Search

The aim of the research was to establish connection between the roles of infertility duration, patient age, various extragenital and genital pathologies in ASA pathogenesis. The work is based on retrospective analysis of 496 outpatient cards, which covered detailed anamnestic data and results of past complex clinico-laboratory tests. Criteria for inclusion in the study was infertility during marriage for at least 18 month, high concentration of ASA-s in booth blood and sperm. It was found that there is no statistically significant connection between the ASA and past illnesses, profession, family history, accompanying autoimmune diseases and extragenital pathologies. Chlamydia trachomatis, Ureaplasma urealyticum, and Mycoplasma hominis compared to other STDs, cause statistically significant increase of ASAs concentration in blood serum, as well as in ejaculate (p<0,001). Testicle associated pathologies plays an important role in development of antisperm immunity, especially orchitis and epididymitis, during which statistically insignificant increase of levels of ASA has been detected in blood, as well as in semen (p<0,001). Thus, we can conclude that, Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, orchitis and epididymitis causes malfunction of blood-testicular barrier, which resulted in inflammatory and toxic damage of spermatogenic epithelium, which in turn plays significant role in the development of autoimmune infertility.

The aim of the research was to study humoral immunity status of infertile men with high concentration of antisperm antibodies in blood plasma, sexually transmitted diseases (STD) and various pathologies of reproductive system. Analysis of 496 outpatient cards has been conducted. It was found, that patients with high levels of ASA >150 mg/l, or average 100-150 mg/l, had statistically significant (p=0,001) high content of Ig A and Ig G relative to the control group. Men with serum ASA concentration >100 mg/l, had statistically insignificant increased levels of all 3 types of immunoglobulins relative to the control group. Patients infected with Chlamydia trachomatis proved to have decreased IgA and IgG, 0,95±0,12 and 6,64±0,5 respectively (p<0,001). As for the patients infected with Ureaplasma urealyticum, decreased levels in Ig A and Ig M have been reported as 0,75±0,29 and 1,08±0,08 respectively (p<0,05). In the course of prostate gland inflammation statistically significant deficiency of Ig A and IgG was evident relative to the control group, 0,75±0,10 g/l and 5,94±0,54 g/l respectively (p<0,001). As for the males with varicocele, Ig A and Ig M decrease is noticeable relative to the control group, 1,06±0,21 g/l and 0,61±0,19 g/l respectively (p<0,05).

Objective: To explore the distribution of Ureaplasma urealyticum (UU) serotypes in cervix secretion and examine the relationship between serotype and host age, clinical phenotypes and vaginal Lactobacilli., Methods: A total of 444 cervical secretion samples were collected from healthy subjects and 342 cervical secretion samples from females with genital diseases between October and December 2012 at Sir Run Run Shaw Hospital, Zhejiang University School of Medicine. Biovar-typing was performed by PCR based on multiple-banded antigen (MBA) gene. And serotyping was performed by real-time PCR based on specific nucleotide sequences., Results: The positive rate of UU in disease group (62.6%, 214/342) was significantly higher than that in healthy group (44.1%, 196/444, P < 0.05). The main serotypes in both groups were 1, 3, 6, 9 and mixed infection.No significant difference existed between host age and UU serotype (P > 0.05) . The distribution of serotype 3 in disease and Lactobacilli abnormal group was significantly higher than that in healthy and Lactobacilli normal groups (13.1% (28/214) vs 5.1% (10/196) , 12.2% (27/221) vs 5.8% (11/189) , both P < 0.05) whereas the distribution of serotype 6 in disease and Lactobacilli abnormal groups was significantly lower than that in healthy and Lactobacilli normal groups (14.0% (30/214) vs 30.1% (59/196) , 16.3% (36/221) vs 28.0% (53/189) , both P < 0.05)., Conclusions: 1, 3, 6, 9 and mixed infection are the main UU serotypes in female cervix.Serotype 3 and mixed infection may be associated with female genital infection.

