Joint drainage Pus should be removed from an infected joint either by needle aspiration or arthroscopically. Repeated joint lavage may be required. A prosthetic joint with suspected infection should al- ways be referred to an orthopedic surgeon. CHAPTER 16 Musculoskeletal infection 447 References Jordan KM, Cameron JS, Snaith M, Zhang W, Doherty M, Seckl J, Hingorani A, Jaque s R, Nuki G on behalf of the British Society for Rheumatology and British Health Profession als in Rheumatology Standards, Guidelines and Audit Working Group (SGAWG). British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the Managem ent of Gout. Rheumatology, 2007; 46: 1372 \200\2234. Other conditions Crystal arthritis \200 Aspirate joint and consider injection of intra-articular corticosteroids. Use NSAIDs or col chicine as appropriate. In \202 ammatory arthritis Aspirate joint and consider intra-articular corticosteroids. Us e NSAIDs and oral/intramuscular steroids as necessary. Treat underlying in \202 ammatory a rthritis. Mathews C, Field M, Jones A, et al. BSR, BHPR, BOA, RCGP and BSAC guidelines for the manage ment of the hot swollen joint in adults. Rheumatology 2006; 45: 1039 \200\22341. Haemarthrosis Aspirate joint arthroscopically to dryness. Investigate for causes of bleedin g if no history of trauma. See also Synovial \202 uid analysis Bacterial infections Crystal arthritis Resources Guidelines BSR, BHPR, BOA, RCGP and BSAC. Guidelines for the Man- agement of the Hot Swollen Joint in Adults. BSR and BHPR. Guidelines for the Management of Gout. SEPTIC ARTHRITIS 448 Septic arthritis De \201 nition Septic arthritis is a pyogenic infection within a joint, and is a medical e mergency with an associated mortality and morbidity. Prompt diagnosis and appropriate treat ment are imperative to limit cartilage destruction, and to preserve a good functional outco me. Immunode \201 ciency virus (HIV) infection should be con- sidered in intravenous drug abus ers. Pre-existing joint disease: the risk of haematogenous spread is increased due to incre ased blood \202 ow into abnormal joints. Co-morbidities: diabetes, malignancy, chronic or gan fail- ure, e.g. established renal or liver disease, skin disease. Prosthetic joints. Classi \201 cation Classi \201 cation is usually on the basis of the causative organ- ism . Staphylococcus aureus is the commonest organism isolated in septic arthritis. Staphylococcus aureus immunopathology \200 Staph. aureus septic arthritis causes the most severe joint destruction because of the rang e of extracellular toxins and degradative enzymes produced by this par- ticular organism. S ome strains are encapsulated, which aids the virulence of the organism. Staphylococcal adhe sions, expressed on the bacterial surface, enable the organism to adhere to and invade host tissue, and facilitate penetration of joints. Soft tissue infection is much more likely to be caused by staphylo- coccal strains without the ability to express adhesin. Some toxins, named superantigens, are responsible for the release of cytokines, such as tumor necrosis factor and interferon gamma, which result in fever, hypotension, and the features of severe systemic sepsis. The immune response of the host is also central to the severity of presen tation of infection. T cell action, which occurs in the adaptive immune response, aggravate s the damage caused by joint sepsis, and elimination of T cell activity reduces mortality a nd joint damage. B cell deple- tion appears to have no effect on outcome following septic a rthritis. The innate immune system protects against infection by staphylococci, and the sev erity of infection is more marked in hosts in which there are complement de \201 ciencies. Epidemiology Incidence \200 Septic arthritis is relatively rare and is estimated at 6 per 100 000 per year in developed countries, with those under 15 and over 55 representing the highest risk groups. Septic ar thritis is more likely to occur in individuals with pre-existing joint disease, e.g. prosth etic joints or in \202 am- matory arthritis. In patients with rheumatoid arthritis, the in cidence is estimated to be around 70 per 100 000 per annum. Common causative organisms Gram positive septic arthritis \200 Gram positive cocci cause 50 \200\22370% of bacterial septic arthritis with Staph. aureus, S. epidermidis, and strepto- cocci (pyogenes, group B and G) the most commonly isolated org anisms. In contrast, Group C Streptococci, pneumococci, and Gram positive bacilli are more rarely implicated. Gram negative septic arthritis \200 Gram negative infection is most commonly caused by Neisseria species, with N. gonorrheoa an d N. meningitides the most common agents. Haemophilus in \202 uenzae, previously a commonl y impli- cated pathogen in pediatric infection, is less frequently seen since the introduct ion of the HIB (Haemophilus in \202 uenzae type b) vaccine. Gram