Guest guest Posted June 12, 2001 Report Share Posted June 12, 2001 I suggest you consult with Dr. Fisher at the Wills Eye Hospital in Philadelphia -------------------------------------------------------------------------------- Subject: information on autoimmune disease http://www.niaid.nih.gov/publications/autoimmune/autoimmune.htm -------------------------------------------------------------------------------- Subject: mycoplasma pneumonia and otitis media 1: Pediatr Infect Dis J 2000 Jul;19(7):666-8 Related Articles, Books, LinkOut Detection of Mycoplasma pneumoniae by polymerase chain reaction in middle ear fluids from infants with acute otitis media. Raty R, Kleemola M. Department of Virology, National Public Health Institute, Helsinki, Finland. riitta.raty@... PMID: 10917232 [PubMed - indexed for MEDLINE] -------------------------------------------------------------------------------- Subject: Reactive arthritis and uveitis I noticed that Ureaplasma has been implicated in this article about reactive arthritis. ureaplasma urealyticum is also implicated in lung disease of pre maturity and low birth weight. I wonder if these associations could also be made with other complications in later life such as Lupus, Sarcoidosis, RA etc. If ureaplasma are associated with ReA can they also be associated with the common uveitis found in ReA? Mike National guideline for the management of sexually acquired reactive arthritis Clinical Effectiveness Group (Association for Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases) Aetiology Reactive arthritis (ReA) is a sterile inflammation of the synovial membrane, tendons, and fascia triggered by an infection at a distant site, usually gastrointestinal or genital. ReA triggered by a sexually transmitted infection (STI) is referred to as sexually acquired reactive arthritis (SARA). This includes sexually acquired Reiter's syndrome described as the triad of urethritis, arthritis, and conjunctivitis, with or without other cutaneous or mucous membrane lesions such as keratoderma blennorrhagica, circinate balanitis/vulvitis, uveitis, oral ulceration, cardiac or neurological involvement. Most commonly, lower genital tract infections, either urethritis or cervicitis, are associated with SARA with objective features of SARA being present in 0.8-4% of cases [1-3]. The place of upper genital tract infection, such as prostatitis and salpingitis, is unresolved. Previously, it was suggested that infection with the human immunodeficiency virus (HIV) was directly associated with SARA but current evidence suggests this is not so [4,5]. The precise mechanisms linking infective agents with SARA are not clearly understood so links with specific micro-organisms are partly speculative. Chlamydia trachomatis, the commonest identifiable cause of non- gonococcal urethritis (NGU), has been the micro-organism most strongly linked to SARA being identified in 35-69% of cases, using non-nucleic acid amplification techniques [2,6-9]. Neisseria gonorrhoeae has been linked with up to 16% of cases, as distinct from its role in septic, gonococcal arthritis [1,10-13]. The precise role of this micro-organism in relation to SARA remains unknown. Ureaplasma urealyticum has been linked with a few cases and may be a cause of SARA in a minority [14,15]. A causal role for other genital tract pathogens and commensals including mycoplasmas is possible but there is currently insufficient evidence for evaluation. Mechanisms of pathogenesis in SARA are also unclear, although it appears to involve an immune response to urogenital micro-organisms. SARA appears to occur over 10 times more frequently in men than in women, although underrecognition in women may be a problem [1,13,16,17]. Possession of the HLA-B27 gene increases susceptibility to SARA by up to 50-fold [2,7,11,16,18]. It is also now clear that DNA and/or surface antigens of C trachomatis [8,19-25], U urealyticum [24,26], and other mycoplasmas [27] may be detected within joint material from individuals with SARA. It is possible that the persistence of viable micro-organisms intra-articularly is an important factor in the causation and perpetuation of the arthritis. Clinical features History There may be a past or family history of spondyloarthritis or iritis [1,12,17,18,28]. Sexual intercourse, usually with a new partner, within 3 months before the onset of arthritis [2,7,16]. Symptoms