Recent eLetters
Displaying 1-10 letters out of 119 published
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Time to improve HIV testing and recording of HIV diagnosis in UK primary care - a response
Submit responseRichard Ma makes some excellent points in his editorial (1). I would like to 'correct' a misperception but add to the current debate about HIV-testing and subsequent care within UK general practice. Ma states that it was the use of highly active antiretroviral therapy (HAART) which precipitated the debates around shared care of patients with HIV infection. Unfortunately this is not true. For those old enough to remember, the serious debate began when patients with HIV and AIDS were denied local services and traditional primary care, particularly when entering the terminal stages of their illness (2). It was also apparent that patients living in one part of the country but receiving care in London were having problems accessing general practitioner (GP)-type services (3). It is true that HAART seemed to focus the mind - it became fairly obvious that prescribing could be one of the facets of care which could be examined in the "shared-care" process. However, in the present context let's examine some of the dynamics in shared care. Primary care is undoubtedly becoming more involved in the care of patients with HIV/AIDS though it has been argued that general practice could still do more (4), for example in trying to uncover the unidentified 21000 people with HIV infection in the UK (5). Yet up to now the problem has been that patients have liked the highly successful hospital model, a model that has either implicity or in some cases explicity "taken over" GP care. In truth this gold standard model is not sustainable and this is the reason why general practice has to be more involved. The barriers to full primary care involvement have been outlined before (1,3,4) but patient fears about disclosure, confidentiality and stigma are still present. Things change in general practice as they do in Medicine; early in the UK it would necessarily take an hour to 'counsel'a patient about an HIV test, now we can do the test in the privacy of our consulting room and give the result to the patient 2 minutes later (we are about to embark on point-of-care testing in our practice). The real questions are these: (a) How can we expect a more pressured primary (6) to take up the challenge of increasing testing when the priorities within general practice seem to increase all the time (6). Furthermore it is appropriate to be mindful of the often complex needs of the various heterogenous groups which are affected by HIV infection (gay men, African men, women and children, drug-users)? As the recent research paper states "further work is needed on the mechanisms required to deliver increased HIV testing in primary care"(7). (b) Next and increasingly important especially if more cases of HIV infection are uncovered in GP, what is the optimal location for a systematic approach to HIV/AIDS - the chronic condition? In other words what system or systems will be responsible for regular patient monitoring of CD counts & viral loads, surveillance of cervical smears and perhaps immunisations as well as offering basic prevention activities, for example smoking cessation advice in those already at higher risk of ischaemic heart disease? References:
1. Ma, R. (Editorial) Time to improve HIV testing and recording of HIV diagnosis in UK primary care: Sex Transm Infect 2009;85:486 doi:10.1136/sti.2009.038091
2. Smits,A., Mansfield,S., Singh,S. (1990). Facilitating care of patients with HIV infection by hospital and primary care teams. British Medical Journal 300, 241-243. ISSN: 0959-8146 3. Mansfield,S., Singh,S. (1993). Who should fill the care gap in HIV disease? Lancet 342(8873), 726-728. ISSN: 0140-6736
4. Singh,S., Dunford,A., Carter,Y.H. (2001). Routine care of people with HIV infection and AIDS: should interested general practitioners take the lead? British Journal of General Practice 51(466), 399-403. ISSN: 0960 -1643
5. Health Protection Agency. HIV in the United Kingdom: 2009 Report. 2009, London, Health Protection Agency also available athttp://www.hpa.org.uk/web/HPAwebFile/HPAweb_C/1227515298354 (accessed 7.1.2010)
6. Oakeshott, P; Aghaizu A; Prime, K; Hay P. Promoting long acting reversible contraception & HIV-testing: more work for harassed GPs. BJGP (2009) Vo 59 (569) 895-6 7. Evans HER, Mercer CH,Rait G et al. Trends in HIV testing and recording of HIV status in the UK primary care setting: a retrospective cohort study 1995-2005. Sex Transm Infect 2009;85:520-6.
