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Biomedical subjects

D Taylor-Robinson

Publications and source records attributed to D Taylor-Robinson.

At least 127 records · Page 7Linked to original sources
PubMed1994

Mycoplasma genitalium in the joints of two patients with arthritis.

Mycoplasma genitalium was sought in synovial fluids from 13 patients, of whom five had Reiter's syndrome, four had rheumatoid arthritis, and one each had systemic lupus erythematosus, psoriatic arthritis, rheumatic fever and undefined arthritis. The mycoplasma was detected by a PCR assay in the knee joint of a 25-year-old man with Reiter's syndrome, from whom urethral ureaplasmas were isolated and whose synovial fluid mononuclear cells responded to ureaplasmal antigens in a proliferation assay. Mycoplasma genitalium was also detected in the knee joint during an exacerbation of arthritis in a 58-year-old man who had had seronegative juvenile polyarthritis that had evolved to seronegative rheumatoid arthritis.

Adult↗
PubMed1994

Mycoplasma fermentans and HIV-associated nephropathy.

We describe a patient in whom HIV-associated nephropathy developed in association with the detection of Mycoplasma fermentans. This mycoplasma was found in renal tissue by means of a polymerase chain reaction when nephropathy was first evident, and subsequently in urine, blood and the throat. The evidence presented strengthens the causal association of this micro-organism with HIV-induced nephropathy.

AIDS-Associated Nephropathy↗
PubMed1994

Immunological events in regressing genital warts.

Little is known of the in vivo role of the immune system in controlling human papillomavirus infection in the genital tract. The authors have studied 125 closely monitored patients with genital warts. Of these 125 patients, wart regression was seen in 28 patients. This study provides evidence that clearance of human papillomavirus from the genital tract is characterized by an active cell-mediated immune response. Regressing warts (n = 14) contained significantly more T lymphocytes (P < .05, Wilcoxon rank sum test) and macrophages (P < .01) than did nonregressing controls (n = 14). CD4-positive lymphocytes predominated in regression, both within the wart stroma and the surface epithelium, where there was a significant change in the ratio of CD4+ to CD8+ cells (P < .01). Lymphocytes in regression also showed greater expression of activation markers, and the majority were of the "antigen-experienced" phenotype. There was no difference in Langerhans cell numbers, although there was significant induction of the immune accessory molecules HLA-DR and ICAM1 (P < .05) on keratinocytes, and E-selectin and VCAM1 (P < .05) on endothelial cells in regressing warts. The changes in regression are consistent with a delayed-type hypersensitivity reaction to foreign antigen, and the ability to induce and mount such a response may be a critical determinant of effective natural immunity to the genital HPVs. Specific targeting of delayed-type hypersensitivity responsiveness may increase the efficacy of strategies for immuno-intervention against HPV infection in the genital tract.

Adult↗
PubMed1994

Protection of mice against vaginal colonisation by Mycoplasma pulmonis.

Resistance against vaginal colonisation by Mycoplasma pulmonis in strain TO mice after exposure to the mycoplasma was investigated. Eighteen mice from which M. pulmonis had been eliminated from the vagina, either naturally or by antibiotic therapy, were resistant to vaginal recolonisation. Specific antibody was measured by an indirect microimmunofluorescence technique and the geometric mean titre (GMT) for each group of mice is presented. Almost all of 31 mice that had developed circulating antibody (GMT 83) or local antibody (GMT 40), or both, after vaginal exposure were resistant to re-colonisation, as were those in which antibodies could not be detected. Seven other mice which had been colonised only in the oropharynx previously and which possessed antibody--circulating (GMT 64) or local (GMT 30), or both--were resistant to vaginal colonisation, but 13 mice with little or no antibody after lack of colonisation at either anatomical site were susceptible. All of 15 mice given killed M. pulmonis organisms intravenously, despite developing circulating antibody in high titre (GMT 122), were susceptible to vaginal colonisation, as were 14 of 15 mice that developed circulating (GMT 15) and local antibodies after being given killed organisms intravaginally. However, 25 mice with high titres of circulating (GMT 154-170) or local (GMT 20) antibody, or both, after receiving live organisms intravenously, were less susceptible to vaginal colonisation (17 becoming colonised) than were 21 non-immunised mice (all becoming colonised) and the organisms were eradicated more rapidly from the former. Despite this, the mice that were colonised following intravenous inoculation of live organisms had pre-challenge antibody titres that were as great as those that were not colonised.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

A longitudinal study of bacterial vaginosis during pregnancy.

