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We describe a case of clinical signs of acute cholecystitis as a complication to genital Chlamydia infection. Transabdominal ultrasound and magnetic resonance-scanning were normal. Cholescintigraphy showed an obstruction of the ductus cysticus. The patient was treated with antibiotics and two weeks later was without symptoms.
CONTEXT: Black women are disproportionately infected with gonorrhea and chlamydia. Because of the potential impact of these infections on women's reproductive health, it is important to determine whether different factors are predictive of infection in women of different races. METHODS: Data from 31,762 women aged 15-24 who were tested for gonorrhea and chlamydia at Missouri family planning clinics in 2001 were used to calculate the prevalence of each infection by selected variables. Logistic regression analysis was used to assess factors associated with the risk of infection. RESULTS: Overall, 0.7% of women had gonorrhea, and 4% had chlamydia. The gonorrhea rate was 4% for blacks and 0.4% for whites; the chlamydia rate, 9% and 4%, respectively. Independent predictors of gonorrhea in both races were symptoms, recent sexual contact with a partner who had STD symptoms, and chlamydia infection. Predictors specific to whites were visiting the clinic for STD care and having a new partner or multiple partners in the past year. Being aged 15-21 was associated with an elevated risk of gonorrhea for blacks only. In both racial groups, chlamydia infection was associated with younger age, contact with a symptomatic partner, cervicitis, cervical friability and gonorrhea positivity. Additional predictors among whites were having a new partner, having multiple partners and having pelvic inflammatory disease; no other factors were significant for blacks. CONCLUSIONS: The prevalence and predictors of gonorrhea and chlamydia infection differ significantly between blacks and whites. Until these disparities are better understood, it will be difficult to establish screening criteria for gonorrhea.
The objective of this review is to critically describe the diagnostic procedures for Chlamydiae infections. Direct identification in culture remains fastidious and lacks sensitivity. Antigen detection techniques include direct immunofluorescence using monoclonal antibodies and immunohistochemistry. Until recently, serologic testing was commonly used for the diagnosis, but sensitivity was low for acute infections. The situation has been greatly improved by the advent of molecular techniques allowing direct identification of chlamydial DNA. The polymerase chain reaction has high specificity and sensitivity. Several commercially available tests can be used for C. trachomatis. For C. pneumoniae, routine tests for gene amplification are still lacking. The diagnosis is based on the combination of direct identification and search for a rise in antibody titer by serologic testing.
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The CD4 T helper cell type 1 (Th1) response is essential for the resolution of chlamydial genital infection in mice. However, not all Th1 clones are equally protective in eradicating the infection. Since oral immunization regimens produce protective immunity, we evaluated the role of the mucosa-associated homing receptor, alpha4beta7, in trafficking to the genital mucosa. Using a panel of CD4, Th1 cell lines and clones, we compared the lymphocyte homing patterns of a Chlamydia-specific, protective clone (P-MoPn), a nonprotective clone (N-MoPn), and a keyhole limpet hemocyanin (KLH)-specific cell line (KLH-1). T cells were labeled with the fluorescent dye PKH-26, adoptively transferred into Chlamydia-infected mice, and monitored at different time points throughout the course of a genital infection. We found that clones P-MoPn and N-MoPn migrated to similar extents to the genital tract and in significantly greater numbers than the KLH-specific T-cell line. Both clones and the KLH-1 line expressed similar levels of the adhesion molecules alpha4, beta1, CD44, and CD11a. However, clones P-MoPn and N-MoPn expressed higher levels of the mucosal homing receptor, alpha4beta7. Also, clones P-MoPn and N-MoPn but not the KLH-1 line migrated to the mesenteric lymph node, suggesting a mucosal recirculation pattern. Moreover, blocking alpha4beta7 adhesion interaction in vivo significantly reduced the recruitment of P-MoPn but not KLH-1 to the genital tract. These findings show that the mucosal homing receptor alpha4beta7 is utilized by a subset of CD4 cells during migration to the Chlamydia-infected genital tract.
Chlamydia trachomatis recently has emerged as the most frequently diagnosed sexually transmitted disease (STD) agent. An estimated three million cases are diagnosed annually in the United States. Because the infection is not reportable, only estimates can be made. The most common STD, it also is often transmitted to infants through infected mothers. Prevention and treatment of the disease in newborns require different procedures from those for gonorrhea, as do diagnostic and treatment methods for infected adults. Chlamydia also appears to pose a threat to pregnancy.