Conflict of Interest:
None declared
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Pharyngeal and Rectal Testing for Chlamydia trachomatis in MSM: Evidence Base
Submit responseDear Editors,
Pharyngeal and Rectal Testing for Chlamydia trachomatis in MSM: Evidence Base
Dr Watson requests the evidence base that screening asymtomatic Men who have Sex with Men (MSM) for C. trachomatis in the throat and the rectum confers either the patient or their contacts any benefit. When considering this question it is important to remember that our current knowledge regarding the natural history of chlamydia infection is currently incomplete and consequently when Chlamydia is detected - irrespective of site or symptomatology- it is always regarded as a pathogen.
To date there is strong evidence base that the rectum is a very important reservoir of Chlamydia infection in MSM.1,2,3,4,5,6,7 In recent years several large studies have been undertaken and the prevalence of rectal Chlamydia in MSM attending sexual health clinics has been determined to be in the range of 6.96 - 11%. 1,2,3,4,5,6,7 Whilst it is undeniable that the vast majority of the non-LGV associated rectal Chlamydia infection seen, is asymptomatic,2,4 it is widely acknowledged that it is a reservoir for potential onward transmission. 1,2,3,4,5,6,7
Currently fewer studies have been undertaken examining the pharynx as a site for C. trachomatis infection. However it is noteworthy that in the studies that have been undertaken, the prevalence of pharyngeal C. trachomatis has been consistently found to 1-2% 5,6,7,8. Interestingly studies have also shown that ~66-100% of chlamydia infections in the pharynx occurred without concurrent urethral Chlamydia infection, and consequently if urine testing alone had been performed the infection would have gone undetected. 5,8
Several studies examining MSM behaviour have highlighted that urethral Chlamydia infection can be associated with insertive unprotected anal intercourse, insertive oral sex and other non-intercourse receptive anal practises9,10. This information suggests that extra-genital Chlamydial infection (both pharyngeal and rectal) is transmitted to sexual contacts. These contacts may go on to develop symptoms - this is more likely if a urethral infection is acquired- or maybe in turn, will exist as a further reservoir of Chlamydia infection. Both scenarios are undesirable and where possible would be ideally avoided.
Finally it is important to put this discussion into context: in my original editorial I advocated for the increased use of dual NAATs to test extra-genital specimens (which would enable the detection of both chlamydia and gonorrhoea) and improving the availability of rectal and pharyngeal testing to all MSM who are at risk of infection.11 This is important because any patient attending a sexual health service for an STI screen does so to ensure that they are either (i) absent from infection or (ii) if an STI is detected- to receive appropriate therapy-. Given the high prevalence of asymptomatic extra-genital Chlamydia and gonococcal infections in MSM, offering both pharyngeal and rectal screening would be undeniably beneficial to both the individual concerned and their sexual contacts.
Yours Sincerely
Sarah Alexander
Sexually Transmitted Bacteria Reference Laboratory Health Protection Agency
References
1. Clinic-based testing for rectal and pharyngeal Neisseria gonorrhoeae and Chlamydia trachomatis infections by community-based organizations--five cities, United States, 2007. Centers for Disease Control and Prevention (CDC). MWR Morb Mortal Wkly Rep. 2009 Jul 10;58(26):716-9.
2. Ward H, Alexander S, Carder C, Dean G, French P, Ivens D, Ling C, Paul J, Tong W, White J, Ison CA. The prevalence of lymphogranuloma venereum infection in men who have sex with men: results of a multicentre case finding study. Sex Transm Infect. 2009 Jun;85(3):173-5.
3. van der Helm JJ, Hoebe CJ, van Rooijen MS, Brouwers EE, Fennema HS, Thiesbrummel HF, Dukers-Muijrers NH. High performance and acceptability of self-collected rectal swabs for diagnosis of Chlamydia trachomatis and Neisseria gonorrhoeae in men who have sex with men and women. Sex Transm Dis. 2009;36(8):493-7.