OBJECTIVE: To determine the longitudinal changes in the incidence of vaginosis in pregnancy. DESIGN: A prospective study of women during pregnancy. SETTING: A District General Hospital in North-West London. SUBJECTS: Seven hundred and eighteen pregnant women attending antenatal clinics. At their first attendance and subsequently, Gram-stained vaginal smears were examined and Mycoplasma hominis and Gardnerella vaginalis were sought by culture. RESULTS: Initially, 87 (12%) women had bacterial vaginosis diagnosed on Gram-stained reading of the vaginal smears. Examination of further smears, obtained from 176 women at 36 weeks of gestation, showed that those whose vaginal flora was normal initially, and who went to term, rarely developed vaginosis (three of 127, 2.4%). Samples were obtained at 36 weeks gestation from 32 women who had bacterial vaginosis initially, and went to term. In almost 50% (15 of 32) of these a normal lactobacillus-dominated flora had regenerated. Thirty-five women (5%) had initial vaginal smears graded as intermediate. From this group, six of the 17 (35%) women from whom samples were obtained at 36 weeks gestation still had flora of an intermediate pattern; 10(59%) now had normal flora and only one (6%) had developed bacterial vaginosis. Women with bacterial vaginosis were more likely to be culture-positive for M. hominis than those with normal flora (34/78 versus 10/563, odds ratio 42.73 (18.9 to 102.3) P < 0.001), or to be culture-positive for G. vaginalis than those with normal flora (35/78 versus 21/563, odds ratio 21.0 (10.75 to 41.2) P < 0.001). CONCLUSION: Pregnant women do not commonly develop bacterial vaginosis after 16 weeks gestation, and if present, it remits spontaneously in approximately half of those who reach term. As bacterial vaginosis is associated with increased rates of second trimester miscarriage and preterm delivery, any treatment aimed at its eradication in pregnancy should be given no later than the beginning of the second trimester of pregnancy.

Adult↗
PubMed1994

Mycoplasmas and ureaplasmas in patients with hypogammaglobulinaemia and their role in arthritis: microbiological observations over twenty years.

OBJECTIVES: To study the occurrence of mycoplasmas and ureaplasmas in patients with hypogammaglobulinaemia and the relationship of these micro-organisms to septic arthritis. METHODS: Over a period of about 20 years, 53 men and 38 women with hypogammaglobulinaemia, most of whom were less than 50 years old, were examined clinically and microbiologically. Mycoplasmas and ureaplasmas were sought in the throat, urogenital tract and joints by standard cultural methods, although not consistently in the three sites of all patients. RESULTS: Arginine-hydrolysing mycoplasmas and ureaplasmas occurred with similar frequency in the sputum/throat of the hypogammaglobulinaemic patients, but no more often than might be expected in immunocompetent patients. Ureaplasmas, however, dominated in the urogenital tracts of both men and women, being found in 75% of vaginal specimens. Arginine-hydrolysing mycoplasmas occurred two to six times more frequently and ureaplasmas two to three times more frequently in urine specimens from hypogammaglobulinaemic patients than they did in such specimens from sex- and age-matched non-venereal disease, hospital patients or healthy subjects; these differences were statistically significant (p < 0.05). Enhanced mucosal colonisation probably increases the chance of spread to distant sites, such as the joints. Of the 91 patients, 21 (23%) had septic arthritis involving one or more joints. Mycoplasmas and/or ureaplasmas, but not bacteria, were isolated from the joints of eight (38%) of these patients. However, dissemination to joints apparently had not occurred in some despite the opportunity by virtue of mycoplasmal or ureaplasmal colonisation at a mucosal site. Sometimes antibiotic therapy failed clinically, and microbiologically and recommendations for management are outlined. CONCLUSIONS: Hypogammaglobulinaemic patients appear to be more susceptible to colonisation of mucous membranes, especially of the urogenital tract, with mycoplasmas and ureaplasmas than are immunocompetent individuals. These micro-organisms are responsible for about two fifths of the septic arthritides occurring in these patients.

Adolescent↗
PubMed1994

Chlamydia trachomatis in women: the more you look, the more you find.

