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 Other forms of osteomyelitis Osteomyelitis of the clavicle This condition is rare and repre sents less than 3% of all cases of osteomyelitis, and may be associated with subcla- vian v enous catheterization. Staph. aureus is the common- est implicated organism. Frequency of follow-up There are no clear guidelines recommending the frequency of follow-u p in patients with osteomyelitis. However, per- sistently raised in \202 ammatory markers indicating evidence of ongoing sepsis are an indication for close supervision. Persistent s oft tissue changes on MR, especially in the spine, indicate an unfavorable prognosis. Prognosis Osteomyelitis remains a dif \201 cult management problem and the rate of relapse is as high as in 1 in 5. Multidisciplinary team Close liaison between orthopedic surgeon, microbiolo- gist, and spin al or neurosurgeons in patients with spinal infection is vital. Physiotherapy is important in the rehabili- tation of the patient with osteomyelitis, and exercise aims to improve mus cle tone and strength. Occupational thera- pists should be involved in all patients with fu nctional im- pairment. Patient advice \200 Compliance with antibiotic therapy is vital for eradiac- tion/control of infection. The man agement plan is formed in each case depending on the individual clinical situation of the i ndividual patient. Resources Websites http://www.patient.co.uk/showdoc/40001112/ Figure 16.1 This is a coronal T2 fat saturated image showing a well circumscribed \202 ui d collection within the proximal tibial metaphysis. It is surrounded by a bone enhancing wa ll and ill-de \201 ned enhancement in the adjacent bone. A tract I seen extending proximal ly to the articular surface of the lateral tibial plateau. http://cks.library.nhs.uk/patient_information_ leaflet/Osteomyelitis OSTEOMYELITIS 456 ICD-10 codes M86.0 Acute haematogenous osteomyelitis M86.1 Other acute osteomyelitis M86.2 Subacute osteomyelitis M86.3 Chronic multifocal osteomyelitis M86.4 Chronic osteomyelitis w ith draining sinus M86.5 Other chronic haematogenous osteomyelitis M86.6 Other chronic oste omyelitis M86.8 Other osteomyelitis M86.9 Osteomyelitis, unspeci \201 ed Gold RH, Hawkins RA, Katz RD. Bacterial osteomyelitis: \201 ndings on plain radiography, CT, MR and scintigraphy. Am J Roentol 1991; 157: 365 \200\22370. Reihaus W, Waldbaur H, Seeling W. Spinal epidural abscess: a meta- analysis of 915 patients. Neurosurg Rev 2000; 23: 175 \200\223204. Sia IG, Berbari EF. Osteomyelitis. Best Pract Res Clin Rheumatol 2006; 20: 1065 \200\22381. Waldvogel FA, Medoff G, Swartz MN. Oteomyelitis: a review of the clinical features: therape utic considerations and unusual aspects. N Engl J Med 1970; 282: 198 \200\223206. References Cierny 3d G, Mader JT, Penninck JJ. A clinical staging system for adult osteomyelitis. Clin Orthopaed Related Res 2003; 414: 7 \200\22324. This page intentionally left blank SOFT TISSUE INFECTION 458 Soft tissue infection \200 Cellulitis De \201 nition Cellulitis is an infection of the dermis and subcutis that produ ces a warm, red, tender area of skin. Erysipelas is the term used to describe super \201 c ial cellulitis, which often in- volves the face, but also involves the local lymphatic drai n- age, resulting in raised shiny plaques. Those with immunocompromise. Those patients with cellulitis that is resistant to oral anti- biotic therapy. It is important to consider cellulitis due to MRSA in those patients who a re not responding to standard therapy. If multi-organism infection is likely, broad spectru m antibi- otic therapy is necessary. Occasionally, prolonged antibi- otic therapy lasting 6 weeks is necessary for complete resolution of infection. Clinical features \200 Patients may be systemically unwell with malaise and fever. Locally, the skin appears warm with erythema and may be tender to touch. It is often poorly demarcated, and severe infecti on may result in oedema, vesicles, bullae, and necrosis. The lower limb is most commonly af fected. Skin trauma and animal bites act as portals of entry for skin infection. Recurrent episodes of cellulitis in the same location often re \202 ect local anatomical abnormaliti es, e.g. in the lymphatic system, which occur as a result of previous infection. Differential diagnosis Infection \200 \200 \200 \200 Bacterial. Viral, e.g. herpes simplex virus. Fungal, e.g. Candida. Parasitic, e.g. Mycobact erium. \200 Non-infectious causes \200 \200 \200 Panniculitis, e.g. erythema nodosum, lupus