negative rods cause less than 20% of septic arthri- tis, with E. coli, Proteus mirabilis, Klebsiella, and entero- ba cter the most commonly implicated organisms in this group. Pseudomonas aeruginosa infection is rare and usually found in the elderly. Less than 1% of septic arthritis is caused by an aerobic bacteria. Clinical features High clinical suspicion allows early diagnosis. Key features in the history \200 There is usually sudden onset of severe pain and swell- ing, with functional disability. Pa tients usually, but not always, feel systemically unwell. There may be a history of recent/ continuing distant infection. Rigors occur in patients with fever, but may also be a featur e of crystal arthritis. The age of the patient is relevant as extremities of age make septi c arthritis more likely. There may be a history of pre-existing joint disease. Recent instr umentation, e.g. arthroscopy or joint aspira- tion and injection should be established. Imm unosuppressive therapies, such as glucocorticoid therapy, are important risk factors. Antic oagulation is not a risk factor for infection, but it is important to check clotting prior to joint aspiration in those patients who are anticoagulated. Recent antibiotic treatment s hould be established as iso- lation of the causative organism is more dif \201 cult in thi s setting. Polyarticular infection occurs in up to 22% of cases. \200 Risk factors for septic arthritis \200 \200 \200 \200 Age: the extremes of ages are more susceptible. Gender: similar incidence is seen in men an d women Distal infection: septic arthritis most usually arises from haematogenous spread fr om a distal focus. Instrumentation: sepsis following joint aspiration or arthroscopy is rar e and is estimated at 1 in 15 000 to 1 in 50 000. Immunosuppression: for example, with gluc ocorticoids. Alcoholism. Intravenous drug abuse: the puncture site is the portal of entry f or organisms, and is most commonly contami- nated with Staph. aureus. Underlying concomitan t Human \200 \200 CHAPTER 16 Musculoskeletal infection 449 Useful tips \200 Some patients have no fever and a subacute onset, making diagnosis more challenging. Polyar ticular sepsis is rare and is usually found in patients with predisposing factors. Cellulitis may co-exist, and iatrogenic septic arthritis may occur as a result of inserting a needle through infected skin. In this situation, the diagnosis of septic arthritis may n eed to be made pragmatically on the basis of clinical \201 ndings. If \202 uid cannot b e aspirated from a potentially septic joint, consider asking another experienced doctor, or request- ing an ultrasound-guided aspiration. If a patient is anticoagulated with warfarin , an urgent INR should be checked, and anticoagulation reversal considered if the INR is gr eater than 3.5. An icepack will induce vasoconstriction and may reduce the risk of haemarth rosis. Key features on examination \200 Fever is a non-speci \201 c feature, and may also occur in crystal arthritis. The absence of fever does not exclude septic arthritis. Tachycardia is uncommon in the elderly but is o ften present in younger patients. Hypotension occurs in patients with septicaemia. The join t is tender and the patient is reluctant to move it actively or to allow passive movement. Erythema of the overlying skin is common and there may be an associated cellulitis or bursi tis. Effusion is usually present. Distant infection, e.g. skin, nasopharyngx, chest, urine, endocarditits should be sought. \200 \200 Differential diagnosis \200 \200 \200 \200 \200 Crystal arthritis. Infection in the overlying soft tissues, e.g. bursitis, cellulitis. Mono arthritic presentation of in \202 ammatory arthritis. Trauma. Haemarthrosis. Investigations Laboratory \200 \200 A neutrophilia is typical, but not universally found. An in \202 ammatory response is usua l with CRP responding more quickly than ESR. Renal impairment may re \202 ect systemic sep sis. Liver function tests may be deranged in sepsis. Autoantibodies are not helpful in diag nosing sepsis. Blood cultures are positive in around 33% of septic arthritis and should be collected in all patients. Objectives of management Treat infection \200 \200 \200 \200 If clinical suspicion is high, but initial microscopy of syno- vial \202 uid negative, tr eatment with antibiotics should be commenced. Consult local policy for antibiotic choice in septic arthritis. Antibiotic choice should cover Staph. aureus, the com- monest pathogen, unless clinical features suggest a differ- ent organism, whilst awaiting culture and sensit ivities. Antibiotics must only be started after aspiration of syno- vial \202 uid and col lection of blood for culture. Intravenous \202 ucloxacillin (2 g qds) and benzyl penicill in (1.2 g qds) cover the majority of staphylococcal and streptococcal species. In penicilli n allergic patients, clin- damycin 