Chlamydia species infect epithelial cells at mucosal surfaces, and are major causes of sexually transmitted diseases. Infection is characterized by inflammation which is exacerbated upon reinfection, ultimately leading to tissue damage and scarring. Although central for the development of disease manifestations, little is known about the mechanisms that initiate and sustain the inflammatory response to Chlamydia. Infection of cervical and colonic epithelial cells with Chlamydia trachomatis and Chlamydia psittaci is shown in the present studies to upregulate mRNA expression and secretion of the proinflammatory cytokines IL-8, GRO alpha, GM-CSF, and IL-6. In contrast to the rapid, but transient, cytokine induction following infection with other invasive bacteria, the epithelial cytokine response to Chlamydia was delayed until 20-24 h after infection, persisted throughout the chlamydial growth cycle (2-4 d), and required bacterial protein synthesis. Moreover, epithelial cell lines and primary endocervical epithelial cells released IL-1alpha after Chlamydia infection, and increased secretion of the proinflammatory cytokines could be inhibited by anti-IL-1alpha. This suggests that IL-1alpha, released following lysis of infected epithelial cells, may amplify the inflammatory response by stimulating additional cytokine production by noninfected neighboring cells. These findings suggest a novel pathophysiologic concept wherein the acute host response to Chlamydia at mucosal surfaces is primarily initiated and sustained by epithelial cells, the first and major targets of chlamydial infection.
One mechanism by which interferons (IFNs) can inhibit chlamydial infection is by the induction of the enzyme indoleamine 2,3-dioxygenase (IDO), which restricts the availability of tryptophan, which is required for chlamydial growth. Other immunomodulating agents, including interleukin-1 (IL-1), can interact synergistically with IFNs, resulting in increased IDO activity in macrophages. The objectives of this study were to establish that IL-1 can enhance IFN-mediated inhibition of chlamydial growth by increasing the amount of IDO activity induced by IFNs and to identify immunomodulatory agents in culture supernatants from chlamydia-infected macrophages that interact synergistically with IFNs in restricting chlamydial growth. Monocyte-derived macrophages were treated with IL-1 combined with gamma IFN (IFN-gamma) or IFN-beta. The ability of treated cells to support the growth of Chlamydia psittaci was directly related to the amount of IDO activity induced; as IDO activity increased, so did inhibition of chlamydial growth. Furthermore, concentrations of IFNs were identified at which little IDO activity was induced and chlamydial growth was permitted yet which in the presence of IL-1 resulted in increased IDO activity and restriction of chlamydial growth. The addition of exogenous tryptophan reversed the effect of combined IFN and IL-1 treatment, indicating that IDO activity induced by combined cytokine treatment was responsible for chlamydial inhibition. Supernatants from chlamydia-infected macrophages were capable of potentiating IDO induction by IFN-gamma and of restricting the growth of C. psittaci. Antibody to IL-1 beta neutralized the potentiating effects of supernatants from chlamydia-infected cells on both IDO induction and chlamydial inhibition. Thus, IL-1 produced in response to chlamydial infection may contribute to the elimination of the infection.
Erythromycin and josamycin are the antibiotics of choice in the treatment of pregnant women with Chlamydia infection. On the basis of differing recommendations in the literature regarding treatment period and dosage, two groups of pregnant women were treated with josamycin according to different dosage schedules: Group A: 170 patients treated with 2 x 500 mg daily for 12 days. Group B: 120 patients treated with 3 x 500 mg daily for 8 days. The diagnosis was confirmed by immunofluorescence with monoclonal antibodies. Non-responding patients were treated again with a similar dose. 17% of the patients in group A and 9.1% in group B were still positive for Chlamydia after the first course of treatment. After a second course, 13.6% of group A and none of group B showed positive controls. Failures of therapy after the first treatment course can be attributed to errors in dosage or re-infection, whereas failures after the second course must be due to bad compliance. Our results suggest that pregnant women with Chlamydia infection are most efficiently treated with high dosages of josamycin over a short period of time.
The present study evaluates two strategies for partner notification among young women with genital Chlamydia trachomatis infection. The study included 443 women, aged 14-21 years, who visited one of 20 youth clinics during a two months period in 1991. The youth clinics were randomized to use patient referral or provider referral. In the latter group, 11 of 14 women with genital Chlamydia infection revealed their sexual partners. Only five of 24 sexual partners were notified by a letter, and six of 24 partners turned up for examination. In the patient referral group, 16 of 34 women asked to notify their partner, and ten of 31 partners were examined. Partner notification in young women with genital Chlamydia infection seems to be difficult.
OBJECTIVE: To evaluate the relationship between Chlamydia infection and otitis media with effusion and to establish a method for detection of Chlamydia antibodies in local fluids. METHODS: Sera and tympanocentesis aspirates from 44 patients with otitis media with effusion were collected. The specimens were used to detect the Chlamydia specific IgG, IgM antibodies using micro-immune fluorescent assay; to detect Chlamydia trachomatis plasmid DNA and Chlamydia pneumoniae genome DNA with polymerase chain reaction (PCR); and to separate Chlamydia pneumoniae in tympanocentesis aspirates with Hep-2 cell culture. RESULTS: One Chlamydia pneumoniae positive culture was found in tympanocentesis aspirate culture from one of the 44 patients, with positive Chlamydiae pneumoniae specific IgG antibody and DNA. Chlamydia trachomatis specific IgG antibody was increased in 14 cases sera and local secretion accordingly, with Chlamydia trachomatis plasmid DNA positive by PCR. CONCLUSION: Chlamydia is a common pathogen in otitis media with effusion.