panniculitis. Neutrophilic disease, e.g. Sweet \200\231s syndrome. Connective tissue disease, e.g. acute phase of sys- temic sclerosis, ca lcinosis cutis on dermatomyositis, relapsing polychondritis. Others, e.g. sarcoidosis, eryt hromelalgia, compart- ment syndrome. Neoplastic. Metastatic. Vascular. Metabolic, e.g. gout . Iatrogenic, e.g. drug eruption, radiotherapy, foreign body. Pathogenesis \200 The commonest causative organisms are Staph. aureus and Strep. pyogenes. The commonest site of cellulitis is the lower limb. Multi-organism cellulitis usually arises from infection w ith anaerobes and Gram negative aerobes, and is often implicated in patients with chronic u lcers. Necrotizing infection, where there is crepitus associated with the cellulitis and a thin discharge, may evolve into myonecrosis and is usually caused by Clostridium perfrin- g ens. Bacteroides, Peptostreptococci, Peptococci and Prevotella may also cause myonecrosis. Unusual or opportunistic infections are commoner in patients who are immunocompromised or i mmunosup- pressed. \200 \200 \200 \200 \200 Bursitis Bursae may be classi \201 ed as deep (beneath \201 brous fascia) or super \201 cial, and are closed sacs lined with synovium that in normal circumstances produce a small amount of lubri- cating \202 uid. There are around 150 bursae, and these act as buffers against friction and facilitate movement of adjacent tissues over one another. While some b ursae are present from birth, others are acquired in response to recurrent pressure. Bursit is may arise as part of a localized or sys- temic in \202 ammatory process, or secondary t o infection. Investigations \200 There may be no signi \201 cant elevation of in \202 ammatory markers or a neurophilia. B lood cultures are often negative. Skin biopsy may be useful in patients with resistant infe c- tion, especially when non-infectious causes are included in the differential diagnosis. Skin biopsies should undergo special stains for fungi and mycobacteria, and for culture. Bu llae and ulcers should be swabbed, and the swab sent for culture. \200 Non-septic bursitis \200 Non-septic bursitis due to recurrent trauma or pressure is associated with specific activit ies or occupations. Recurrent pressure over speci \201 c bursae resulting in non- septic i n \202 ammation has been linked with speci \201 c occu- pations. For example, housemaid \200\231s knee is used to describe a prepatellar bursitis and clergyman \200\231s knee is u sed to describe infrapatellar bursitis. Non-septic bursitis is common in gout and rheumatoi d arthritis Imaging Imaging with MR or ultrasound is indicated if there is a possibility of deep soft t issue infection or a local collection, and MR is the imaging technique of choice where asso ci- ated osteomyelitis is suspected. Treatment of routine cellulitis The majority of cases can be managed in an outpatient setti ng with oral antibiotics, the choice of which should cover both Staph. aureus and Strep. py ogenes. Patients who require admission to hospital include: \200 Those who are systemical ly unwell. \200 Those with systemic features of sepsis. Septic bursitis \200 Infection is more likely in super \201 cial, rather than deep bursae because of the increa sed risk of trauma in super- \201 cial tissues. The bursae that most commonly become infe cted are the olecranon, prepatellar, and super \201 cial infrapatellar. CHAPTER 16 Musculoskeletal infection 459 The route of infection is thought to be due to direct inoculation from local trauma, which may be chronic or acute. Infection due to haematogenous spread is rare. Predisposing featur es include diabetes mellitus, alcohol abuse, and previous non-septic bursitis. Bite wounds are associated with mulitorganism infection, and include Eikenella corrodens, H aemophilus sp., and anaerobes such as Veillonella. N. gonorrhoeae is the commonest cause of infection due to haematogenous spread. Mycobacterial tenosynovitis is associated with fres h and salt water exposure, when M. marinum is often isolated. Causative organisms \200 \200 80% of cases are caused by Staph. aureus. The remainder are caused by B haemolytic strepto cocci, coagulase negative staphylococci, enterococci, and occa- sionally Gram negative orga nisms. Brucella, tuberculosis, and Candida have all been isolated in refractory cases of bu rsitis. Clinical features \200 Those tendons most commonly involved are the \202 exor tendons of the hand, although infe ctious tenosynovitis can occur in any tendon sheath. There is usually a history of trauma