450 \200\223600 mg qds IV or 2nd or 3rd generation cepha losporin IV is appropriate. If methacillin resistant staphylococcus aureus (MRSA) is a poss ibility, intravenous vancomycin is the antibiotic of choice. If there is a high risk of Gra m negative sepsis, antibiotic choice should be 2nd or 3rd generation cephalosporin. Close l iaison with microbiology colleagues is advised. The evidence base for the duration of antib iotic therapy is not established but current practice is to treat for a total of 6 week, wi th 2 week of intravenous therapy followed by 4 weeks of oral therapy. Markers of infections , such as in \202 ammatory markers and white cell count should be monitored, and would be expected to fall over the \201 rst 7-14 days. All patients with possible septic arthritis of a prosthetic joint should be referred urgently to the on call ortho- paedic team for as piration and further management. \200 Imaging \200 Plain radiographs are unhelpful diagnostically in early septic arthritis, but establish pre -existing joint disease and non-speci \201 c soft tissue swelling. The earliest plain radi ographs changes are seen after 2 weeks in patients with untreated infection. Ultrasound may be useful in determining synovitis and effusion, and aid accuracy of diagnostic aspiration . Nuclear medicine scans detect non-speci \201 c in \202 amma- tory joint disease. MR sca ns are helpful if soft tissue infection or osteomy- elitis are suspected, but are unhelpful in early infection. Synovial \202 uid aspiration \200 \200 Joint aspiration, with microscopy and culture of the synovial \202 uid, is the single mos t important diagnostic test. Frank pus may be aspirated, making the diagnosis more likely. The sample should be sent to the laboratory immediately it has been taken and not left for routine transportation. Organisms are cultured in 50 \200\22370% of septic arthritis. Cryst al arthritis and sepsis can co-exist. High neutrophil count, high lactate, and low glucose are the typical characteristics in septic synovial \202 uid. PCR on synovial \202 uid i s often non-speci \201 c and 20% of RA cases have detectable bacterial DNA, rendering this an unhelpful test in septic arthritis. Hip aspiration should be undertaken under ultrasoun d/ image intensi \201 er control, and should be considered for other joints if blind aspir ation is unyieldy. \200 \200 Remove pus \200 Pus contains toxins and enzymes released by the organ- ism, which are damaging to cartilage . Pus should there- fore be removed as a matter of urgency. There are no studies comparing arthroscopic lavage with repeated joint lavage, but close liaison with ortho- paedic collea gues is advised. The joint should be aspirated to dryness either by closed needle or arthro scopically, and may need to be repeated. Other tests Cultures/swabs should be collected if distant site of infec- tion is likely, e. g. genitourinary, respiratory. SEPTIC ARTHRITIS 450 Investigations In early infection, in \202 ammatory markers and neutrophil count will be e levated, although they are less reliable in delayed and late infection. Conventional radiog raphs are often unhelpful, but may show loosening and rarefaction of the bone surrounding t he prosthesis. Imaging with US, CT and MR will be more helpful, and should be undertaken fo llowing discussion with radiological colleagues. Pros- thetic joints should be aspirated by orthopedic surgeons, usually in theater under sterile conditions, and only if the risk of prosthetic infection is greater than the risk of intro- ducing infection into a non-infecte d prosthetic joint. Pain relief NSAIDs and analgesia should be given to all patients with no contraindication t o these therapies. Short-term opioid analgesia should be considered in those patients with inad- equate pain control. Rehabilitation \200 It is unclear at which point rehabilitation of the joint should occur. Early mobilization o f the joint is a balance between reducing damage during infection and preventing muscle was ting/contractures. One approach is to start rehabilitation as the indicators of infection o n blood tests are falling, and the patient is feeling more comfortable. Management of prosthetic infection Management depends of the age of the patient and the len gth of time there has been infection present in the joint. Each case is assessed individual ly. Options include: \200 \200 \200 Management of immunosuppressive agents \200 Patients on DMARD therapies for RA are at risk of infec- tion due to their rheumatoid arthr itis and the immuno- suppressive effect of the DMARDs. There is no evidence to suggest stop ping DMARD therapy in patients with septic arthritis. In patients treated with anti-TNFA ag ents, current BSR recommendation is to withhold anti-TNFA therapy for 12 months following i nfection. No studies have explored the possibility of introducing anti-TNFA earlier