During a study of genital infection in inner-city family-planning patients we examined 452 women for Chlamydia trachomatis. The prevalence of infection was 7.3%. There was no significant difference between patients attending because of genital symptoms and those who were attending for routine family-planning advice. Infection was found to be correlated with five main demographic parameters; age less than 25, no stable partnership, hormonal contraception, nulliparity and West Indian Ethnic origin. Using these parameters a simple scoring system was devised which allowed a high-risk population to be defined in whom screening would be economically justified.
The peroxidase-antiperoxidase (PAP) technique was applied in cellular samples for the detection of chlamydial infection. Urethral scrapings were obtained from 316 males with clinically suspected urethritis. Positive PAP staining was detected in 118 (37%) of 316 tested. Cellular samples from the endocervix of 25 (54%) of 46 female contacts of males with positive Chlamydia-infected cells had positive Chlamydia-PAP staining. Chlamydia was also found in 12 (25%) of 48 male with gonorrhea. Serum IgG antibodies against Chlamydia trachomatis were evaluated using an enzyme-linked immunosorbent assay. A total of 29 out of 73 patients had positive Chlamydia serology; of these, 21 were positive for PAP staining, and eight were negative. The determination of Chlamydia antigen by means of the PAP technique appears to be a satisfactory method for detecting Chlamydia in male and female genital specimens; also, the procedure can be done readily in most laboratory settings.
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Since 1989 the reporting of chlamydia infections is regulated by the Contagious Diseases Act, which stipulates that a physician who detects chlamydia is obliged to trace the patient's sexual partner(s). Up to 1994 the annual decrease in the number of chlamydia cases was 20 percent, which did not meet the goal stipulated by the County Council. A questionnaire study was carried out concerning diagnosis, treatment and public health intervention in chlamydia patients seen by general and private practitioners. While the clinical management was seen to adhere to the recommendations of the National Board of Health, adequate tracing of sexual contacts was not carried out in 20-45 per cent of the cases. In a major urban area, such as the County of Stockholm, referral of all chlamydia cases to specialist clinics could possibly improve not only the care of the patients but also the success rate in reaching their sex partners.
Chlamydia trachomatis was isolated from the ovaries of a 39-year-old married woman who presented with secondary amenorrhoea. Treatment with doxycycline was given and menstruation resumed spontaneously.
Assessment of immunological and microbiological efficacy of Chlamydia cervicitis management was made by a complex method with a low intensity laser. The total number of leukocytes, percentage of viable cells and the number of neutrophils were detected in cervical secrets. Functional status of neutrophils was studied by a content of lysosomes on the ground of spontaneous and induced by latex HCT-reducing capacity, phagocytic activity. A system of cytokines was studied by interleukine level (IL-1 alpha, IL-1 beta, TNF-alpha, IL-8) and IFN-gamma content in cervical mucus. Positive clinical effect of the local use of the low intensity laser for Chlamydia cervicitis treatment was accompanied by positive changes in immunological indices of cervical secret, normal concentration of cytokines in cervical secret, restoration of the number and functions of neutrophils. Local use of the low intensity laser contributed to decreased number of opportunistic pathogenic microorganisms and their associations, and restored local flora.
Our previous study has shown that the adoptive transfer of dendritic cells (DCs) freshly isolated from Chlamydia-infected mice (iIDCs), unlike those from control naive mice (iNDCs), can inhibit systemic and cutaneous eosinophilia induced by OVA exposure. In the present study, we examined the mechanism by which iIDC inhibits allergen-specific Th2 cell differentiation in vitro and in vivo. The study revealed that iIDCs exhibited higher surface expression of CD8alpha and the ICOS ligand (ICOS-L), as well as higher IL-10 and IL-12 production than iNDCs. In vitro DC:CD4(+) T cell coculture experiments showed that iIDCs could inhibit allergen-specific Th2 cell differentiation and that the inhibitory effect could be abolished by the blockage of IL-10 or IL-12 activity. More interestingly, the coblockade of IL-10 and the ICOS-L showed synergistic effect in enhancing allergen-driven Th2 cytokine production. Furthermore, adoptive transfer of iIDCs, but not iNDCs, to OVA sensitized mice significantly inhibited airway eosinophilia and mucus overproduction following intranasal challenge with OVA. Overall, the data demonstrate a critical role played by ICOS-L-expressing and IL-10-producing DCs from Chlamydia-infected mice in the infection-mediated inhibition of allergic responses.