OBJECTIVE: To determine the extent to which testing of multiple sites and samples is required to define whether a woman is Chlamydia trachomatis-positive. DESIGN: One-hundred and fifty women attending the Genitourinary Medicine clinic at St Mary's Hospital were enrolled; they had not received antichlamydial antibiotics in the previous three months, were not in a high-risk group for HIV infection, or pregnant, or using an intrauterine contraceptive device. Thirty-two women were re-examined three months after recruitment. METHODS: An urethral specimen was Gram stained (smear) and cultured for gonococci. Another urethral specimen was taken to detect C trachomatis elementary bodies (EBs) by the MicroTrak direct fluorescent antibody (DFA) test (Syva). An endocervical swab specimen was Gram stained (smear) and cultured for gonococci. One of two other endocervical swabs was used for the DFA test and was then placed in medium which was centrifuged in a MicroCentaur at 13,000 rpm for 10 min; the deposit was examined by using the DFA test. The first 15-20 ml of voided urine (first pass urine; FPU) was also centrifuged and the deposit tested similarly. RESULTS: Of 182 cervical smears and/or deposits tested for C trachomatis, 38 were positive; more cervical deposits (37) than smears (26) were positive and, of these, one-fifth of the deposits and one-third of the smears contained fewer than 10 elementary bodies. Of 162 paired urethral smears and FPU deposits available, one or other specimen of 36 pairs was chlamydia-positive, that is 31 smears and 32 deposits; of these, two-fifths of the smears and half of the deposits contained fewer than 10 EBs. Of 150 sets of cervical and urinary tract samples tested, 31 were chlamydia-positive at both sites, six in the cervix alone and four in the urinary tract alone. Of 139 women for whom there were valid first visit sample results, 36 (26%) were chlamydia-positive in the cervix, 34 (25%) in the urinary tract and 41 (29%) had at least one sample from either site positive. Overall, DFA tests of deposits from centrifuged cervical specimens achieved the highest sensitivity (88%) and those of cervical smears the lowest (70%). CONCLUSIONS: Deposits from centrifuged cervical specimens were C trachomatis-positive more often than were cervical smears. Testing deposits from centrifuged urines was as successful as testing urethral smears. One-fifth (cervical deposits) to one-half (urine deposits) of specimens contained fewer than 10 EBs. The urinary tract was chlamydia-positive almost as frequently as the cervix but both sites needed to be tested to define whether a woman was chlamydia-positive.

Cervix Uteri↗
PubMed1994

Ureaplasma urealyticum in Reiter's syndrome.

OBJECTIVE: To evaluate the role of Ureaplasma urealyticum (Uu) in the pathogenesis of Reiter's syndrome (RS). METHODS: Infection with Uu was determined in 31 patients with RS and 28 patients with other arthritides by urethral, cervical and synovial fluid (SF) culture and by measuring anti-Uu serum antibody. Infection with Chlamydia trachomatis was determined by examining SF by a direct immunofluorescence technique, by a polymerase chain reaction and by measuring anti-C. trachomatis serum antibody. The proliferative response of SF and peripheral blood mononuclear cells (PBMC) to Uu antigens in patients with RS was compared to that of a control group. The effect that treatment of 6 patients with RS with ciprofloxacin had on repeated cultures, on titer of anti-Uu antibody and on mononuclear cell reactivity was measured sequentially. RESULTS: The colonization rate of Uu in patients with RS (74%) was significantly greater than in patients with other arthritides (14%). Genital C. trachomatis isolation and serum anti-C. trachomatis antibody were uncommon in both groups (11 and 13%, respectively). SF mononuclear cells of the patients with RS proliferated specifically in response to Uu antigens [up to 6.9 stimulation index (SI)], as did their PBMC (up to 14.5 SI). In some patients, high anti-Uu antibody titers were measured in the serum. Clinical remission was observed in 4 of 6 patients and correlated with eradication of Uu, decrease in antibody titers and disappearance of mononuclear cell reactivity to Uu antigens. CONCLUSION: Our findings suggest that Uu might be a causative agent or a trigger in the development of sexually acquired RS.

Adult↗
PubMed1993

Association of Mycoplasma genitalium with acute non-gonococcal urethritis.

Chlamydia trachomatis is known to be a cause of acute non-gonococcal urethritis (NGU), though the aetiology of this disorder is not fully understood. Mycoplasma genitalium has been isolated from a few men with NGU, but culture has remained difficult and reliable detection became possible only with a specific polymerase chain reaction (PCR). We have used the PCR to examine the role of M genitalium in NGU. M genitalium was detected in urethral samples from 24 (23%) of 103 men with symptoms, signs, or both, of acute NGU, but from only 3 (6%) of 53 men without NGU (p < 0.006). This association was independent of the presence of C trachomatis and could not be explained by differences in age, ethnic, origin, lifetime number of sexual partners or a change in sexual partner during the previous 3 months. The clinical response of the mycoplasma-positive men to doxycycline treatment was at least as satisfactory as that of the chlamydia-positive men. These findings suggest that the association of M genitalium with NGU is likely to be causal, a notion consistent with the known virulence characteristics of this microorganism and its ability to cause urethritis in male sub-human primates.