4. Annan, N.T., A K Sullivan, A Nori, P Naydenova, S Alexander, A McKenna, B Azadian, S Mandalia, M Rossi, H Ward and N Nwokolo. Rectal chlamydia_a reservoir of undiagnosed infection in men who have sex with men. Sex Transm Inf 2009;85;176-179.
5. Ota KV, Tamari IE, Smieja M, Jamieson F, Jones KE, Towns L, Juzkiw J, Richardson SE. Detection of Neisseria gonorrhoeae and Chlamydia trachomatis in pharyngeal and rectal specimens using the BD Probetec ET system, the Gen-Probe Aptima Combo 2 assay and culture. Sex Transm Infect. 2009 Jun;85(3):182-6. Epub 2009 Jan 6.
6. Benn PD, Rooney G, Carder C, Brown M, Stevenson SR, Copas A, Robinson AJ, Ridgway GL. Chlamydia trachomatis and Neisseria gonorrhoeae infection and the sexual behaviour of men who have sex with men. Sex Transm Infect. 2007 Apr;83(2):106-12.
7. Kent CK, Chaw JK, Wong W, Liska S, Gibson S, Hubbard G, Klausner JD. Prevalence of rectal, urethral, and pharyngeal chlamydia and gonorrhea detected in 2 clinical settings among men who have sex with men: San Francisco, California, 2003. Clin Infect Dis. 2005 Jul 1;41(1):67-74. Epub 2005 May 26.
8. D J Templeton, F Jin, J Imrie, G P Prestage, B Donovan, P H Cunningham, J M Kaldor, S Kippax, A E Grulich. Prevalence, incidence and risk factors for pharyngeal chlamydia in the community based Health in Men (HIM) cohort of homosexual men in Sydney, Australia Sex Transm Infect 2008;84:361-363.
9. Jin F, Prestage GP, Mao L, et al. Incidence and risk factors for urethral and anal gonorrhoea and chlamydia in a cohort of HIV-negative homosexual men: the Health in Men Study. Sex Transm Infect 2007;83:113-9.
10. Lafferty WE, Hughes JP, Handsfield HH. Sexually transmitted diseases in men who have sex with men. Acquisition of gonorrhea and nongonococcal urethritis by fellatio and implications for STD/HIV prevention. Sex Transm Dis. 1997 May;24(5):272-8.
11. Alexander, S. The challenges of detecting gonorrhoea and chlamydia in rectal and pharyngeal sites: could we, should we, be doing more? Sex Transm Infect. 2009;85:159-160.
Conflict of Interest:
None declared
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Vaginal bacteria in bacterial vaginosis.
Submit responseDear Editor,
For more than 50 years the etiology of bacterial vaginosis, originally desribed as a sexually transmitted disease (1,2) has been considered controversial. The mainstream of studies on BV have been focused on the microbiology of vagina in concert with the original view of a contagious disease. No doubt, those studies like the present one by Haggerty et al.(3), discussed by Hay (4),have expanded our knowledge and have entertained possibilities of their pathogenic significance. Still, those studies have failed to provide a concept that would explane the basic nature of BV.
An alternative concept of BV as a physiological entity rests on the premise that the female vagina is not only a reservoir of microbes; the adult vagina is in the first place a copulatory organ with a function in the physiology of reproduction (5).This concept derived from observations on direct stained cervicovaginal smears in which the precoital Lactobacilli morphotype flora was seen to be replaced by Haemophilus vaginalis morphotype flora in postcoital smears.The phenomenon was interpreted to indicate that in response to unprotected intercourse, i.e. male ajaculate and vaginal transudate, the vaginal bacterial flora may change rapidly and completely from the predominance of Lactobacilli morphotype to that of Haemophilus ( Gardnerella) vaginalis morphotype and that the change is reversible (6,7,8).