Onset of arthritis within 30 days of sexual contact in 88% of patients with a mean interval of 14 days between the onset of genital tract symptoms and arthritis [1,2,12,16,17]. A recent history of urethral discharge and/or dysuria in approximately 80% of men with SARA, although considerably fewer women are symptomatic [9,7,12,13,16] Pain, with or without swelling and stiffness, at one or more (usually fewer than six) joints, especially at the knees and feet [12,16-18] Pain and stiffness at entheses, especially the posterior and plantar aspect of the heels, which often results in difficulty in walking. Enthesitis and/or fasciitis occurs in approximately 20% of patients [1,11,13,16,17]. Painful movements may also result in 30% from tenosynovitis and in 16% painful swelling of a toe or finger (dactylitis) may occur [16,17]. Low back pain and stiffness is common in the acute episode and sacroiliitis occurs in approximately 10% of patients during the acute episode [1,11-13,16,17,29,30]. Irritable eyes, with or without redness, photophobia, or a reduction in visual acuity. Conjunctivitis occurs in 20-50% of patients with SARA but iritis is less common, occurring in around 2-11% of patients [1,11-13,16,17,30]. Other eye lesions occur rarely [1,11,13]. Systemic symptoms of malaise, fatigue, and fever occur in approximately 10% of patients [16,18]. Signs Genital infection. Manifest in men by urethritis, urethral discharge, and/or epididymo-orchitis and in women by mucopurulent cervicitis, with or without easily induced cervical bleeding, and/or abdominal pain. Infection may be asymptomatic, particularly in women [7,9,12,13,16]. Arthritis, almost invariably affecting one to five lower limb joints in an asymmetrical distribution. Persistent small joint involvement may be erosive. Upper limb involvement is rare in the absence of psoriasis [12,16-18]. Enthesopathy. Tenderness, with or without swelling at the sites of tendon or fascial attachments, especially the achilles tendon and plantar fascia attachments to the calcaneum [1,11,13,16,17]. Tenosynovitis. Tenderness, with or without swelling over tendon sheaths and crepitus on movement. Classic dactylitis may be seen [16,17]. Pain on direct sacral pressure may indicate acute sacroiliitis [1,11,13,16,17] Care should be taken to distinguish this from lumbosacral disc disease or other pathology. Pain and redness of the eye is usually due to conjunctivitis, or rarely iritis [1,11-13,16,17,30]. Slit lamp examination is essential to differentiate them. Rarely, corneal ulceration, keratitis, and intraocular haemorrhage may be seen and optic neuritis and posterior uveitis have been described [1,11,13,17]. Psoriasiform rash which may be typical plaque or guttate cutaneous psoriasis in 12.5% [12], nail dystrophy in 6-12% [12,30], or typical psoriatic lesions of the glans penis or labia (circinate balanitis or vulvitis) in 14-40% [1,11,13,16,17,30], tongue (geographical tongue) in about 16% [30], or pustular psoriasis on the soles of the feet (keratoderma blennorrhagica) in up to 33% [1,11-13,16,17,30]. The latter may occur rarely on the palms of the hands. Stomatitis and oral ulceration occur in approximately 10% [11-13,17]. Heart lesions are almost invariably asymptomatic although tachycardia and rarely pericarditis and aortic valve disease may occur. Electrocardiographic abnormalities, including conduction delay, are recorded in 5-14% of patients [11-13,17]. Renal pathology, such as proteinuria, microhaematuria, and aseptic pyuria, is seen in about 50% and is usually asymptomatic. Glomerulonephritis and IgA nephropathy rarely occur [18]. Rare manifestations include thrombophlebitis of the lower limbs, subcutaneous nodules, nervous system involvement including meningoencephalitis, and nerve palsies [1,12,13,17]. Fever and weight loss occur in a minority of patients, approximately 10% [16,18,29]. Complications In the majority of individuals with SARA the disease is self limiting with a mean first episode duration of 4-6 months [1,16,17,30]. Approximately 50% have recurrent episodes at variable intervals [1,12,17,28]. The complications of SARA are principally due to aggressive arthritis and are more likely if the individual possesses the HLA-B27 gene [11,16]. Chronicity with symptoms persisting for more than 1 year in approximately 17% of patients [17]. Erosive joint damage especially affects the small