i n which introduc- tion of the causative organism, such as via an animal bite or scratch, oc curs. Haematogenous spread is, however, recognized and in particular with N gonorrhoeae. In the hand, communication may exist between the ten- don sheath and adjacent bursae, allowin g spread of infection into adjacent tissues. In the thumb or little \201 n- ger a communi cating bursa allows infection on both the dorsum and palm of the hand in the shape of a hor se- shoe, with the collection termed a horseshoe abscess. The typical \201 ndings include tenderness, symmetrical enlargement of the affected \201 nger, a \202 exed \201 nger at rest, and exquisite pain on passive extension. Gonococcal infection most commonly affec ts the exten- sor tendons, unlike other infections. Mycobacterial infection presents with a chronic, insidi- ous onset. Atypical infection presents 2 \200\2234 weeks after inoculatio n, and a nodular cellulitic process, called a \201 sh tank granuloma, develops. There may be an obvious puncture wound that may reveal evidence of infection. Necrosis of the tendon may occur if infection is untreated. Host immunity is important in determining response to infection, and immunocompromised or immunosup- pressed patients may have more extensive in fection than those with normal immunity. Clinical features \200 The typical presentation is of pain and erythema over the affected bursa. There may be a hi story of trauma. There may be a previous history of bursitis. Patients may be systemically unwell with a fever. Joint mobility is preserved in uncomplicated bursitis. \200 \200 \200 Investigations \200 The total white cell count is normally elevated, typically with a neutrophilia. There may b e an elevation of in \202 ammatory markers. Imaging may reveal bursal \202 uid, bursal s ynovitis, and associated abscesses. Aspiration of the affected bursae may reveal purulent \202 uid, which should be sent for gram stain, culture, and microscopy under polarized lig ht. Fluid should be examined for acid fast bacilli in resistant cases. \200 Treatment \200 Uncomplicated super \201 cial bursitis responds well to anti- biotics. Gram stain and cult ures should guide antibiotic choice. If cultures are negative, antibiotics should cover Sta ph. aureus and streptococci. Standard therapy starts with intravenous antibiotics until the infection starts to settle, followed by oral antibiotics. Total duration of antibiotics is usually up to 4 weeks, although some cases settle within this time allowing dis- continuat ion of therapy. Broad spectrum antibiotics may be required in patients with resistant bursi tis. Surgical incision and drainage may be required in cases where resolution is slow. \200 Investigations \200 There may be an elevated total white cell count, but this is not a universal \201 nding. Plain radiographs are unhelpful. Ultrasound may reveal in \202 ammation within the tendon sheath. MR is useful in to determine the extent of infection. \200 Diagnosis Diagnosis is made on the basis of Gram stain and culture, either by needle aspira tion or at the time of surgical exploration. Prognosis The prognosis of bursitis is good, although infection due to tuberculosis or Bruc ella may require prolonged therapy, and may relapse on cessation of treatment. Treatment \200 Infectious tenosynovitis De \201 nition Infectious or suppurative tenosynovitis occurs whe n infec- tion occurs in a closed synovial tendon sheath. Prophylactic antibiotics should be administered to all patients with animal bites. If infec tious tenosynovitis is suspected, empirical antibi- otics should be started following needl e aspiration of the tendon sheath. Antibiotic choice should be guided by the history and li keliest organism Surgical treatment is advised due to the high rate of tendon necrosis, and should be undertaken in all but the earliest cases of infection, and in these cases too if infec- tion is not improving with antibiotics in the \201 rst 24 h. Causative organisms The organisms implicated in infectious tenosynovitis de- pend on the ex posure and trauma. \200 Streptococci, Staph. aureus, and S. epidermidis are mostly implicated, with Gram negative o rganisms and entero- cocci implicated less commonly. SOFT TISSUE INFECTION 460 Repeat debridement and extensive tenosynovectomy may be necessary in cases where infection is resistant to antibiotic therapy. Creatinine kinase is usually within the normal range, and blood cultures are positive in up to 30% of cases. Staph. aureus is the commonest organism, implicated in 