than th is. In patients prescribed regular long term glucocorticoid therapy, additional glucocortic oid should be considered to prevent Addisonian crises. Irrigation of the joint. Single stage procedure to replace the prosthesis. Two-stage proced ure, with treatment with antibiotics between removal of the \201 rst prosthesis and the r eplace- ment with a second. Long-term antibiotics and leaving the prosthesis in place. Remo val and arthrodesis. Amputation of the affected limb. Close liaison with microbiology colle agues is essential. In those patients who undergo a revision, antibiotics can be mixed into the cement, and can make up to 20% of the cement mixture, although the addition of antibio tics may compromise the cement resulting in weakness. \200 Prosthetic joint infection The possibility of prosthetic joint infection should be re- ferr ed to the on call orthopedic team who will be aspi- rate the joint under sterile conditions , usually in theater, a technique which should not be undertaken by teams other than the or thopedic surgeons except in exception circumstances because of the potential risk of introd ucing infection into a non-infected prosthetic joint. Unusual sites for septic arthritis \200 Septic arthritis of the symphysis pubis is rare and often follows uro-gynecological surgery . The differential diag- nosis includes osteitis pubis, a non-infectious in \202 amma- tor y condition seen in athletes. Septic arthritis of the sacroiliac joint is uncommon and usua lly occurs as a result of Staph. aureus infection. Intravenous drug abusers are particularl y at risk. Endo- carditis should be excluded. Brucella infection can result in unilateral s acroilitis. Predisposing factors for prosthetic infection. \200 \200 \200 \200 \200 \200 \200 \200 Poor nutritional status. Underlying joint disease, e.g. rheumatoid arthritis. Obesity. Diab etes mellitus. Malignancy. Remote infection. Skin disease. Revision surgery (the risk of in fection in revision sur- gery is estimated at 4% compared with 0.5% in \201 rst replaceme nts). Advice to patients with septic arthritis \200 \200 \200 Bed rest during the acute episode is recommended. Pain management aids early rehabilitation . Soft tissue swelling may occur and doesn \200\231t necessarily indicate worsening of infe ction. Completing the course of antibiotics and good compli- ance is vital to the eradicati on of infection and prevent- ing antibiotic resistance. Exercise should be undertaken withi n the limits of pain and as the signs and symptoms of infection improve. Modi \201 cation of risk factors for risk factors, for example, high blood sugars in diabetic patients shoul d be addressed. The risk of permanent deformity/loss of function may be should be discussed , especially in patients with a delayed diagnosis. Clinical features \200 Early infection occurs within 3 months of surgery. Patients present with pain and systemic symptoms. On examination, the patient is pyrexial and has a tachycardia. Examination of the wound and joint reveal erythema, tenderness, and sometimes a hot, gaping wound. Early infe ction is usually due to Staph. aureus or Gram nega- tive bacilli. Delayed infection occurs between 3 and 24 months after surgery, and is associated with subtle signs. Persistent pain arises as a result of in \202 ammation and early loosening. Late infection occurs after a n uncomplicated 2-year period following surgery and is always due to haematog- enous spread . The main sources of infection are skin, respiratory, urinary, and dental sources. Prognosis and natural history \200 Mortality is reported in up to 11%, but in elderly patients with rheumatoid arthritis and p oylarticular sepsis, mor- tality may be as high as 50%. Functional impairment is as high as 70%. CHAPTER 16 Musculoskeletal infection 451 Monitoring infection A settling neutrophil count, in \202 ammatory markers and fever are r eassuring. If these indicators of infection are not settling, consider: \200 \200 \200 \200 \200 Resources Guidelines C. Mathews, M. Field, A. Jones, et al on behalf of the British Society for Rheumatology Standards, Guidelines and Audit Working Group Rheumatology. BSR & BHPR, B OA, RCGP, and BSAC. Guidelines for the Management of the Hot Swollen Joint in Adults 2006; 45: 1039 \200\22341. Reculturing of blood and synovial \202 uid. Establishing patient compliance with antibiot ics. Dose/route of delivery of antibiotics. Reviewing antibiotic sensitivities. Searching f or distal or other deep seated infection, e.g. disciitis. Internet sites for patient group www.patient.co.uk/showdoc/27000235 ICD-10 codes M00 \200\223M03 Infectious arthropathies. M00.0 M00.1 M00.2 M00.8 Follow-up Follow-up is recommended at the end of antibiotic therapy and once more following cessation of antibiotic therapy. For those patients with permanent functional disability, joint replacement is an