The aim of the research was to explore women with reproductive problems and pregnant women on Mycoplasma and Ureaplasma as well as to investigate spread of these microbes in the women of reproductive age. There were investigated 100 women with reproductive problem and 96 pregnant women. It was found that 64% of women with reproductive problem and 60% of pregnant women had Ureaplasma urealyticum with high titer (more then 1000 cells in ml), but Mycoplasma hominis was detected approximately in equal % of non-pregnant and pregnant women (12% - non-pregnant women; 16% - pregnant women). It is recommended to investigate women before planning pregnancy.

Background: There are few studies on coinfection with genital mycoplasmas and ureaplasmas in men with gonococcal urethritis (GU). The role of these species in postgonococcal urethritis (PGU) is poorly understood. Thus, we conducted a study to determine the prevalence of coinfection with genital mycoplasmas and ureaplasmas among men with GU and to assess the role of these pathogens in PGU., Methods: Three hundred ninety men infected with culture-confirmed Neisseria gonorrhoeae participated in the study. Chlamydia trachomatis, Mycoplasma genitalium, Mycoplasma hominis, Ureaplasma parvum biovar 1, and Ureaplasma urealyticum biovar 2 in first-voided urine samples were detected by polymerase chain reaction-based assay at the patients' initial visits. PGU was judged to be present if the urethral smear was positive for polymorphonuclear leucocytes 7-14 days after treatment for gonorrhea. The association between each microorganism and PGU, measured by the odds ratio, was estimated by multivariate logistic regression analysis., Results: C. trachomatis, M. genitalium, M. hominis, U. parvum biovar 1, and U. urealyticum biovar 2 were detected in 85 (21.8%), 16 (4.1%), 8 (2.1%), and 33 men (8.5%), respectively. In patients with chlamydia-negative GU, coinfection with M. genitalium was associated with a 14.54-fold greater risk of PGU (95% confidence interval, 2.91-72.74), and coinfection with U. urealyticum biovar 2 was associated with a 3.64-fold greater risk of PGU (95% confidence interval, 1.24-10.63)., Conclusions: Coinfection with M. genitalium or U. ureaplasma biovar 2 in men with GU was significantly associated with PGU, independent of C. trachomatis. Men with GU should be treated presumptively with antibiotics that are active against C. trachomatis, M. genitalium, and U. urealyticum biovar 2.

The genital mycoplasmas represent a complex and unique group of microorganisms that have been associated with a wide array of infectious diseases in adults and infants. The lack of conclusive knowledge regarding the pathogenic potential of Mycoplasma and Ureaplasma spp. in many conditions is due to a general unfamiliarity of physicians and microbiology laboratories with their fastidious growth requirements, leading to difficulty in their detection; their high prevalence in healthy persons; the poor design of research studies attempting to base association with disease on the mere presence of the organisms in the lower urogenital tract; the failure to consider multifactorial aspects of diseases; and considering these genital mycoplasmas only as a last resort. The situation is now changing because of a greater appreciation of the genital mycoplasmas as perinatal pathogens and improvements in laboratory detection, particularly with regard to the development of powerful molecular nucleic acid amplification tests. This review summarizes the epidemiology of genital mycoplasmas as causes of neonatal infections and premature birth; evidence linking ureaplasmas with bronchopulmonary dysplasia; recent changes in the taxonomy of the genus Ureaplasma; the neonatal host response to mycoplasma and ureaplasma infections; advances in laboratory detection, including molecular methods; and therapeutic considerations for treatment of systemic diseases.

Intrauterine infection is an important cause of some birth defects worldwide. The most common pathogens include rubella virus, cytomegaloviurs, ureaplasma urealyticum, toxoplasma, etc. General information about these pathogens in epidemiology, consequence of birth defects, and the possible mechanisms in the progress of birth defects, and the interventions to prevent or treat these pathogens' infections are described. The infections caused by rubella virus, cytomegaloviurs, ureaplasma urealyticum, toxoplasma, etc. are common, yet they are proved to be fatal during the pregnant period, especially during the first trimester. These infections may cause sterility, abortion, stillbirth, low birth weight, and affect multiple organs that may induce loss of hearing and vision, even fetal deformity and the long-term effects. These pathogens' infections may influence the microenvironment of placenta, including levels of enzymes and cytokines, and affect chondriosome that may induce the progress of birth defect. Early diagnosis of infections during pregnancy should be strengthened. There are still many things to be settled, such as the molecular mechanisms of birth defects, the effective vaccines to certain pathogens. Birth defect researches in terms of etiology and the development of applicable and sensitive pathogen detection technology and methods are imperative.