Acute Disease↗
PubMed1993

Mycoplasma fermentans in individuals seropositive and seronegative for HIV-1.

Mycoplasmas have been suggested as a co-factor to explain various puzzling features of infection by human immunodeficiency virus 1 (HIV-1). We sought Mycoplasma fermentans by means of a semi-nested polymerase chain reaction (PCR) in samples of peripheral-blood mononuclear cells (PBMC), throat swabs, and urine samples from 117 HIV-seropositive patients (of whom 114 were homosexual men). M fermentans was detected in 12 (10%) PBMC samples, 15 (23%) of 65 throat samples, and 4 (8%) of 55 urine samples from the seropositive subjects. The organism was detected in similar proportions among 73 HIV-seronegative patients recruited from a sexually transmitted diseases clinic (9%, 20%, and 6%, respectively); again, most of the men (40 of 50) in this group were homosexual. We found no association between infection by the mycoplasma and stage of disease, CD4 count, or HIV-1 load. These findings do not, however, eliminate the possibility that the mycoplasmal infection could affect the speed of disease progression.

Blotting, Southern↗
PubMed1993

Infection due to Chlamydia trachomatis in pregnancy and the newborn.

Bacteria in the genus Chlamydia comprise three species, C. trachomatis, C. psittaci and C. pneumoniae. C. trachomatis infection is common, varying in prevalence in women from 0% to 37%. In the United States, the prevalence rate is estimated currently to be about 5%. Pregnancy may predispose to an increased chance of infection with C. trachomatis, through physiological immunosuppression and/or cervical ectopy. Maternal antibodies to C. trachomatis provide limited, if any, protection for the newborn. C. trachomatis causes pelvic inflammatory disease--which can result in tubal infertility or ectopic pregnancy and postabortal or late postpartum endometritis. It may also cause chorioamnionitis and premature delivery of the fetus. The incidence of vertical transmission of chlamydiae from mother to baby varies; if the mother is untreated, 20-50% of the newborns will develop conjunctivitis and 10-20% will develop pneumonia. C. psittaci infection in pregnancy is rare, but can cause spontaneous abortion. Whether C. pneumoniae infection in pregnancy has any influence on the outcome has not been ascertained. C. trachomatis can be detected by one or more of several methods; enzyme immunoassays are the least sensitive, but the most widely used. Screening for C. trachomatis in pregnancy may be of benefit in areas of high prevalence, and is generally regarded as being cost-effective if the prevalence rate is more than 5%. Pregnant women are best treated with erythromycin, 250 mg four times daily for 7 days. This will prevent infection of the newborn in more than 90% of cases. The infected neonate should be treated with erythromycin, given systemically and also with topical tetracycline if conjunctivitis is present.

Chlamydia Infections↗
PubMed1993

Mycoplasma pulmonis infection of the murine oropharynx protects against subsequent vaginal colonization.

Intranasal inoculation of 12 young adult mice (strain TO) with Mycoplasma pulmonis protected all of them against vaginal colonization when they were challenged intravaginally 60 days later with the same mycoplasmal strain. In contrast, all 15 mice without a respiratory infection became colonized vaginally (geometric mean titre [GMT] 4.6 x 10(6) colour-changing units [c.c.u.]) when challenged in the same way. The GMT of serum antibody, measured by a microimmunofluorescence technique, prior to challenge was 200 and 8 for the oropharyngeally infected and unexposed mice, respectively. The GMT of antibody in vaginal washings from the two groups was 6 and 3, respectively. All four nude BALB/c mice were susceptible to vaginal colonization (GMT 5.6 x 10(6) c.c.u.) after oropharyngeal infection (GMT 5.1 x 10(4) c.c.u.) resulting from intranasal inoculation, as were all six nude mice (vaginal GMT 1.4 x 10(7) c.c.u.) that had not been inoculated intranasally. In contrast, all ten of their immunocompetent counterparts were resistant to vaginal colonization after oropharyngeal infection (GMT 1.3 x 10(3) c.c.u.), whereas all nine such mice that had not been infected oropharyngeally were susceptible to vaginal colonization (GMT 7.6 x 10(6) c.c.u.). These results show the important role that a respiratory infection has in protecting the vagina against colonization and that protection is dependent on a functioning T-lymphocyte system.

Animals↗
PubMed1993

Models of infection due to mycoplasmas, including Mycoplasma fermentans, in the genital tract and other sites in mice.