option. However, eradication of infection must be undertaken before surgery is contem- plated. Staphylococcal arthritis and polyarthritis Pneumococcal arthritis and polyarthritis Other s treptococcal arthritis and polyarthritis Arthritis and polyarthritis due to other speci- \201 ed bacterial agents pyogenic arthritis, unspeci \201 ed. M00.9 References Kaandorp CJ, Dinant HJ, van der Laar M, et al. Incidence and sources of native a nd prosthetic joint infection: a community based pro- spective survey. Annl Rheumat Dis 199 7; 56: 470 \200\2235. Current controversies \200 It remains unclear if glucocorticoid therapy or bisphos- phonates may modify the in \202 a mmatory response during infection, and therefore reduce the potential structural and functi onal damage in a joint. It is unlikely there will ever be trials of intra-articular glucoco rticoid or bisphos- phonates in patients with septic arthritis. However, there is some limi ted data in children to suggest a bene \201 cial effect on functional outcome at 1 \200 \2232 years following sepsis in those who received a short course of oral prednisolone. The re are no studies comparing joint lavage with arthro- scopic washout, although removing pus from the joint, by either technique, is appropriate. There are no studies comparing the di fferent durations of antibiotic therapy, and the proposed 6 weeks of anti- biotic therapy h as been adopted as standard practice on the basis of clinical experience. The potential for a vaccine to protect against Staph. aureus, remains a theoretical development for the futu re, although efforts to date have been unsuccessful. Odio CM, Ramirez T, Pharmd GA, et al. Double blind, randomized, placebo-controlled study of dexamethasone therapy for hema- togenous septic arthritis in children. Pediat Infect Dis J 2003; 22: 883 \200\2238. Patti JM, Bremell T, Krajewska-Pietrasik D, et al. The Staphylococcus aureus collagen adhes in is a virulence determinant in experimen- tal septic arthritis. Infect Immun 1994; 62: 15 2 \200\22361. Shirtliff ME, Mader JY. Acute septic arthritis. Clin Microbiol Rev 2002; 15: 527 \200\22344. Tarkowski A. Infectious arthritis. Best Pract Res Clin Rheumatol 2006; 20: 1029 \200\22344. Verdrengh M. Carlsten H. Ohlsson C. Tarkowski A. Addition of bisphosphonate to antibiotic a nd anti-in \202 ammatory treatment reduces bone resorption in experimental Staphylococcus aureus- induced arthritis. J Orthopaed Res 2007; 25: 304 \200\22310. GONOCOCCAL ARTHRITIS 452 Gonococcal arthritis Neisseria gonorrhoeae is the second commonest cause of all sexually transmitted infection i n the UK. Transmission is via the mucosa, of the urethra, endocervix, pharynx, rectum, and the conjunctiva of the newborn. Occasionally, infection may involve the fallopian tubes, or can result in bacteraemia, involvement of the skin and/or arthritis. N. gonorrhoeae is an obligate human pathogen and a fastidious organism, and therefore requires a nutritious medi um and supplements such as glucose and iron for growth. Other musculoskeletal manifestations include pyomyosi- tis and osteomyelitis. Hepatitis and meningeal involve- ment are other life-threatening complications. Investigations \200 Leucocytosis and high in \202 ammatory markers are typi- cally found. Synovial \202 uid microscopy and culture is likely to reveal Gram negative diplococci in around 50% of cases, with a similar yield from blood cultures. Both intra- and extracellular organisms may be s een on Gram stain. Isolation of the organisms is dif \201 cult and transfer of syn- ovial \202 uid to culture media should be undertaken as soon as possible and if practical, at t he bedside. Cultures from the mucosa of the genital tract have a yield of around 80%. A det ailed sexual history is imperative to identify which mucosal surfaces should be swabbed and in order to arrange contact tracing. Involvement of col- leagues in the sexual health team is advised. Co-existing chlamydial infection should be excluded, along with other sexually transmitted diseases. PCR has a role in diagnosis, although is less useful than routine cu lture as antibiotic resistance and sensitivity are not possible with this technique. Speci \201 city of PCR is high at 97% and sensitivity is between 78 and 80%. Nucleic acid ampli \201 cation is a technique that enables earlier detection of gonococcal infection. Epidemiology and risk factors \200 Young people are most commonly infected, with current rates highest in males aged 20 \200 \22324 years and females aged 16 \200\22319 years. The highest rates are found in London an d predomi- nantly urban areas. Gonococcal infection tends to be concentrated in core preven tion groups. In the UK these include homo- and bisexual men, and black ethnic minority popu lations. Multiple sexual partners leads to higher risk of exposure, and other co-existing s exually transmitted infections. In 2006, there