The change in bacterial dominance is in line with the observation that the male ejaculate may immediately neutralize the basic vaginal acidity to protect the ejaculated spermatozoa, and that a return to the basic acidity may take place shortly after the effect of the ejaculate is over (5).
However, in case the restoration of the precoital physiology fails, as has been observed in women who have engaged in unprotected intercourse repeatedly and at short intervals (9), the low acidity associated with Gardnerella flora would persist and invite an invasion of anaerobic microbes and an inflammatory symptomatic form of BV would develope - meaning in fact the return to the once abandoned "nonspecific" vaginitis (1).
It seems feasible that BV is by origin a physiological postcoital condition, not a contagious disease;consequently Hv/G vag. bacterium would be a natural organism in the vagina rather than a contagious microbe and the Hv/G vag. flora another physiological flora in women of reproductive age.
Of note, the results of the inoculation experiments, presented as an evidence for a contagious nature of Hv vaginitis (1,2) were likely to be a coitus-induced change of Lactobacilli flora, as in those experiments the sex life of the study subjects was not considered. Likewise the isolation of Hv bacteria from most consorts of "infected" women and in one case from a previously "healthy" wife and her husband immediately following marriage would rather speak for a coitus-induced change of flora.
Bacterial vaginosis is a potential condition in sexually active women worldwide and it is getting to be more of a problem each passing year. In view of the prevaling concept of BV, the physiological concept should be discussed and criticized in an open forum.
Pentti A. Leppäluoto Finnish Cancer Society (ret.) leppaluoto@kolumbus.fi
References
1. Gardner HL, Dukes CD. Haemophilus vaginalis vaginitis. A newly defined specific infection previously classified "nonspecific" vaginitis. Am J Obstet Gynecol 1955;69:962-76.
2. Criswell BS, Ladwig CL, Gardner HL, Dukes CD. Haemophilus vaginalis. Vaginitis by inoculation from culture. Obstet Gynecol 1969;33:195-9.
3. Haggerty CL, Totten PA, Ferris M, Martin DH, Hoferka S,Astete SG, Ondondo R, Norori J and Ness RB. Clinical characteristics of bacterial vaginosis among women testing positive for fastidious bacteria. Sex Transm Inf 2009;85:242-8.
4. Hay P. How important are the newly described bacteria in bacterial vaginosis? Sex Transm Dis 2009;85:240-1.
5. Masters WH, Johnson VE. Human sexual response. London UK: J&A Churchill Ltd;1966. p.88-100.
6. Leppäluoto PA.The etiology of the cocci-type "streptokokkentyp" vaginal smear. Acta Cytol 1971;15:211-5. Errata: wrong pictures. Idem. 1971;15:577.
7. Leppäluoto PA.The coitus-induced dynamics of vaginal bacteriology. J Reprod Med 1971;7:169-75.
8. Leppäluoto PA. Autopsy of bacterial vaginosis: a physiological entity rather than a contagious disease. Acta Obstet Gynecol Scand 2008;87:578-9.
9. Döderlein A.Das Scheidensekret und seine Bedeutung fur das Puerperalfieber. Die Arten des Scheidensekrets. Leipzig:Verlag Eduard Besold (Arthur Georgi); 1892.p.46.
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Human papilloma virus, sexual behaviour and logical places of infection and malignancy
Submit responseThe locations on body of sexual transmited infections with Human papilloma viruses, can corelate with "inovationes" in sexual behaviour. It is logical that the viral afectiones (condilomata, precancerous lesions and carcinoma) can be located on cervix, vulva, glans penis, anal region, oral region and tongue, haed and neck, larinx, oesophagus and breast! Very important is the maybe causal connection between human papilloma virus infection and the breast carcinoma! Data revealed that apart from the heart and the kidney, the virus has been found in all other organs that have been analyzed so far, i.e., prostate, urinary bladder, oral cavity, larynx, esophagus, stomach, colon, liver, vagina/vulva, endometrium, ovary, breast, penis, anus, skin, and lung. Some of the detection rates are remarkable, e.g., colon cancer up to 97%, lung cancer 80%, and breast cancer 74% (Petersen I, Klein F., 2008)*. Maybe the new antiviral therapy and the Gardasil vaccination can be helpful by different type of malignancy, especially by very frequent and dangerous brest, anal and ovarian cancers.