Ureaplasma urealyticum respiratory tract colonization in preterm infants has been associated with a high incidence of pneumonia and the development of bronchopulmonary dysplasia. However, study of this human pathogen has been hampered by the absence of animal models. We have developed the first juvenile mouse model of Ureaplasma pneumonia and characterized the histopathology during the month following inoculation. C3H/HeN mice were inoculated intratracheally with a mouse-adapted clinical Ureaplasma isolate (biovar 2) or sham inoculated with 10B broth. Culture of lung homogenates and PCR of DNA from bronchoalveolar lavage fluid (BAL) confirmed the presence of Ureaplasma in 100% of inoculated animals at 1 day, 60% at 2 days, 50% at 3 days, and 25% at 7 and 14 days. Ureaplasma was undetectable 28 days postinoculation. There were marked changes in BAL and interstitial-cell composition with increased number of polymorphonuclear leukocytes 1 to 2 days and 14 days postinoculation and macrophages at 2 and 14 days postinoculation. The Ureaplasma infection caused a persistent focal loss of airway ciliated epithelium and a mild increase in interstitial cellularity. There were no differences in BAL protein concentration during the first 28 days, suggesting that pulmonary vascular endothelial barrier integrity remained intact. Comparison of BAL cytokine and chemokine concentrations revealed low levels of tumor necrosis factor alpha (TNF-alpha) at 3 days and monocyte chemoattractant protein 1 at 7 days in Ureaplasma-infected mice but a trend toward increased TNF-alpha at 14 days and increased granulocyte-macrophage colony-stimulating factor and interleukin-10 at 28 days. These data suggest that Ureaplasma alone may cause limited inflammation and minimal tissue injury in the early phase of infection but may promote a mild chronic inflammatory response in the later phase of infection (days 14 to 28), similar to the process that occurs in human newborns.

Three serovars (5, 8 and 10) of Ureaplasma urealyticum were inoculated intravaginally into groups of oestradiol-treated young adult BALB/c strain mice. Hormone treatment was essential for vaginal colonisation. The proportion of mice colonised initially and the persistence of colonisation were different with the three serovars; half of those given serovar 8 were still colonised after 84 days. A strain of serovar 5 after a further 50 subcultures in vitro was a little less persistent than it was before such subculture, but not in a way to suggest that subculturing was the main reason for differences in the behaviour of the serovars. At autopsy of six mice that were still colonised vaginally 158 days after inoculation of serovar 8, spread to the upper genital tract was shown to have occurred in three of them and dissemination to the liver and kidney in one. Compared with immunocompetent mice of strain CB20, such dissemination was not a feature in genetically related mice with severe combined immunodeficiency. This is not in keeping with the situation in hypogammaglobulinaemic patients in whom ureaplasmas and other mycoplasmas are known to disseminate. However, differences in the proportion of immunocompetent mice colonised or in ureaplasmal persistence with different serovars may act as a marker for differences in human pathogenicity and is worthy of further study.

The comparison of the genomes of two very closely related human mucosal pathogens, Mycoplasma genitalium and Mycoplasma pneumoniae, has helped define the essential functions of a self-replicating minimal cell, as well as what constitutes a mycoplasma. Here we report the complete sequence of a more distant phylogenetic relative of those bacteria, Ureaplasma urealyticum (parvum biovar), which is also a mucosal pathogen of humans. It is the third mycoplasma to be sequenced, and has the smallest sequenced prokaryotic genome except for M. genitalium. Although the U. urealyticum genome is similar to the two sequenced mycoplasma genomes, features make this organism unique among mycoplasmas and all bacteria. Almost all ATP synthesis is the result of urea hydrolysis, which generates an energy-producing electrochemical gradient. Some highly conserved eubacterial enzymes appear not to be encoded by U. urealyticum, including the cell-division protein FtsZ, chaperonins GroES and GroEL, and ribonucleoside-diphosphate reductase. U. urealyticum has six closely related iron transporters, which apparently arose through gene duplication, suggesting that it has a kind of respiration system not present in other small genome bacteria The genome is only 25.5% G+C in nucleotide content, and the G+C content of individual genes may predict how essential those genes are to ureaplasma survival.