were 19 007 cases diagnosed in sexual health clinics in the United Kingdom. The true number of cases is estimated to be considerably gr eater. Mucosal infection progresses to disseminated infection in 0.5 \200\2233% of patients . The associated arthritis is seen in sexually active young adults, with a ratio of men to women of 1:3. One expla- nation for this difference is that women may present later and, th erefore, with more widely disseminated infection. Only 25%, mostly men, report genital infe ction. The incidence of gonococcal infection is falling in both the USA and Europe as a res ult of education programs, and is currently lower in Europe than in the USA. The host facto rs that aid dissemination include preg- nancy, menstruation, and immunosuppressed states su ch as lupus, HIV, and hypocomplementaemia. The Health Protection Agency has a role in monit oring the rates of gonococcal infection and antibiotic resist- ance in the UK. Management \200 Antibiotic resistance has resulted in increased need to obtain microbiological con \201 rm ation prior to treatment. Antibiotic resistance has increased since the late 1980s, and has limited the use of penicillin in patients with gonococcal infection. In England and Wales, cipro \202 oxacin was the recom- mended \201 rst-line therapy until resistance reached 5% in 2002. Since then guidelines have been revised to recommend the use of the third gener ation cephalosporins, ce \201 xime (oral) or ceftriaxone (intramuscular). Azithromycin is not a recommended \201 rst-line therapy for gonorrhea, but should be used at a 2-g dose, rather than the 1-g dose used for Chlamydia infections. Parenteral antibiotics are recommen ded for the \201 rst 24 \200\22348 h, and this should be followed by a further 7 days of oral antibiotics. Repeat cultures should then be considered to ensure eradication. In gonoc occal arthritis, the joints should be washed out/ repeatedly aspirated to remove purulent \202 uid. Patients should be screened for other sexually transmit- ted infections Partners should be contacted for appropriate investiga- tion and treatment, and contact screening. \200 Clinical features \200 The polyarthralgia of gonococcal infection is asymmetri- cal, may be severe, and be associa ted with a fever. The pattern of joint involvement is typically migratory and may resolve s pontaneously. The skin rash is typically discrete, with papular, pustular or vesicular lesi ons and is not itchy. The rash appears on the limb and trunk, but there is sparing of the f ace and scalp. Arthritis occurs in less than half of cases although teno- synovitis occurs in two-thirds, and can be dif \201 cult to dif- ferentiate from arthritis. Monoarticular j oint involvement is more common than polyarticular disease, with knees, wrists, ankles, and \201 n- ger joints being the most commonly affected. In cases where diagnosis is delayed , endocarditis, myo- carditis, pericarditis, and conduction abnormalities indicate cardiac involvement. Resistance mechanisms Resistance to penicillin can result from the acquisition of a plasmid , which inactivates penicillin, (penicillinase-producing N. gonorrhoeae) or from multiple m utations, which reduce the permeability of the membrane (chromosomally-mediated CHAPTER 16 Musculoskeletal infection 453 Current controversies The development of a protective vaccine against Neisseria gonorrhea i s an area of ongoing research. resistant N. gonorrhoeae). Resistance to cipro \202 oxacin arises as a result of mutations in the DNA gyrase gene, and the topoisomerase gene IV, which are responsible for super- co iling of DNA within the bacterial cell. Resistance is usu- ally high-level and affects all the quinolones. Resources ICD-10 codes A54.4 Gonococcal infection of unsculosketel system M01.3 Arthritis M 73.0 Bursitis M90.2b Osteomyeitis M68.0 Synoritis M68.0 Tenosynovitis Differential diagnosis The differential diagnosis includes all causes of hot swollen joint, including septic arthritis due to all causes, monoar- thritis due to in \202 ammatory art hritis, trauma, etc. Advice \200 Limiting the number of sexual partners, and consistent and correct use of condoms helps to reduce the inci- dence of gonorrhea and other sexually-acquired infec- tions. Compliance wi th the full prescribed course of antibiot- ics ensures both eradication of infection and re duces the risk of antibiotic resistance. Contact tracing is vital to prevent transmission o f gono- coccal infection to other sexual partners, and to prevent morbidity due to unrecogn ized or silent infection. Websites www.bashh.org http://www.hpa.org.uk/infections/topics_az/ hiv_and_sti/Stats/STIs/gonorrhea/default.htm References Ghosn SH, Kibbi AG. Cutaneous gonococcal infections. Clin Dermatol 2004; 22: 476 \200\22380. Gray-Swain MR, Peipert JF. Pelvic in \202 ammatory disease in adoles- cents. Curr Opin Obstet Gynecol 2006; 18: 