* Pathologe. 2008 Nov;29 Suppl 2:118-22.
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Evidence, please
Submit responseIt is a shame that Dr Alexander's opening sentence: "It is important that all men who have sex with men (MSM) accessing sexual health-care are tested for Neisseria gonorrhoeae and Chlamydia trachomatis (CT) at all anatomical sites where they may be at risk of infection.", is not referenced.
I should appreciate being directed to the evidence that screening asymtomatic MSM for CT in the throat or rectum confers them or anyone else with any benefit. A simple number needed to screen per defined benefit would do.
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Anal sex need not be highly prevalent to affect HIV incidence among heterosexual populations
Submit responseThe results published by Kalichman et. al. on anal intercourse (AI) practices among heterosexuals in South Africa [1] and the associated editorial by Boily et. al. [2] are important contributions to our understanding of HIV transmission. While a small proportion of men (14%) and women (10%) report engaging in heterosexual AI [1], this mode of exposure could be important to overall HIV transmission rates because the risk of transmission through receptive AI is approximately 10-times greater than through receptive vaginal intercourse (VI) [3-9]. In particular, women who engage in AI may be at much higher risk of acquiring HIV as ~43% of their reported sexual acts involve anal sex [1]. Based on the results from the Kalichman et. al. cross-sectional study we estimate the relative contribution of AI to HIV incidence among heterosexual populations in South Africa. The estimated risk of HIV transmission per unprotected act is approximately 0.08% for receptive VI, 0.8% for receptive AI, and 0.04% for insertive VI or AI [3-7]. Assuming condoms are 95% effective in reducing the risk of HIV transmission [10-14] and using a binomial equation [15] we estimate the cumulative risk of HIV transmission over numerous risk exposures (at the median frequencies of VI, AI, and mean condom use reported in [1]) for both men and women who engage in AI and for those who only engage in VI. The risk of HIV transmission to females in a discordant partnership is greatly increased if they engage in AI. Assuming each female only has one discordant sexual partner, we estimate that the 3-monthly risk of HIV acquisition for females who only engage in VI is 0.2% but the risk increases by 7.5-times, to 1.5%, if they also engage in AI, with 89% of their risk attributable to AI. Although only 10% of heterosexual women engage in AI, we estimate that 45% of the total female population incidence of HIV occurs among these women. Our estimates suggest that the prevalence of HIV in females who engage in anal sex should be much higher than in the rest of the population. Although Kalichman et. al. did not report prevalence by gender, their study indicated that 9% of those who did not engage in anal intercourse were HIV-positive compared with 22% among those who engaged in anal intercourse [1]. Our simple calculations, underpinned by the frequency of reported AI and VI among heterosexuals [1] and known transmission risk estimates, highlight that heterosexual anal intercourse does not have to be very common in a population to have a large impact on HIV incidence particularly among females. The Kalichman et. al. study highlights the importance of accurately surveying the type and frequency of sexual behaviour within populations and the need to openly study and discuss heterosexual anal intercourse. Heterosexual anal sex may contribute more to HIV epidemics than previously assumed.
References
1. Kalichman, S., et al., Heterosexual Anal Intercourse among Community and Clinical Settings in Cape Town, South Africa. Sexually transmitted infections, 2009: p. 411-5.
2. Boily, M.-c. and R.F. Baggaley, The role of heterosexual anal intercourse for HIV transmission in developing countries: are we ready to draw conclusions? Sexually Transmitted Infections, 2009. 85: p. 6-8.