70% of cases in th e developed world. Fungi and microsporidia are rarely seen in patients who are not immunoco mpromised. Myositis Infectious myositis may be caused by viruses, bacterial infection, fungi, and para sites. The pattern may be focal or diffuse depending on the cause, but in general, bacteria and fungi cause focal myositis whereas viral and parasitic myositis is more diffuse. Treatment A combination of surgical drainage and broad spectrum antibiotics is usually requ ired, pending microbiological cul- ture. Culture of the pus obtained at the time of drainag e is mandatory to isolate the underlying organism. Antibiotic cover should cover Staph. aur eus. If MRSA is suspected, vancomycin should be introduced as part of the broad spectrum co ver. Close liaison with microbiological col- leagues is necessary pending culture sensitivi ties. Treat- ment results in an excellent prognosis in those patients who do not have septi caemia, and should be continued intravenous for 3 \200\2234 weeks. Viral myositis A large number of viral infections may result in myalgia or myositis and inc lude adenovirus, Coxsackie B, Echovirus, Epstein-Barr, Hepatitis B, HIV, HTLV-1, mumps, Par vovirus, Rubella virus, Varicella zoster and West Nile virus. In \202 uenza virus, especia lly in \202 uenza B virus may result in myositis, with a preponderance for the muscle in t he calf. Coxsackie B infection causes chest wall myalgias, and is known as Bornholm disease or pleurodynia syndrome. Psoas abscess Psoas infection often arises from nearby sources, such as the gastrointestina l tract, e.g. in patients with Crohn \200\231s dis- ease, diverticular disease, or malignan cy. Other sources of infection include gynecological infection or rarely haema- togenous sp read. Staph. aureus or mycobacterium tubercu- losis may arise from vertebral osteomyelitis. Bacterial myositis Bacterial myositis is classi \201 ed as: \200 \200 \200 Staphylococcal. Streptococcal. Gram negative organisms, e.g. Enterobacteria, Pseu- domonas, Aeromonas, etc. Anaerobes, e.g. clostridium, bacteroides, Fusobacterium, Peptostreptococcu s, etc. Systemic infection, such as endocarditis, may also result Clinical features Patients present with back or lower abdominal pain, fever, and pain on we ight bearing, with an antalgic gait. The psoas sign (passive extension of the hip) may be p ositive. in myalgias, with small abscess formation the cause. Investigations CT or MR are the investigation of choice. Pyomyositis Pyogenic myositis is classi \201 ed as: \200 \200 \200 Treatment Treatment consists of surgical drainage and antibiotic therapy tailored to the or ganism. Gram negative cover should be considered, especially if a gastrointestinal origin i s implicated. Clostridial myonecrosis (gas gangrene). Group A streptococcus necrotizing myositis. Non-clo stridial myositis, e.g. anaerobic streptococcal myonecrosis. Pyomyositis is commoner in the developing world than in the west, and results from trauma, poor nutrition, and con- comitant infection. Immunocompromised patients, such as those with HIV infection, patients prescribed glucocorti- coids, or those with co-morbidities such as diabetes melli- tus or malignancy are at increased risk. Infection is thought to arise fro m bacteraemia and seedlings of infection within a focal area of muscle. Three stages occur of pyomyositis occur: \200 \200 \200 Gas gangrene This is a rapidly progressive infection with necrosis of muscle tissue and sev ere systemic upset. The infectious agent is almost always clostridium perfringes and the co m- monest presentation is following trauma, where the wound has been contaminated with soil or dirt, although infection may arise in wounds following gastrointestinal surgery, in- fe ction sites, or in ischaemic tissue. Clostridium septicum may result in gas gangrene, but i n the absence of an entry wound. Bacteraemia is usually associated with gastrointes- tinal pathology, such as colitis or malignancy. C. novyi, and other clostridia species account fo r a small number of cases of gas gangrene. Bacteria are deposited within the muscle. Suppurative stage, with abscess formation. System ic infection with septicaemia. Clinical features Pain and swelling of the affected muscle, with systemic upset is typical, although often there is little to \201 nd clini- cally as the infection is deep. As the abscess grows, the cardinal features of in \202 ammation become more apparent. The most co mmonly areas affected are the large muscle groups of the lower limb, and is multifocal in