joints of the feet with 12% exhibiting foot deformities, although severe deformity is rare [1]. Persistent locomotor disability occurs in approximately 15%, principally caused by erosive damage with deformity of the metatarsophalangeal, ankle or knee joints, or as a consequence of sacroiliitis or spondylitis [11,28]. No accurate estimates of the prevalence of ankylosing spondylitis are available although it has been described in up to 23% of patients with severe disease [29]. It is unclear whether the development of ankylosing spondylitis is a complication of the ReA or the independent development of two conditions in the same genetically predisposed population. Inadequately treated, or recurrent, acute anterior uveitis may rapidly lead to cataract formation and blindness in a minority [11- 13,28]. Diagnosis The diagnosis of SARA involves three components. Recognition of the typical clinical features of spondyloarthropathy. Demonstration of evidence of genitourinary infection by the identification of: Urethritis in men. Urethral discharge, dysuria, and/or epididymo- orchitis may be present. Asymptomatic cases are not infrequent. Microscopic confirmation is by a Gram stained urethral smear demonstrating ³ 5 polymorphonuclear leucocytes (PMNLs) per high power (x 1000) microscopic field, or ³ 10 PMNLs per high power (x 1000) microscopic field on a first void urine sample. Mucopurulent cervicitis in women. A purulent or mucopurulent endocervical exudate, with or without easily induced cervical bleeding, and/or lower abdominal pain may be present. However, cervical infection is frequently asymptomatic. The identification of genital pathogens, particularly C trachomatis or N gonorrhoeae. Full screening for STIs is essential. Please refer to the relevant guidelines on NGU, C trachomatis infection, and gonorrhoea. Investigation of specificity and activity of arthritis. Management General advice The principles of management are governed by the expectation that SARA is a self limiting disease in the majority of patients. Patients should be advised to avoid unprotected sexual intercourse until they and their partner(s) have completed treatment and follow up for any genital infection identified. Patients should be given a detailed explanation of their condition with particular emphasis on the long term implications for the health of themselves and their partner(s). This should be reinforced by giving them clear and accurate written information. Further investigation The following investigations are essential, often useful or sometimes useful [6,11-13,16-18,28-31]. Genitourinary medicine (GUM) specialists are advised to liase with and/or refer to other specialists including rheumatologists, ophthalmologists, and dermatologists for all patients with significant involvement of extragenital systems. It is advised that all patients with SARA are referred to an ophthalmologist, if possible, for slit lamp assessment. Essential investigations should be performed by GUM specialists while other investigations are suggested following appropriate referral. Essential Full screening for STIs Acute phase response Erythrocyte sedimentation rate (ESR) or C reactive protein (CRP) or Plasma viscosity (PLV) Full blood count Urinalysis. Investigations which are often useful Liver and kidney function tests HLA-B27 x rays of affected joints and sacroiliac joints Electrocardiogram Echocardiogram Ophthalmic evaluation including slit lamp assessment. Investigations which are sometimes useful HIV antibody test Blood cultures Stool culture (if enteritic ReA is suspected) Serology for C trachomatis including IgM and IgA antibody Synovial fluid analysis for cell count, Gram stain, crystals, and culture Synovial biopsy Exclusion tests for other diseases with rheumatological features- for example, rheumatoid factor (rheumatoid arthritis), plasma urate (gout), chest x ray, and serum angiotensin converting enzyme (ACE) level (sarcoidosis). Treatment Treatment is directed at several distinct elements of the condition. It is advisable that advice/assessment is obtained from relevant specialists as indicated above. Constitutional symptoms Rest Non-steroidal anti-inflammatory drugs (NSAIDs). Genital infection Antimicrobial therapy for any genital infection identified should be as in uncomplicated infection. Please refer to the relevant infection guidelines. Whether short course antibiotic