3. de Vincenzi, I., A longitudinal study of human immunodeficiency virus transmission by heterosexual partners. European Study Group on Heterosexual Transmission of HIV. N Engl J Med, 1994. 331(6): p. 341-6.
4. Padian, N.S., et al., Heterosexual transmission of human immunodeficiency virus (HIV) in northern California: results from a ten- year study. Am J Epidemiol, 1997. 146(4): p. 350-7.
5. Vittinghoff, E., et al., Per-contact risk of human immunodeficiency virus transmission between male sexual partners. Am J Epidemiol, 1999. 150(3): p. 306-11.
6. Gray, R.H., et al., Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda. Lancet, 2001. 357(9263): p. 1149-53.
7. Wawer, M.J., et al., Rates of HIV-1 Transmission per Coital Act, by Stage of HIV-1 Infection, in Rakai, Uganda. J Infect Dis, 2005. 191(9): p. 1403-9.
8. Koblin, B.A., et al., Risk factors for HIV infection among men who have sex with men. AIDS, 2006. 20(5): p. 731-9.
9. Read, T.R.H., et al., Risk factors for incident HIV infection in men having sex with men: a case-control study. Sexual Health, 2007. 4: p. 35-39.
10. Davis, K.R. and S.C. Weller, The effectiveness of condoms in reducing heterosexual transmission of HIV. Family Planning Perspectives, 1999. 31: p. 272-9.
11. Weller, S.C. and K.R. Davis, Condom effectiveness in reducing heterosexual HIV transmission. Cochrane Database Syst Rev, 2002. (1): p. CD003255.
12. Pinkerton, S.D. and P.R. Abtramson, Effectiveness of condoms in preventing HIV transmission. Social Science and Medicine, 1997. 44: p. 1303-12.
13. Weller, S.C., A meta-analysis of condom effectiveness in reducing sexually transmitted HIV. Social Science and Medicine, 1993. 36(12): p. 1635-44.
14. Fitch, T.J., et al., Condom Effectiveness: Factors that influence risk reduction. Sexually Transmitted Diseases, 2002. 29: p. 811-7.
15. Wilson, D.P., et al., Relation between HIV viral load and infectiousness: a model-based analysis. Lancet, 2008. 372(9635): p. 314- 20.
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The financial burden of HPV on the NHS was underestimated leading to wrong choice of vaccine.
Submit responseSir: The editorial by Sheldon R Morris1 concludes that the rationale for a vaccine that includes HPV 6 and 11 is compelling. The British Association for Sexual Health & HIV also thought the evidence was compelling and said so in a press release2. The choice of Cervarix over Gardasil was indeed a sad day for Sexual Health in the UK3. The key to the decision in the UK was the perceived cost to the NHS of genital warts. This is explored extensively in the editorial by Morris, who concluded that for the bivalent vaccine to be economic it would potentially need to cost 50% less than the quadrivalent vaccine. Economic evaluation by Jit et al4 on which the Joint Committee for Vaccination and Immunisation base their conclusions, is inherently flawed. Jit et al only looked at one small study from a DGH to make the extraordinary conclusion that genital warts only cost the NHS £134 per episode. The burden of laryngeal papilloma (also caused by types 6 and 11) was not considered. However, one of the largest multi-centre studies done in the United Kingdom5, which included two authors from that same DGH, concluded in 2003 that using one of the cheapest and commonest treatments, ie. Podophyllotoxin cream, the total average direct and indirect cost per patient was £573. Studies in USA and Canada may not reflect costs in the United Kingdom where the vast majority of warts are treated on the NHS. For example, if I was treating a genital wart patient (which I don’t) using my own home as an office, I could probably do it for £160 an episode (first visit – £80 for trichloroacetic acid and a private prescription for Podophyllotoxin or Imiquimod, and two follow-up visits of £40 plus / minus further prescriptions. However, the NHS has to take into consideration the vast structure and administrative costs that goes with running a public service. Even using PBR (payment by results), it’s £153 for a new visit in Chester with £90 per follow-up, bringing the cost up to £333 for just a first visit and two follow-ups. The BASHH press release emphasised the potential early pay back from including 6 & 11, and indeed this has proved to be the case in Australia where within a year of the vaccination programme being complete there was a 48% reduction in new female genital wart cases presenting to one of the biggest STD clinics6. I have continued to write to Ministers of Health asking for an explanation of this decision, but I can’t get an answer to the one simple question – why was the key economic factor for the valuation of a multi million pound contract, that had huge implications for NHS Sexual Health services, based on one small study from a DGH ?