Ureaplasma urealyticum is relatively common in the respiratory tract of very low birth weight infants and has been hypothesized to be involved in the development of chronic lung disease. The purpose of this study was to investigate whether U. urealyticum could stimulate macrophages to produce proinflammatory cytokines in vitro, which are early pathologic changes in the lung during the development of chronic lung disease. A human monocytic cell line (THP-1) differentiated to macrophages, a rat alveolar macrophage cell line (Nr8383), and human lung macrophages from tracheobronchial aspirate fluid in preterm infants were exposed to U. urealyticum antigen for 24 h. The protein levels of human IL-6, tumor necrosis factor-alpha (TNF-alpha), and rat TNF-alpha were measured with ELISA. Rat IL-6 was analyzed with a specific bioassay. The mRNA levels of these cytokines were detected by reverse transcriptase-PCR. The production of TNF-alpha and IL-6 increased after stimulation with U. urealyticum in both the human and rat macrophage cell lines. In tracheobronchial aspirate fluid macrophages, U. urealyticum increased the production of TNF-alpha from 14 to 84% and IL-6 from 46 to 268% above control levels. U. urealyticum also induced gene expression of TNF-alpha and IL-6. In conclusion, U. urealyticum could be an important factor in the development of chronic lung disease because of its ability to induce alveolar macrophage proinflammatory cytokine production.

We trace the evidence-based evolution of ureaplasmal male infertility as an established clinical entity. We review epidemiology data, possible pathogenic mechanisms of Ureaplasma urealyticum in infertility, and the results of isolation studies and therapeutic trials. Future developments are outlined.

The presence of Ureaplasma urealyticum, Mycoplasma hominis, and Chlamydia trachomatis was explored in 50 public restroom toilet bowls. We used culture, antigen detection, polymerase chain reaction, and survival assay. Five bowls (10%) were contaminated with at least one organism. U. urealyticum was found in four bowls, M. hominis in three, and C. trachomatis in one. U. urealyticum survived on the toilet rim for up to 2 hours.

The in-vitro effects of several concentrations of Ureaplasma urealyticum on the motility, membrane integrity and morphology of washed spermatozoa from healthy donors were studied. A significant reduction in sperm motility and signs of membrane alteration, directly related to U.urealyticum concentration and contact time were observed. Scanning electron microscopy examination showed masses of U. urealyticum attached to the head and middle piece of some of deformed spermatozoa. It is suggested that U.urealyticum is involved in sperm changes leading to male infertility, particularly when there is heavy U. urealyticum colonization or specific infections with this microorganism.

The possibility that Ureaplasma urealyticum might play an important role in human infertility was first raised more than 20 years ago, but this association remains speculative. Considering the hypothesis that the pathogenicity of Ureaplasma urealyticum may depend on its serotypes, the clastogenic effects of different strains of Ureaplasma urealyticum, at concentrations of 10(3) CCU (color changing units)/ml, 10(4) CCU/ml and 10(5) CCU/ml, were evaluated in vitro in short-term cultures of human lymphocytes. Total or partial mitotic inhibition was produced by Ureaplasma urealyticum serotypes 2, 3 and 10 independent of the concentration (10(3) CCU/ml, 10(4) CCU/ml or 10(5) CCU/ml) of the microorganisms employed. In contrast, the clastogenic effects observed with serotypes 1, 7 and 12 varied according to the concentration employed in the test. Mitotic alterations were observed in Ureaplasma urealyticum serotypes 5, 6, 7, 8, 9, 11 and 12. Chromatid gaps (53.0%) and chromatid breaks (13.9%) were the most frequent types of alterations observed. The results of this in vitro assay demonstrated that the clastogenic effects varied with the Ureaplasma urealyticum serotypes evaluated.