a round 20% of cases. Diagnosis may be challenging. For example, an il- iopsoas abscess may r esemble appendicitis and an obtura- tor internus abscess may mimic septic arthritis of the hip. History Rapid tissue necrosis presents with swelling, lack of bleed- ing and loss of elasti city. The pathological process occurs as a result of a toxin \200\223 alpha toxin, which s plits lecithin and inhibits leukocytes. The history varies from 6 h to 21 days following in jury, and is associated with severe pain. The wound is often offensive smelling and in \202 ammed. Gas bubbles may appear in the adjacent skin, resulting in crepi- tus and gas ma y be emitted from the wound. Patients are normally systemically unwell with hypotension and shock. Investigations Imaging with MR or CT are the preferred methods of imag- ing in pyomyositis. There is normally an acute phase re- sponse seen on routine blood tests and a leucocytosis is usual except in patients who are immunocompromised. Investigations The total WBC is normally elevated. Haemolysis may re- sult. Blood cultures are positive in 15% and a Gram stain on the biopsied tissue may con \201 rm Gram positive bacilli. CHAPTER 16 Musculoskeletal infection 461 Treatment Urgent surgical exploration and debridement, with fasci- otomies or amputation is required. Antibiotic regimes include high dose intravenous penicillin and clindamycin. cause a rise in CK. 3 weeks following infection, serological tests will become positive and diagnosis is normally made on this basis, rather than on muscle biopsy; this may show larv ae, but identifying which species they belong to may be dif \201 cult. Outcome Even with aggressive treatment, mortality is high, and in the region of 25%. Treatment Albendazole or mebendazole are effective, but mostly in the gastrointestinal phas e of the infection. Muscle larvae are very dif \201 cult to treat. In life-threatening com plications, there is a role for high dose glucocorticoid therapy. Dis- ease prevention incl udes careful food preparation and cooking. Group A streptococcal necrotising myositis This is a common cause of cellulitis and soft ti ssue infec- tion. Occasionally, this organism results in myositis, for which the terms are group A streptococcal necrotizing myositis, streptococcal myonecrosis, or gangrenous myosi- tis. It usually arises in patients under 50 and with no other co-morbidities or history of trauma, but often arises in conjunction with a systemic, toxic shock-like syndrome. Cysticercosis This parasitic infection arises from the ingestion of under- cooked pork infe cted with Taenia solium eggs. Infected water is also implicated as a source of infection. T he eggs enter the body via the gastrointestinal tract and reach the muscles via the bloodst ream. They may be deposited in the central nervous system, heart, and eye, in addition to m us- cle. Incubation takes from weeks to years. Presentation \200 Stage 1: prodromal illness, often with sore throat and myaligia/arthralgia lasting 3 \200 \2237 days. Stage 2: rapid onset and worsening of pain, usually in the leg, with skin invol vement including discolouration and bullae formation. Stage 3: overwhelming sepsis with mul ti-organ failure. Symptoms Myalgias, fever and eosinophilia may occur, although the neurological manifestatio ns include seizures, headaches, or psychiatric manifestations. Investigations Microbiological culture of tissue removed at surgical ex- ploration and debr idement is mandatory. Leucocytosis and high in \202 ammatory markers may not be present in the early stages. Creatine kinase may be elevated. Investigations Serological tests are the main method of diagnosis. Plain radiographs may re veal calci \201 ed casts within the muscles. This appearance is described as puffed rice i n appearance. Treatment Urgent surgical debridement, and high dose penicillin and clindamycin are necessa ry, but mortality may be as high as 85%. Treatment Treatment is with praziquantel or albendazole with con- comitant glucocorticoid t herapy as antifungal agents may cause swelling of the infected lesions, which is of particu lar clinical relevance in neurological infection. Anaerobic streptococcal myonecrosis This is very similar to gas gangrene and may be caused by streptococcal infection, both anaerobic and group A, or Staph. aureus. Treatment is with surgical debridement and antibiotics. Other parasitic infections Other parasitic infections include acute schistosomiasis, Chaga \200\231s disease, and toxocariasis. Resources ICD-10 codes L03 M71.0 Bursitis M71.2 Bursitis M73.0 Bursitis M73.1 Bursitis M65. 