Dr Colm O'Mahony MD. FRCP. BSc. DIPVen. Department of Sexual Health (GUM) Countess of Chester Foundation Trust Hospital. Liverpool Road. Chester. CH2 1UL
References 1. Morris, SR HPV vaccine strategies: the cost of HPV and the choice of vaccine Sex Transm Infect 2009;85:315-316
2. BASHH Press Release 29 October 2007. RSM BASHH secretariat. www.bashh.org press section.
3. O’Mahony, C. Government decision on national human papillomavirus vaccine programme is a sad day for sexual health. Sex Transm Infect 2008;84:251
4. Jit M, Hong Choi Y, Edmonds WJ Economic evaluation of human papillomavirus vaccination in the United Kingdom BMJ 2008;337:a769
5. Lacy CJN et al Randomised controlled trial and economic evaluation of podophyllotoxin solution, podophyllotoxin cream, and podophyllin in the treatment of genital warts. Sex Trasm Infect August 2003;79:270-275
6. Fairley, K. Decline in presentations of genital warts one year after implementation of quadrivalent Human Papillomavirus vaccination program in young women. 25th International Papillomavirus Conference, Malmo (Sweden), 8-14 May 2009
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The challenge of detecting gonorrhoea (GC) – we can, we should, we already do more.
Submit responseDear Editor,
In a recent leading article Alexander (1) citing in particular recent work with men who have sex with men (MSM) in the USA (2), has suggested that when examining extra-genital specimens from high risk patient groups, GC culture should be replaced by GC nucleic acid amplification tests (NAATs). We agree with this conclusion but believe that the higher sensitivity of GC NAATs should be promoted to allow impact on wider populations. There is already growing evidence in the UK that GC NAATs (with alternative target confirmation to avoid issues of low positive predictive value) can accurately detect substantial numbers of cases beyond those found by culture and by current diagnostic service structures. A Scottish study (3) found more than double the cases of GC when testing throat and rectum of men by NAATs instead of culture but also reported extra cases among females tested.
We have recently reported on detection of GC (when testing for Chlamydia) by use of the APTIMA Combo2 (AC2) assay with alternative target confirmation (4). In a GU medicine clinic AC2 detected some 20% extra cases of GC beyond culture. Also compared to self-referral at a GU medicine clinic, community tests made a substantial contribution to the overall number of GC cases found (40 community versus 35 Macclesfield GU clinic). There were no culture- positive but AC2 negative results in any of our patients. Of over15000 tests performed both at the community and at the GU medine clinic, only one was positive for GC by AC2 but unconfirmed by the alternative assay. In the community, over 60% of GC infections occurred in chlamydia negatives so dual testing at the outset would find more GC cases than reflex testing of those screened chlamydia positive. Wider considered use of GC NAATs should be encouraged.