Mycoplasma hominis was isolated in pure culture from septic synovial aspirates from an individual (patient A) during 16 different bouts of exacerbation over a 70-month period of observation. Two isolates, 10(7) and also 10(6) color-changing units (CCU) of the 1620 isolate and 5 x 10(4) CCU of the 1628 isolate, caused inflammation in chimpanzees inoculated intraarticularly. Inflammation was also induced with 10(7) CCU of the 2010B isolate, serovar VII of Ureaplasma urealyticum, recovered from an agammaglobulinemic individual (patient B) with septic polyarthritis and with 3 x 10(6) CCU of the PI-1428 isolate of Mycoplasma pneumoniae. Inflammation persisted for up to 36 days and was self-limiting. The aspirates contained up to 220,000 white blood cells/mm3 and up to 10(7) CCU/mL. There was good correlation between the severity of inflammation and the numbers of organisms, but antibody was not detected in aspirates during the peak severity of disease. As the numbers of organisms, decreased, detectable levels of antibody increased, thus suggesting that antibody may have been bound to antigen. Chimpanzees previously infected with either the 1628 isolate of M. hominis or the 2010B isolate of U. urealyticum were protected on challenge with > 100 times the minimal dose causing arthritis. Chimpanzees showed little or no inflammation when inoculated intraarticularly with 5 x 10(8) CCU of the type strain PG-21 of M. hominis or with the type strain CO of U. urealyticum or when inoculated intravenously with 3 x 10(8) CCU of the arthrogenic 1620 isolate of M. hominis.

Cultures positive for Ureaplasma urealyticum in babies weighing < 1000 g have been associated with both chronic lung disease (CLD) and death, but no definite causality has been established. To further investigate the role of the organism in CLD, we colonized premature baboons with U. urealyticum and compared resulting pathology with that in uninoculated control animals. Using an established model of prematurity, the 140-day-gestation baboon, three animals were colonized with U. urealyticum via endotracheal tube. All had hyaline membrane disease, indistinguishable from disease in human infants, and U. urealyticum infection. Samples obtained from nasopharynx, trachea, pleural fluid, and, at necropsy, lung tissue produced positive cultures. Culture of blood from one animal yielded U. urealyticum. On pathologic examination, after 6 days of ventilation, all three of the infected animals had the specific pathologic finding of bronchiolitis with epithelial ulceration not seen in four uninfected control animals. Thus, U. urealyticum is capable of causing a pathologically recognizable pulmonary lesion in premature primates with hyaline membrane disease.

Recent studies show an association between the presence of Ureaplasma urealyticum in tracheal aspirates and bronchopulmonary dysplasia. We hypothesized that among infants with birth weights < or = 1,250 g and respiratory disease, those with U. urealyticum in their tracheal aspirates would have radiographic evidence of more-severe pulmonary disease more often than would those without this organism. A total of 292 low-birth-weight infants who had endotracheal aspirate cultured within 7 days of birth were enrolled. The radiographic outcome variables were pneumonia, early severe bronchopulmonary dysplasia (precocious), and chronic lung disease. Microorganisms were isolated from 128 infants (44%); U. urealyticum was isolated from 44 (15%). Pneumonia was significantly more common in infants with than without U. urealyticum (30% vs. 16%, P = .03). U. urealyticum also was associated with precocious bronchopulmonary dysplasia independent of prematurity, race, and sex (odds ratio, 2.2; P < .05). Tracheal isolation of U. urealyticum within 7 days of birth is associated with pneumonia and precocious bronchopulmonary dysplasia.

It is becoming apparent that a high rate of variability of surface structures is a ubiquitous property among mycoplasmas. The present study demonstrates how variations in the size of the V-1 antigen (a major surface antigen of Mycoplasma pulmonis thought to be associated with virulence) are reflected by phenotypic differences (cytadherence) that may play a role in virulence of the organism. Furthermore, a similar antigen is described for the human pathogen Urea-plasma urealyticum, and data are presented on the analysis of clinical isolates that demonstrate the potential for variation in the size of this antigen in vivo. Although no direct connection of antigen variation to natural disease has yet been presented, the data further document the tremendous potential for virulence-related diversity possessed by these organisms and emphasize the importance of a valid animal model for discerning the true relationship between variation and virulence.