treatment of the acute genital infection influences the non-genital aspects of SARA is controversial, with the probability being that it does not once the arthritis is manifest (level of evidence Ib, grade of recommendation A) [16,30,32-34]. Arthritis First line therapy Rest with the restriction of physical activity, especially weight bearing activity where leg joints are involved. Balance with the use of physiotherapy to prevent muscle wasting (IV, C) [18,35,36]. Physical therapy with the use of cold pads to alleviate joint pain and oedema (IV, C) [18,35,36]. NSAIDs are well established as efficacious agents in many inflammatory arthritides and form the mainstay of therapeutic management. It is important that they are used regularly to achieve the maximum anti-inflammatory effect. There is no definite drug of choice (IIb, [18,35-39]. Intra-articular corticosteroid injections, especially valuable for single troublesome joints. Proved value in other inflammatory arthritides but there are no randomised placebo controlled trials (RPCTs) of its use in SARA (IV, C) [18,35,40-42]. Second line therapy (moderate/severe arthritis/failure of first line) As above plus Systemic corticosteroids. If used, consideration should be given to anti-osteoporosis prophylaxis. Corticosteroids are valuable as short courses usually beginning with oral doses of 10-25 mg daily where severe symptoms arise from several joints, often in the presence of constitutional illness. In rheumatoid arthritis it has been shown to suppress inflammation but there are no RPCTs of its use in SARA (IV, C) [18,35,43]. Sulphasalazine. Indicated where disabling symptoms persist for 3 or more months, or evidence of erosive joint damage is present. Sulphasalazine reduces the duration of active synovitis but probably does not influence ultimate recovery. High doses, 3 g daily, are associated with significant toxicity, especially gastrointestinal, which may necessitate cessation of treatment, whereas 2 g daily appears equally effective and better tolerated (Ib, A) [18,35,44-46]. Methotrexate. Indicated where disabling symptoms persist for 3 or more months, or evidence of erosive joint damage is present. Doses range from 7.5-15 mg orally as a single weekly dose. Oral folic acid should be given, usually as a single 5 mg dose weekly, with or on the day after the methotrexate dose. Methotrexate is favoured by many physicians because of the ease of weekly oral administration and the favourable responses seen in rheumatoid disease and psoriatic arthritis. Only case reports of its use in SARA have been published (IV, C) [18,35,36,47]. Azathioprine. Indicated where disabling symptoms persist for 3 or more months, or evidence of erosive joint damage is present. Doses of 1-4 mg/kg/body weight per day may be used (III, [18,35,48]. Gold salts and d-penicillamine. These drugs are occasionally used when persistent polyarthritis is present. No RPCTs have been published concerning their use in SARA (IV, C) [18,35]. Antibiotics. Short course antibiotic therapy used for the treatment of concomitant urogenital infection may reduce the risk of recurrent arthritis developing in individuals with a history of ReA but otherwise there is little evidence of benefit in arthritis (Ib, A) [16,30,32-34]. Lymecycline administered for 3 months, in one study, has been shown to reduce the duration of arthritis in C trachomatis triggered SARA but the role of long term antimicrobial therapy, particularly in non-chlamydial SARA, is not yet established (Ib, A) [33,49-51]. Medical synovectomy using yttrium-90 or osmic acid. Both methods have been shown to have short term benefit in chronic mono-articular synovitis [41]. The place of medical synovectomy in SARA has not been established. Surgery. Exceptionally, surgical treatment including synovectomy and arthroplasty, is valuable [35]. Enthesitis Rest (IV, C) [18] Physiotherapy and ultrasound NSAIDs (IV, C) [18] Local corticosteroid injection (IV, C) [41,42] Radiotherapy for persistent disabling heel pain, exceptionally Surgery, exceptionally. Mucous membrane and skin lesions No treatment for mild lesions Keratinolytic agents, such as topical salicylate or corticosteroid preparations, in mild to moderate cases (IV, C) [18,47] Calcipotriol cream/ointment in mild to moderate cases (IV, C) [52] Methotrexate, if severe lesions (IV, C) [18,47] Retinoids, if severe lesions (IV, C) [18,53]. Eye lesions Should be managed with ophthalmological advice. Slit lamp assessment is essential to diagnose uveitis which if untreated may result in irreversible visual loss. Therapy for uveitis consists of eye drops or oral corticosteroids and mydriatics (IV, C) [18]. Post-inflammatory pain and fatigue Explanation and patience Low dose tricyclic drugs, such as amitriptyline 10-25 mg at night, if severe symptoms. Prophylaxis In addition to the advice to avoid unprotected sexual intercourse until they and their partner(s) have completed treatment and follow up for any genital infection identified, patients should be advised to avoid potentially " triggering infections " in the future, either urogenital or enteric. Hence, safer sexual practice should be discussed and the importance of food hygiene stressed. Pregnancy and breast feeding All medications should be avoided during pregnancy and breast feeding where possible. Antibiotics. Please refer to the relevant infection guidelines. NSAIDs may potentially produce subfertility as a result of the luteinised unruptured ovarian follicle syndrome [54]. NSAIDs used regularly during pregnancy may produce premature closure of the fetal ductus arteriosus, oligohydramnios, delayed onset, and increased duration of labour [55,56]. Corticosteroids are low risk but if the daily use is 10 mg or more, fetal/infant adrenal suppression may occur [56]. Sulphasalazine appears to have only small theoretical risks but may induce oligospermia in men [56,57]. Azathioprine should not be initiated during pregnancy, if possible. Women should avoid conception while taking azathioprine and for at least 6 months after [56]. Methotrexate and retinoids are teratogenic and contraindicated during pregnancy and breast feeding. Both men and women using methotrexate should avoid conception during drug taking and for at least 6 months after. Women using retinoids should be advised to use adequate contraception for at least 1 month before treatment, during treatment, and for at least 2 years after stopping treatment [56]. Gold salts should be avoided during pregnancy and breast feeding. Women should avoid conception during and for at least 6 months after treatment [56]. Sexual partners Partner notification, treatment, and the contact tracing period is dependent on the genital infection identified. Please refer to the relevant infection guidelines. Follow up GUM follow up is dependent on the genital infection identified. Please refer to the relevant infection guidelines. Extragenital manifestations should be followed up under the direction of the relevant specialist. Auditable outcome measures Duration of inability to work Need for admission to hospital Presence of erosive joint damage Duration to full recovery Number of joint and/or extra-articular recurrences over a 2 year period after the initial episode Presence of long term disability. Authors and centres Keat, Northwick Park and St Mark's NHS Trust; Carlin, Nottingham City Hospital NHS Trust. Membership of the CEG Clinical Effectiveness Group: chairman, Radcliffe (MSSVD); Imtyaz Ahmed-Jushuf (AGUM); Frances Cowan (MSSVD); Mark FitzGerald (AGUM); Janet (Royal College of Physicians GU Medicine Committee). Conflict of interest None. Evidence base In compiling these guidelines evidence has been sought from Medline, Cochrane Library, authoritative reviews, and Sexually Transmitted Diseases (STD): Netherlands Guidelines 1997. Additional papers referenced by articles identified by the search strategy were also reviewed. Searches have been made from 1966 to October 1998 using the keywords " Reactive arthritis, " " Reiter's syndrome, " " Infectious arthritis, " " Spondyloarthropathy " AND " Aetiology, " " Microbiology, " " Venereal diseases, " " Sexually transmitted diseases/bacterial/viral, " " Chlamydia infections/Chlamydia trachomatis, " " Neisseria gonorrhoeae, " " Ureaplasma infections/Ureaplasma urealyticum, " " Mycoplasma infections/Mycoplasma hominis Mycoplasma genitalium, " " Herpesviridae infections/Herpes genitalis/Herpes simplex, " " HIV infections/HIV, " " Acquired immunodeficiency syndrome, " " Pathology, " " Diagnosis, " " Epidemiology, " " Prevention & control, " " Surgery, " " Rehabilitation, " " Therapy, " " Drug therapy, " " Treatment, " " Antibiotics, " " Antimicrobial therapy, " " Azathioprine, " " Azithromycin, " " Corticosteroid therapy, " " Cyclosporin, " " D- penicillamine, " " Doxycycline, " " Erythromycin, " " Gold salts, " " Lymecycline, " " Management, " " Methotrexate, " " Minocycline, " " M yocrisin, " " Non-steroidal anti-inflammatory drugs, " " Ofloxacin, " " Osmic acid, " " Radiotherapy, " " Steroids, " " Sulphasalazine, " " Synovectomy, " " T etracycline. 