Progesterone induces susceptibility in murine genital tracts to Mycoplasma pulmonis, Mycoplasma pneumoniae, and Mycoplasma genitalium when each is given intravaginally. In contrast, estradiol, but not progesterone, induced such susceptibility to Ureaplasma urealyticum, Mycoplasma hominis, and Mycoplasma fermentans, the "incognitus" and PG18 strains of the latter behaving similarly. None of the mice that had been given M. fermentans intravaginally died, whereas others that had been given large numbers of M. fermentans organisms intraperitoneally died within a few days. M. pulmonis spreads from the respiratory tract to other sites more often in T cell-depleted mice than in immunocompetent mice. In addition, the "incognitus" strain of M. fermentans given intravenously killed BALB/c nude mice but did not kill immunocompetent control mice of the same strain or CBA nude mice. The effect is not unique to M. fermentans since M. hominis inoculated intravenously also killed CBA nude mice or made them ill. Such observations raise the possibility that immunosuppression caused by the human immunodeficiency virus could allow mycoplasmas to flourish and exacerbate disease.

Animals↗
PubMed1993

Mycoplasma fermentans--HeLa cell interactions.

A survey of previous evidence for the intracellular localization of mycoplasmas within nonphagocytic cells indicated that it was insufficient to conclude unequivocally that such localization occurred. Illustrations of the seemingly intracellular existence of Mycoplasma fermentans in the tissues of patients with AIDS and other patients rekindled interest in the topic of mycoplasmal entrance into epithelial cells. Accordingly, the "incognitus" and PG18 strains of M. fermentans were sought and demonstrated within HeLa cells by electron microscopy following treatment of the cell cultures with gold-labeled antiserum specific to the mycoplasma, together with ruthenium red staining. The phenomenon is not unique to this mycoplasma, being demonstrated also with Mycoplasma hominis. In hindsight, some of the earlier investigators who hinted at intracellular localization were probably correct in doing so.

HeLa Cells↗
PubMed1993

Occurrence of Mycoplasma genitalium in different populations and its clinical significance.

Mycoplasma genitalium is predominantly flask-shaped with cytadsorptive and glass-adhering properties. These biological features of pathogenicity are reflected in its ability to cause urethritis and salpingitis in subhuman primates when given experimentally, although its role in human disease is less clear. M. genitalium was initially recovered by culture of specimens from two of 13 men with acute nongonococcal urethritis (NGU), but culture remains a laborious and insensitive means of detection. This organism has, however, been detected in the urethra of > or = 20% of men with acute NGU by using a polymerase chain reaction (PCR) and in a similar proportion of men with chronic NGU. The possibility of sexual transmission of M. genitalium is supported by the fact that by using the PCR it has been detected in the lower genital tract of about 20% of women who were attending a clinic for sexually transmitted diseases. It has also been detected, together with Mycoplasma pneumoniae, in a joint of a hypogammaglobulinemic patient who was suffering from polyarthritis after pneumonia and has been isolated, again with Mycoplasma pneumoniae, from the throat in culture. Such detection raises the question of the preferred mucosal site of M. genitalium, which has yet to be determined.

Animals↗
PubMed1993

The contrasting effects of progesterone and oestrogen on the susceptibility of mice to genital infection with Mycoplasma pulmonis.

The genital tract of young female mice was rendered susceptible to colonisation with Mycoplasma pulmonis by pre-treating them with progesterone (usually 2.5 mg) given subcutaneously at weekly intervals for 4 weeks. Colonisation was influenced by the size of the inoculum and by the dose of progesterone; at least 2.5 x 10(4) organisms and at least 0.5 mg of hormone (administered on four occasions) were required. The duration of colonisation was related also to the size of the inoculum and the dose of progesterone. Similar results were obtained in TO, BALB/c and CBA strains of mice. Progesterone treatment induced the dioestrous stage of the reproductive cycle within 5 days and the cycle of the majority of untreated, mycoplasma-susceptible mice was also at this stage. However, mice, particularly of the CBA strain, were far less susceptible when not given progesterone and the mycoplasmas tended to persist for a shorter time. Mice treated with oestradiol, even in small doses, became completely refractory to infection with M. pulmonis. In vitro, progesterone inhibited the growth of M. pulmonis, as did oestradiol, but vaginal washings from progesterone-treated mice were no more inhibitory than those from untreated mice. Thus, the success of progesterone in enhancing colonisation could not be attributed to a direct stimulatory effect of the hormone at the mucosal surface and we suggest that it may be due to a greater availability of progesterone-induced receptors for mycoplasmas in the dioestrous phase of the reproductive cycle than in the oestrous phase.

Animals↗