This study examined the association between Ureaplasma urealyticum colonization and the development of chronic lung disease (CLD) in 93 premature infants who were treated with surfactant and who had birth weights < 1251 g. Nasopharyngeal and tracheal cultures for U. urealyticum were obtained at 2 +/- 1 and at 14 +/- 1 days after birth and were positive in 17 (18%) of 93 patients. Infants born vaginally were 4.5 times more likely to be colonized than were those born by cesarean section. Colonization with U. urealyticum was associated with 1.66 (95% confidence interval, 1.24-2.20, P = .024) times the risk of developing CLD and with a greater incidence of > or = 2+ polymorphonuclear leukocytes in the tracheal aspirate at 2 +/- 1 days of age compared with uncolonized infants (P = .025). We conclude that U. urealyticum colonization is associated with CLD even after surfactant treatment. The presence of U. urealyticum is also associated with inflammatory cells in the tracheal aspirate.

Evidence related to the association of Ureaplasma urealyticum with premature birth is reviewed. U. urealyticum is a common inhabitant in the vagina of pregnant women. It is recovered from the vaginas of approximately 70% of pregnant women. The presence of U. urealyticum in the vagina is not associated with premature birth. Therapy to eradicate U. urealyticum from the vagina during pregnancy does not reduce the incidence of premature birth. Recovery of U. urealyticum from the amniotic fluid has not been associated with prematurity. However, in three of six reports, the recovery of U. urealyticum from the chorioamnion has been associated with prematurity, and U. urealyticum is rather consistently associated with histological chorioamnionitis. This review suggests that U. urealyticum in the lower genital tract is not associated with premature birth but that its presence in the chorioamnion is weakly associated with prematurity and strongly associated with histological chorioamnionitis.

Multiple insults may induce bronchopulmonary dysplasia (BPD) in premature infants, including the recently reported association of BPD with neonatal Ureaplasma urealyticum colonization. One mechanism of damage could involve stimulation of proinflammatory cytokine release from pulmonary fibroblasts. We therefore compared the effects of U. urealyticum, oxygen, and lipopolysaccharide (LPS) on the release of interleukin (IL)-1 beta, IL-6, and IL-8 from neonatal fibroblasts. Fibroblasts were grown in multiwell plates and divided into the following experimental conditions: fibroblasts alone, fibroblasts plus U. urealyticum (10,000 cfu/mL), and fibroblasts plus LPS (2 micrograms/mL). Plates were then exposed to room air or hyperoxia for 48 h, and supernatants were assayed for IL. U. urealyticum-infected fibroblasts produced a significant increase in IL-6 (P < .05) and a dramatic increase in IL-8 (P < .05) that was independent of hyperoxic exposure and significantly increased over that produced by LPS or hyperoxia alone. U. urealyticum is a potent inducer of fibroblast cytokine release in vitro and may contribute to the development of BPD.

A critical appraisal of four cohort studies examining the relationship between Ureaplasma urealyticum and chronic lung disease (CLD) of prematurity is presented. Three studies were concurrently conducted, but the fourth was conducted 4 years later when surfactant replacement was a widespread practice. Although infants were enrolled in all studies soon after birth before they had developed CLD, there were differences in patients population, the definition of colonization with U. urealyticum, neonatal management, and the definition of CLD of prematurity. Despite the differences, all four studies found an association between colonization and development of CLD of prematurity. A combined estimate of relative risk for the four studies was 1.91 (95% confidence interval, 1.54-2.37). When infants were categorized into groups by birth weight, the association was not observed in infants who weighed > 1,250 g. The association was also not observed in infants who weighed < 750 g, but the risk of CLD of prematurity in the uncolonized control group was already 82%. Because the cohort study design allows for the possibility that one or more additional factors associated with U. urealyticum may be the true cause(s) of CLD of prematurity, there is strong but not definitive evidence that U. urealyticum causes CLD of prematurity.