503 \200\22310. Prognosis \200 Olshen E, Shrier LA. Diagnostic tests for chlamydia and gonor- rhoeal infection. Semin Paediat Infect Dis 2005; 16: 192 \200\2238. Untreated gonorrhea may result in pelvic in \202 ammatory disease in women, the consequenc es of which include chronic pain and dysparunia, infertility, and an increased risk of ecto pic pregnancy. Infection in the mother can be transmitted to the baby during delivery, resu lting in neonatal conjunctivitis, which is responsive to antibiotic treatment. Chronic infe ction may result in joint damage, but early treatment is associated with a favorable outcom e with no long-term sequelae. Rice PA. Gonococcal arthritis (disseminated gonococcal infection). Infect Dis Clin N Am 2005; 19: 853 \200\22361. Tapsall JW. Antibiotic resistance in Neisseria gonorrhoeae. Clin Infect Dis 2005; 41(Suppl 4): S263 \200\2238. OSTEOMYELITIS 454 Osteomyelitis Osteomyelitis is one of the most dif \201 cult infectious dis- eases to treat. Progressive bony destruction and the for- mation of sequestra are hallmarks of this infectious process . It can arise as a result of: \200 \200 \200 Diagnosis is usually made of the combination of clinical, radiological, and culture of bone specimens. Management It is vital to obtain samples for microbiology prior to com- mencing antibiotic therapy. Bone sampling, blood culture, and surgical sampling, are all possible methods of i solating the causative organism. Culture of bone reveals the organ- ism in 94% of cases. Wo und swabs, however, in patients with sinus formation, are susceptible to normal skin \202 ora colonization, and are therefore less sensitive and give rise to false positive culture s. Haematogenous seedling. Contiguous spread of infection. Direct inoculation into intact bone . Classi \201 cation There are two main systems of classi \201 cation. \200 The Waldvogel classi \201 cation uses the duration of dis- ease, the mechanism of infectio n, and the presence of vascular insuf \201 ciency within the bone. Cierny \200\223Mader cl assi \201 cation is based on portion of bone involved, the physiological status of the hos t, and other risk factors including pre-existing co-morbidities, such as malignancy, vascul ar disease, and diabetes. Treatment A combination of surgical exploration, debridement, and adequate doses and durati on of the appropriate antibiotic to eradicate infection is required. The aims of surgery ar e to drain infected tissue, debride necrotic tissue, and re- move infected metal ware. Dead space is eliminated, and stabilization of bone with either bone grafts or using exter- nal \201 xation devices may be necessary, depending on the extent of the infection. There is no evidence base guiding the length of treatment of antibiotic therapy, but standard pract ice determines a course of 4 \200\2236 weeks of an antibiotic which is able to penetrate bo ne well. Long bone osteomyelitis Long bone osteomyelitis may arise either from haematog- enous or co ntiguous spread of infection with the most commonly implicated organism being Staph. aureus . How- ever, coagulase-negative staphylococcus, aerobic Gram negative bacteria (such as ent erococci, Pseudomonas, Proteus and E. coli) and Peptostreptococcus species are also fairly commonly isolated from cultures in osteomyelitis. Less commonly, infection may be due to my cobacterial in- fection, Mycoplasma, Salmonella, Brucella, or fungal agents. Open fracture osteomyelitis Between 2 and 25% of open fractures are complicated by infectio n, and the type of fracture, the degree of soft tissue damage and contamination of the woun d at the time of injury in \202 uence the likelihood of the development of infec- tion. A delay in surgical reduction and debridement of more than 5 h has been shown to be associate d with a higher risk of infection. The tibia is the commonest site of osteomyelitis followi ng an open fracture, usually in young men between 20 and 30 years of age. Infection results in non-union, chronic infection, and eventually, if untreated or refractory to treatment, amputation may be required. Clinical features The presenting symptoms in subacute infection are vague and usually non-s peci \201 c, for example, low grade fever and poorly localized pain of insidious onset. Ex amination may reveal fever, with local swelling and tenderness over the affected site. In t hose with co-existing soft tissue infection, the tissues may be tender and erythematous, an d with a discharging sinus. Rarely patients may be acutely systemi- cally unwell, with sign s of sepsis. Signs of distant infection, such as endocarditis should be sought in all cases . A high index of suspicion is necessary in all cases. Clinical features Infection usually becomes clinically obvious a few months after the injur y, with symptoms of bone pain and fever, and erythema and localized pain on examination. Investigations \200 Although there may be a neutrophilia in acute cases, a normal total white cell count may be found in chronic cases. In \202 ammatory markers, such as ESR and CRP are usually elevate d, and may be used to monitor response to treatment. Imaging of bone using plain radiograph s may indicate bone destruction and destruction of the cortex of the bone after 14 days fol lowing the onset of infection. MR and CT, however, provide greater resolution of bone and s oft tissue. Figure 16.1 is an example of the MR appearance of osteomyelitis. Metal, such as that in pros- thetic joints, interferes with image quality and therefore signi \201 cantl y reduces the ability of these techniques to provide detail in adjacent bone. Isotope bone scans are non-speci \201 c. Radiolabelled white cell scans may help localize infection. Mi crobiological investigations include blood cultures, bone biopsy, and culture either follow ing needle biopsy or surgical exploration. Investigations The need for microbiological cultures and the surgical management of open fr acture osteomyelitis is identical to that of long bone osteomyelitis. Often more than one o r- ganism may be isolated as skin \202 ora are more likely to be implicated in infection following open fracture than in os- teomyelitis due to haematogenous spread of an organism. Management of infection risk in open fractures Parenteral antibiotic therapy should be admi nistered within 6 h of injury and for a period of 7 \200\22310 days. More prolonged prophyl actic antibiotic therapy is not indicated as there is no evidence this reduces the risk of chronic infection and bacterial resistance may result. Vertebral osteomyelitis and disciitis Vertebral osteomyelitis and disciitis usually arise f rom hae- matogenous spread from a distant focus of infection in the skin, the gastrointesti nal, the genitourinary, or the respira- tory tracts. The origin of infection may remain obs cure. Gram negative aerobic bacilli and Candida are seen in pa- tients who abuse intravenou s drugs. The segmental arterial CHAPTER 16 Musculoskeletal infection 455 circulation of the vertebrae is the most likely route of haematogenous spread to the spine. Lumbar vertebral infection is the most common site of infection and may result in epidural extension. If the abscess becomes more extensive, involvement of the subdural space may oc cur with paravertebral, mediastinal, retroperitoneal, and psoas muscle infection arising as a complication. Disc space infec- tion may also arise. spinal or nerve root involvement. These new symptoms should be investigated with further ur gent imaging and may require surgery. Bony fusion occurs after 1 \200\2232 years of infecti on. Osteomyelitis in diabetics \200 15% of patients with diabetic foot ulcers will develop osteomyelitis and, of these, 16% wil l require amputation to eliminate infection. 36% of patients develop recurrent infections. It can be dif \201 cult to differentiate between super \201 cial foot ulcers and osteomye litis, but in general, the larger the ulcer (>2 cm) and the greater the depth (>3 mm) and t he more bone that is visible, the higher the risk of osteomyelitis. Surgical resection or a mputation is often necessary, and the duration of antibiotic therapy should last for at lea st 4 weeks and be guided by clinical response. Clinical features The symptoms comprise insidious pain and spinal tenderness. 15% have symp toms and signs of nerve root compression at presentation. Fever is present in less than hal f of patients. Investigations \200 In \202 ammatory markers are normally elevated as is the neutrophil count. The organism ma y be isolated on blood cultures. MR is the imaging technique of choice and details the absc ess clearly. \200 Osteomyelitis in patients with rheumatoid arthritis Patients with rheumatoid arthritis have a higher risk of osteomyelitis due to Staph. aureus, mycobacterial, and fun- gal infection than in the general population. Presentation, especially if there are multiple foci of inf ection, may present as a generalized rheumatoid \202 are. CT-guided biopsy may be undertaken of the abscess, but will only reveal an organism in arou nd 50% of cases. Staph. aureus and coagulase negative staphylococci are the com- monest org anisms. Management \200 \200 Management is normally conservative. Surgical debridement should be reserved for those pati ents with neurological compromise who are not responding to conservative treatment with ant ibiotics, or those who have signi \201 cant bone destruction. Antibiotics should be contin ued for 4 \200\2236 weeks and repeat imaging with MR will con \201 rm resolution of the in fection. Inflammatory markers can be used to monitor the response to treatment in combinati on with the patient \200\231s clinical state. Neurological examination should be performed daily or if new symptoms develop to ensure early detection of