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Molecular evidence for the presence of chlamydia in the synovium of patients with Reiter's syndrome. Arthritis Rheum 1992;35:521-9. Bas S, Griffais R, Kvein TK, et al. Amplification of plasmid and chromosome chlamydia DNA in synovial fluid of patients with reactive arthritis and undifferentiated seronegative oligoarthropathies. Arthritis Rheum 1995;38:1005-13. Branigan PJ, Gérard HC, Hudson AP, et al. Comparison of synovial tissue and synovial fluid as the source of nucleic acids for detection of Chlamydia trachomatis by polymerase chain reaction. Arthritis Rheum 1996;39:1740-6. Li F, Bulbul R, Schumacher HR Jr, et al. Molecular detection of bacterial DNA in venereal-associated arthritis. Arthritis Rheum 1996;39:950-8. Nikkari S, Puolakkainen M, Yli-Kerttula U, et al. Ligase chain reaction in detection of chlamydia DNA in synovial fluid cells. Br J Rheumatol 1997;36:763-5. Vittecoq O, Schaeverbeke T, Favre S, et al. Molecular diagnosis of Ureaplasma urealyticum in an immunocompetent patient with destructive reactive polyarthritis. Arthritis Rheum 1997;40:2084-9. Tully JG, Rose DL, Baseman JB, et al. Mycoplasma pneumoniae and Mycoplasma genitalium mixture in synovial fluid isolate. J Clin Microbiol 1995;33:1851-5. Csonka GW. Long-term follow-up and prognosis of Reiter's syndrome. Ann Rheum Dis 1979;38(suppl):24-8. Good AE. Reiter's syndrome: long-term follow-up in relation to development of ankylosing spondylitis. Ann Rheum Dis 1979;38 (suppl):39-45. Popert AJ, Gill AJ, Laird SM. A prospective study of Reiter's syndrome. An interim report on the first 82 cases. Br J Vener Dis 1964;40:160-5. Bas S, Cunningham T, Kvien TK, et al. The value of isotype determination of serum antibodies against chlamydia for the diagnosis of chlamydia reactive arthritis. Br J Rheumatol 1996;35:542-7. Frydén A, Bengtsson A, Foberg U, et al. 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Comparison of sulfasalazine and placebo in the treatment of reactive arthritis (Reiter's syndrome): a Department of Veterans Affairs ative Study. Arthritis Rheum 1996;39:2021-7. Egsmose C, Hansen TM, Andersen LS, et al. Limited effect of sulphasalazine treatment in reactive arthritis. A randomised double blind placebo controlled trial. Ann Rheum Dis 1997;56:32-6. Owen ET, Cohen ML. Methotrexate in Reiter's disease. Ann Rheum Dis 1979;38:48-50. Calin A. A placebo controlled, crossover study of azathioprine in Reiter's syndrome. Ann Rheum Dis 1986;45:653-5. Lauhio A, Leirisalo-Repo M, Lähdevirta J, et al. Double-blind, placebo-controlled study of three-month treatment with lymecycline in reactive arthritis, with special reference to chlamydia arthritis. Arthritis Rheum 1991;34:6-14. Pott HG, Wittenborg A, Junge-Hulsing G. Long-term antibiotic treatment in reactive arthritis. Lancet 1988;1:245-6. R, on HR, Tempest B, et al. Chlamydial infection and arthritis. J Rheumatol 1989;16:846. 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All rights reserved. -------------------------------------------------------------------------------- Sorry guys and gals, I only look this stuff up. I didn't write it. The problem is that most people have mollicutes in their system anyway. The question is does another virus or pathogen's presence allow them to become active and cause the problem, as in molecular mimicry or are they the 'trigger' of the autoimmune disease. These very early microbes have been overlooked to a great degree in their potential to cause disease. The micobacteria require cholesterol for their survival. the uyrealiticum require urea to survive. I keep finding cross references in disease process with microbacteria (also known as mycoplasma) and viruses. We all know that M. tuberculosis causes uveitis and arthritis and lung disease. Why not these other 27 as well? Wishing all good health, Mike B -------------------------------------------------------------------------------- Quote Link to comment Share on other sites More sharing options...
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