0 M65.1 M60.0 Myositis Other bacterial causes of myonecrosis Other causative agents include Bacillus and Aeromonas . Cellulitis Parasitic infection Trichinosis This parasitic infection occurs after eating under-cooked i nfected meat, normally pork. Incubation is 1 \200\2232 weeks fol- lowing ingestion. The lar vae penetrate the intestinal wall of the host and are then spread by haematogenous carriage . Infectious tenosynovitis Infectious tenosynovitis Symptoms Mild gastrointestinal symptoms may occur, then muscle pain and tenderness develop. Involved muscles often in- clude those in the head and neck, such as the masseter, peri-or bital, and tongue muscles. The diaphragm may also be involved. Neurological and cardiac com plications also occur. References Kroshinsky D, Grossman ME, Fox LP. Approach to the patient with presumed cellulitis. Semin Cutan Med Surg 2007; 26: 168 \200\22378. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis. Infect Dis Clin N Am 2005; 991 \200\2231005. Wadia NH, Katrak SM. Muscle infection: viral, parasitic, bacterial, and spirochaetal. In Sc hapira AHV, Griggs RC (eds) Muscle Diseases. Boston: Butterworth Heinemann, 1999: 339 \200 \22362. Investigations An eosinphilia is usually found, but may be the only abnor- mality on blood tests. Signi \201 cant infection is required to RHEUMATIC FEVER 462 Rheumatic fever De \201 nition Rheumatic fever is a delayed, multisystem disease that occurs following gro up A streptococcal infection of the pharynx. The pathogenesis and immune mechanisms are still not completely understood. The host \200 \231s humoral and cell-mediated immune response to the bacterium s antigens determine the s everity of the individual clinical response, although the virulence of the streptococcal sp ecies is also important. The strains of group A streptococcus associated with acute rheumat ic fever may express an M protein or antiphagocytic component in their cell wall. A decreas ing incidence of acute rheumatic fever in the United States over the past 50 years is corre lated with the falling incidence of streptococcal pharyngitis in chil- dren. This may be du e to changing strains of group A streptococcal infection. Spectrum of disease Rheumatic heart disease is a major cause of morbidity and mortality in low and middle income countries, and among underprivileged communities in high income coun- tries. Primary prevention of acute rheumatic fever is pos- sible with adequate antibiotic treatment of streptococcal throat infections. Diagnostic criteria \200 The modi \201 ed Jones criteria are commonly used to diag- nose the initial attack of acut e rheumatic fever. The probability of acute rheumatic fever is high when there is evidence of recent streptococcal infection (increase in the antistreptolysin O titre) with either tw o major, or one major and two minor manifestations. Permanent damage to heart valves may re sult from recurrent attacks of rheumatic fever. The other major manifestations are transien t and do not lead to permanent damage but are important in the diagnosis. Clinical presentation of acute rheumatic fever Key features in history and examination \200 There is normally a history of sore throat, which pre- cedes other symptoms by an average o f 3 weeks (range 1 \200\2235 weeks). The modi \201 ed Jones criteria for the diagnosis of acute rheumatic fever are necessary as the presentation is variable. A high index of clinic al suspicion is necessary. Arthritis \200 A migratory pattern of joint involvement is seen, with several joints being affected at any one time, with synovi- tis persisting for around a week before settling. However, despite the use of NSAIDs, the pain is often more severe than the clinical \201 ndings. Those joi nts involved normally include the large weight bearing joints, with a very small minority p resenting with only small joint involvement. Modi \201 ed Jones criteria for diagnosis of acute rheumatic fever, 1992 Major criteria \200 Carditis \200 Polyarthritis \200 Erythema marginatum \200 Subcutaneous nodules \200 Chorea Carditis \200 Cardiac symptoms are variable, and include non-speci \201 c chest discomfort or symptoms o f heart failure. New or changing murmurs may be found on examina- tion. The commonest is a mitral regurgitant murmur, although aortic regurgitation is also a feature. If extensive va lvular disease occurs, signs of congestive cardiac failure may be detected, needing urgent and aggressive therapy. Varying degrees of heart block are