition and Treatment of Chlamydial Infections from Birth to Adolescence

Abstract

The "silent epidemic" of Chlamydia trachomatis threatens to cause reproductive damage and infertility in many of the 50 million women who acquire it each year. Female reproductive tract infection has more recently been linked to stillbirth and premature delivery. Innate immune cells and mediators appear to be the primary players in pathogenesis, with neutrophils playing a prominent role in disease development. Although adaptive antibody and CD4 T cell responses appear primarily protective, these responses are inefficient. Infections are frequently chronic as a result, and when infection is diagnosed and treated with appropriate antibiotics, repeated infection is the rule. The lack of acute symptoms in many infected individuals contributes to the high prevalence of chlamydial infection. Although chronic sequelae are relatively rare in men, and many women sustain infection without developing pelvic inflammatory disease or chronic sequelae, the extremely high prevalence of chlamydial infection leads to significant morbidity and healthcare costs. A vaccine is urgently needed to prevent infection, but given the difficulties of inducing a CD4 T cell memory response that can home quickly to the genital tract, induction of sterilizing immunity may not be possible. A vaccine that prevents disease by lowering bacterial burden and dampening production of tissue-damaging responses may be possible. Until an efficacious vaccine is developed, screening and treatment programs appear to be the best method of disease prevention.

Chronic Chlamydial Diseases: From Atherosclerosis to Urogenital Infections

“…C. trachomatis infection in pregnant women has been also linked to chorioamnionitis, placentitis, premature rupture of membranes, and preterm birth [36], however, existing evidence is weak [32]. In men, C. trachomatis causes nongonococcal urethritis, epididymitis, prostatitis, and proctitis [37].…”

“…Genetic predisposition and host immune response are also important in pathogenesis of long term complications of genital C. trachomatis infection [32]. Specific HLA DQ alleles and polymorphisms in the promoter of IL-10 and TNF alpha are associated with high risk of tubal infertility [22•], whereas polymorphisms in TLR-2 are associated with protection against tubal disease following C. trachomatis infection [36].…”

Site-Specific, Insertional Inactivation of incA in Chlamydia trachomatis Using a Group II Intron

“…Of paramount importance to human health is C. trachomatis , the causative agent of sexually transmitted infections and trachoma, the former of which remains the leading reportable bacterial infection both in the United States and world-wide [2], [3]. These pathogens share a unique physiology in which the bacteria undergo a biphasic developmental cycle initiated when the extracellular, non-replicative form known as the elementary body (EB) binds to the surface of a susceptible eukaryotic cell [4].…”

Capsid protein Vp1 from chlamydiaphage φCPG1 effectively alleviates cytotoxicity induced by Chlamydia�trachomatis

“…In the USA, 1,598,354 chlamydial infections were reported in 2016, corresponding to a rate of 497.3 cases per 100,000 individuals, and from 2008 to 2015, the rate of reported chlamydial infections increased from 32.48 to 37.18 cases per 100,000 individuals in China ( 2 ). C. trachomatis -induced genital tract infections may cause inflammation, edema and mucosal discharge ( 3 ), and ascending uterine infections may lead to pelvic inflammatory disease, tubal scarring, ectopic pregnancies and infertility ( 4 ).…”