M Mahto
Department of GU Medicine
Cheshire East Community Health (Central and Eastern Cheshire PCT)
Macclesfield, SK11 6JL, UKH Mallinson
Haytor
Crosby
Liverpool
L23, UKCorrespondence to: Dr M Mahto, Consultant Physician
Genitourinary Medicine Department
Assura Health and Wellness Centre
Sunderland Street
Macclesfield, SK11 6JL, UK Email - mrinalini.mahto@echeshire-tr.nwest.nhs.ukReferences
1. Alexander S. The challenges of detecting gonorrhoea and chlamydia in rectal and pharyngeal sites: could we, should we, be doing more? Sex Transm Infect 2009;85:159-160
2. Ota KV, Tamari IE, Smieja M et al. Detection of Neisseria gonorrhoeae and Chlamydia trachomatis in pharyngeal and rectal specimens using the BD Probetec ET system, the Gen-probe Aptima Combo2 assay and culture. Sex Transm Infect 2009;85;182-6
3. Scottish Guidelines for Molecular testing of Neisseria gonorrhoeae. See http://www.hps.scot.nhs.uk/training/presentations.aspx?id=167
4. Mahto M, Zia S, Ritchie D and Mallinson H. Diagnosis, management and prevalence estimation of gonorrhoea: influences of Aptima Combo 2 assay with alternative target confirmation. International Journal of STD and AIDS 2009;20:315-319
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A surgical perspective
Submit responseDear Editor,
Although lymphogranuloma venereum (LGV) as a cause of severe proctitis is well known amongst genitourinary and gastroenterological specialists, it remains absent from a common list of causes of rectal bleeding amongst General Practitioners and Surgeons. An example is a case of a homosexual man who presented as a 2 week rule urgent referral to the Colorectal clinic with painless rectal bleeding and went on to have endoscopy and biopsies for proctitis. It would not have been unreasonable to start this patient on steroids or mesalazine enemas for symptom control while awaiting the results of biopsies. In this instance, however, it was only after telephone consultation with an HIV specialist and referral to the Genitourinary Medicine clinic that a diagnosis of LGV proctitis was reached several weeks later. Steroids’ would almost certainly have made this condition worse and may even have resulted in a rectal perforation.
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LGV doesn’t spread in the overall Chlamydia trachomatis-infected population in France
Submit responseDear Editor,
Helen Ward (3) ask the question about the extent of the Lymphogranuloma venereum (LGV) in the wider population than that of men who have sex with men (MSM). A rospective sentinel survey set up in France following the European alert in January 2004 tried to answer this question. From April 2002 to December 2008, rectal samples from MSM were collected by the French National Reference Centre for Chlamydia infections from mainly 3 labs in Paris and some labs in France. All the C. trachomatis-positive rectal samples were genotyped. Over 1041 positive specimens genotyped, 725 L2 serovars and 316 non-LGV associated serovars (mainly Da,G, and J) were identified. Simultaneously, C. trachomatis-positive genital specimens were tested for the presence of LGV strains by a specific genovar L Taqman Real-time PCR (2). A total of 2662 urogenital specimens (1095 urethral or male urine specimens and 1567 vaginal, cervical or female urine specimens) were tested. These specimens were obtained between 2004 and 2008 in Paris, Bordeaux, and from Pasteur Cerba laboratory, a central French laboratory that received specimens from all over the country. No LGV strain was found except one in the urethral male sample of one HIV(+) gay man. This is the second case of urethritis due to a C. trachomatis genovar L2 in France, the first one having been already published in 2006 (1). We can conclude that, in France, LGV remains essentially a rectal infection in MSM.
Acknowledgments: we thank Dr Georges Kreplack, Patrice Sednaoui, Catherine Scieux Sabine Trombert, for providing C. trachomatis-positive specimens from Paris and Cerba laboratory.
References
1. Herida, M., G. Kreplack, B. Cardon, J. C. Desenclos, and B. de Barbeyrac. 2006. First case of urethritis due to Chlamydia trachomatis genovar L2b. Clinical Infectious Diseases 43:268-269.
2. Morre, S. A., J. Spaargaren, J. S. A. Fennerna, H. J. C. de Vries, R. A. Coutinho, and A. S. Pena. 2005. Real-time polymerase chain reaction to diagnose lymphogranuloma venereum. Emerging Infectious Diseases 11:1311- 1312.
3. Ward, H., and R. F. Miller. 2009. Lymphogranuloma venereum: here to stay? Sex Transm Infect 85:157.
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