recognized. First degree heart b lock is asymptomatic and other sympto- matic forms may require pacing. Minor criteria \200 \200 \200 \200 Prolonged P \200\223R interval on electrocardiogram Arthralgia Fever Acute phase reactants Plus supporting evidence of a preceding streptococcal infection for both major and minor cr iteria Epidemiology \200 Chorea \200 Acute rheumatic fever is prevalent in developing coun- tries, where there is overcrowding a nd poor access to health care. The highest reported incidence of acute rheumatic fever is i n indigenous populations of Australia and New Zealand, although incidence is yet to be esta blished in many developing countries. The estimated annual number of cases in those popula- tions with a high incidence is 374 per 100 000 population in the 5 \200\22314 years age gr oup with 60% estimated to develop rheumatic heart disease. In the west, the incidence has d ropped to fewer than 1 per 100 000 population. An abrupt, non-rhythmic, involuntary movement disor- der is characteristic of Sydenham \200 \231s chorea or St Vitus \200\231 dance. Classically, these movements disappear during slee p but recur on waking and are present at rest. Facial muscles may also be involved and invo luntary grimacing and smiling may occur. Muscle weakness can be detected in the milking sig n when the patient is asked to squeeze the \201 ngers of the examiners hand. The patients grip contracts and releases continuously as if the patient were milking. Inappropriate beh avior is a manifestation of neurologi- cal involvement Skin involvement \200 Etiology and pathophysiology \200 Subcutaneous nodules lasting less than a month are painless and \201 rm. They vary in siz e, but may be as large as 2 cm, when they may mimic rheumatoid nodules. It is well established that group A beta haemolytic strep- tococcus causes acute rheumatic fever, but not by a direct toxic effect. CHAPTER 16 Musculoskeletal infection 463 Erythema marginatum is a pink or red rash generally found on the trunk and limbs, but with sparing of the face. The term marginatum describes the resolution of the rash from the cent er giving a ring like appearance. The lesions may come and go, and are normally associ- ate d with carditis. Intramuscular penicillin is preferred as it is more effec- tive than oral penicillin and en sures better compliance. Surgery Urgent valve replacement may be life saving in a patient with decompensating cardia c failure, and is a more com- mon cause of heart failure than myocardial disease in rheumat ic fever. If possible, repair of a damaged valve is preferred to prosthetic replacement. Minor manifestations \200 \200 Fever, up to 40 C, normally settles after 1 \200\2233 weeks. Abdominal pain is non-speci \201 c and usually begins at the start of the illness. Acute phase reactants are a non-spec i \201 c \201 nding. Physical therapies Current practice is that physical activity should be re- stricted until the acute episode has settled, and then should be built up slowly. There is no evidence-bas e for this advice. Investigations \200 Follow-up Regular follow-up is necessary and optimizes timing of val- vular heart disease s urgery. Throat cultures should be performed but are usually negative by the time rheumatic fever pr esents. Antistreptolysin O and anti-DNAse in paired sera at baseline and 2 weeks later may indicate recent strepto- coccal infection if there is an elevation in titres. ECG and echoc ardiography are useful to diagnose and monitor cardiac involvement, and will detect mild ca ses of carditis in patients who are asymtomatic. ECG is nec- essary to pick up elongated P \200\223R intervals. Typical valvu- lar lesions such as valve lea \202 et and chordal thic kening, lea \202 et shortening, mitral annular dilation, lea \202 et pro- lapse, and chor dal elongation are easily identi \201 ed. Synovial \202 uid is sterile. Joint involvemen t may be picked up on plain radiographs as non-speci \201 c soft tissue swelling. Patient advice \200 Good compliance with antibiotics is imperative to ensure lower risk of rheumatic heart dise ase. Patients should be encouraged to seek medical attention for future sore throats. Resources Guidelines WHO guidelines. Report of a WHO Expert Consultation. World Health Orga nization. ISBN-13 9789241209236 \200 Internet sites http://cks.library.nhs.uk/patient_information_ leaflet/Rheumatic_fever Natural history \200 \200 Mortality occurs in 5%. 60% develop rheumatic heart disease within 10 years of infection. http://www.patient.co.uk/showdoc/40000571/